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Schmidt, Lindsay, and Jeffrey Myers. "Bronchioloalveolar Carcinoma and the Significance of Invasion: Predicting Biologic Behavior." Archives of Pathology & Laboratory Medicine 134, no. 10 (October 1, 2010): 1450–54. http://dx.doi.org/10.5858/2010-0227-cr.1.
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Abstract A resected adenocarcinoma illustrates challenges in diagnosing bronchioloalveolar carcinoma (BAC). Bronchioloalveolar carcinoma is defined by lack of invasion, something that may be difficult to assess in scars. Small (≤0.5 cm) invasive foci have little impact on the good prognosis associated with low-stage tumors. The term microinvasive adenocarcinoma or minimally invasive adenocarcinoma has been proposed for otherwise typical BACs and small invasive foci measuring 0.5 cm or less. Larger areas of invasion are associated with a more aggressive course and more reliably distinguish BAC from other variants of adenocarcinoma. Separating BAC from other forms of adenocarcinoma is important owing to differences in prognosis and emerging therapeutic strategies.
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Chang, Kevin Y., and Wellington K. Hsu. "Spinal Biologics in Minimally Invasive Lumbar Surgery." Minimally Invasive Surgery 2018 (April 5, 2018): 1–15. http://dx.doi.org/10.1155/2018/5230350.
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As the use of minimally invasive spine (MIS) fusion approaches continues to grow, increased scrutiny is being placed on its outcomes and efficacies against traditional open fusion surgeries. While there are many factors that contribute to the success of achieving spinal arthrodesis, selecting the optimal fusion biologic remains a top priority. With an ever-expanding market of bone graft substitutes, it is important to evaluate each of their use as it pertains to MIS techniques. This review will summarize the important characteristics and properties of various spinal biologics used in minimally invasive lumbar surgeries and compare their fusion rates via a systematic review of published literature.
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Vrbničanin, Sava, and Dragana Božić. "Biological invasions: The example of weed species." Acta herbologica 23, no. 2 (2014): 97–112. http://dx.doi.org/10.5937/actaherb1402097v.
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Heiss, Kirsten, Hui Nie, Sumit Kumar, Thomas M. Daly, Lawrence W. Bergman, and Kai Matuschewski. "Functional Characterization of a Redundant Plasmodium TRAP Family Invasin, TRAP-Like Protein, by Aldolase Binding and a Genetic Complementation Test." Eukaryotic Cell 7, no. 6 (April 25, 2008): 1062–70. http://dx.doi.org/10.1128/ec.00089-08.
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ABSTRACT Efficient and specific host cell entry is of exquisite importance for intracellular pathogens. Parasites of the phylum Apicomplexa are highly motile and actively enter host cells. These functions are mediated by type I transmembrane invasins of the TRAP family that link an extracellular recognition event to the parasite actin-myosin motor machinery. We systematically tested potential parasite invasins for binding to the actin bridging molecule aldolase and complementation of the vital cytoplasmic domain of the sporozoite invasin TRAP. We show that the ookinete invasin CTRP and a novel, structurally related protein, termed TRAP-like protein (TLP), are functional members of the TRAP family. Although TLP is expressed in invasive stages, targeted gene disruption revealed a nonvital role during life cycle progression. This is the first genetic analysis of TLP, encoding a redundant TRAP family invasin, in the malaria parasite.
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Medina Villaamil, Vanessa, Guadalupe Aparicio Gallego, Francisco Gomez Veiga, Manuel Valladares Ayerbes, Maria Quindós Varela, Natalia Fernandez Nunez, Aurea Molina Diaz, Isabel Santamarina Cainzos, and Luis Miguel Anton Aparicio. "Using biologic knowledge to discover molecular correlations between human renal cell carcinoma pathways." Journal of Clinical Oncology 32, no. 4_suppl (February 1, 2014): 451. http://dx.doi.org/10.1200/jco.2014.32.4_suppl.451.
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451 Background: Renal cell carcinoma (RCC) is known to be resistant to chemotherapy. There is need for the identification of biomarkers capable to determine RCC prognosis factors and metastatic potential obtainable from non-invasive or minimally invasive techniques. Our aim was to derive predictive models which could predict more accurately than any one factor alone. Methods: To studythe cascade of events leading to the formation and progression of RCC, we assessed 29 markers by immunohistochemistry and qRT-PCR using tissue micro-array (TMA). Results: Multivariate logistic regression showed the best proteins combination for node status (NOTCH1 and GLUT5) and pelvis invasion (EGFR and DLL3). ROC curve analyses were made to analyse the accuracy of the best candidate proteins; it should be noted NOTCH1 and GLUT5 for node status prediction (AUC=0.833, 95% CI, 0.744-0.922; p<0.001) and EGFR and DLL3 for pelvis invasion (AUC=0.777, 95% CI, 0.631-0.922; p=0.007). Furthermore, we carried out the correlation between these candidate proteins and all mRNA measured in order to deepen in the cellular transcripts traffic associated with them. To highlight the correlation between high DLL3 protein levels and low Hif1-β expression, and the negative correlation between GLUT5 protein and low levels of Baxβ. Conclusions: In the age of individual therapy, the approach to percutaneous image-guided RCC biopsy procedures plays an expanded role. Applying a 2 mm punch needle for constructing a TMA we could describe for the first time how are combined and correlated 29 markers in regression equations to predict in the most optimal way a number of pathological variables associated with RCC. [Table: see text]
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Osek, Jacek, and Kinga Wieczorek. "Listeria monocytogenes—How This Pathogen Uses Its Virulence Mechanisms to Infect the Hosts." Pathogens 11, no. 12 (December 7, 2022): 1491. http://dx.doi.org/10.3390/pathogens11121491.
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Listeriosis is a serious food-borne illness, especially in susceptible populations, including children, pregnant women, and elderlies. The disease can occur in two forms: non-invasive febrile gastroenteritis and severe invasive listeriosis with septicemia, meningoencephalitis, perinatal infections, and abortion. Expression of each symptom depends on various bacterial virulence factors, immunological status of the infected person, and the number of ingested bacteria. Internalins, mainly InlA and InlB, invasins (invasin A, LAP), and other surface adhesion proteins (InlP1, InlP4) are responsible for epithelial cell binding, whereas internalin C (InlC) and actin assembly-inducing protein (ActA) are involved in cell-to-cell bacterial spread. L. monocytogenes is able to disseminate through the blood and invade diverse host organs. In persons with impaired immunity, the elderly, and pregnant women, the pathogen can also cross the blood–brain and placental barriers, which results in the invasion of the central nervous system and fetus infection, respectively. The aim of this comprehensive review is to summarize the current knowledge on the epidemiology of listeriosis and L. monocytogenes virulence mechanisms that are involved in host infection, with a special focus on their molecular and cellular aspects. We believe that all this information is crucial for a better understanding of the pathogenesis of L. monocytogenes infection.
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Ochsenkühn, Thomas, Constanze Waggershauser, Cornelia Tillack-Schreiber, Isabel Braun, Maximilian Sohn, Franz Bader, June Munich, and Fabian Schnitzler. "SAFETY OF PERIOPERATIVE BIOLOGICS IN PATIENTS WITH IBD UNDERGOING RESECTIVE BOWEL SURGERY: THE MUNICH IBD CENTER EXPERIENCE." Inflammatory Bowel Diseases 29, Supplement_1 (January 26, 2023): S2. http://dx.doi.org/10.1093/ibd/izac247.003.
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Abstract BACKGROUND AND AIMS The risk of biologics in the peri-operative setting in IBD is still discussed controversially. Recently, the large prospective PUCCINI trial could demonstrate that direct exposure to TNF-blockers within 12 weeks before abdominal surgery was not associated with a higher risk of infectious complications. However, in daily clinical practice experiences on biological treatment perioperatively are limited. In our current retrospective trial, we addressed the safety of different biologicals in a peri-operative setting. METHODS Eligible IBD patients in this single center study were recruited from our Munich IBD center between January 2012 and May 2022, who underwent bowel surgery at our Department of Surgery. Direct exposure to biologics was defined as exposure to biologics within 12 weeks before abdominal surgery. To evaluate safety, the postoperative outcome focused on minor complications, defined as infectious complications, wound healing complications and major complications, defined as insufficiency of the anastomosis and abscess formation at the surgery site postoperatively. RESULTS A total of 447 IBD patients (334 CD/113 UC, 51.9% female) were included and were followed for a median time of 45 months [range 0-113]. Median age was 44 years [19-89], median age at diagnosis was 24 years [5-84] and median age at surgery was 41 years [16/85]. Median disease duration until surgery was 11 years [0-47]. With 74.3%, the majority of IBD patients had moderate to severe IBD disease activity at date of surgery. A total of 73.9% (326/447) had medical treatment at date of surgery, 61.5% (275/447) were treated with biologics within 3 months before surgery and 42.3% (189/447) had biologics within 4 weeks before surgery. Overall, 36.9% of patients (164/447) received infliximab, 13.0% (58/447) adalimumab, 1.1% (6/447) golimumab, 5.8% (26/447) vedolizumab, 6.5% (29/447) ustekinumab, perioperatively. The majority of surgeries was planned electively (97.1%, 434/447), and performed laparoscopically (67.8%, 303/447). Minor and major postoperative complications occurred in 20.8% (93/447) of patients. Serious complications were observed in a total of 9 patients, six patients had acute bleeding complications postoperatively, 1 patient developed peritonitis and 2 CD patients died postoperatively, one with and one without biologics. No significant differences regarding complications and safety were observed between patients with versus without biologic treatment. Interestingly, CD patients with direct exposure to biologics were more likely to undergo minimal-invasive surgery (63.1%, 135/214) than patients without exposure (28.3%, 34/120, p<0.05). CONCLUSIONS This retrospective single center study of 447 IBD patients could demonstrate that biologic treatment before sugery, even within 4 weeks, is not associated with a higher risk of complications.
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Biswas, Tithi, Charulata Jindal, Timothy L. Fitzgerald, and Jimmy T. Efird. "Pathologic Complete Response (pCR) and Survival of Women with Inflammatory Breast Cancer (IBC): An Analysis Based on Biologic Subtypes and Demographic Characteristics." International Journal of Environmental Research and Public Health 16, no. 1 (January 4, 2019): 124. http://dx.doi.org/10.3390/ijerph16010124.
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In this US-based study of the National Cancer Database (NCDB), we examined 8550 patients diagnosed with non-metastatic, invasive inflammatory breast cancer (IBC) who received surgery from 2004–2013. Patients were grouped into four biologic subtypes (HR+/HER2−, HR+/HER2+, HR−/HER2+, HR−/HER2−). On average, women were 56 years of age at diagnosis and were followed for a median of 3.7 years. The majority were white (80%), had private health insurance (50%), and presented with poorly differentiated tumors (57%). Approximately 46% of the cancers were >5 cm. Most patients underwent mastectomy (94%) and received radiotherapy (71%). Differences by biologic subtypes were observed for grade, lymph node invasion, race, and tumor size (p < 0.0001). Patients experiencing pathologic complete response (pCR, 12%) vs. non-pCR had superior 5-year overall survival (OS) (77% vs. 54%) (p < 0.0001). Survival was poor for triple-negative (TN) tumors (37%) vs. other biologic subtypes (60%) (p < 0.0001). On multivariable analysis, TN-IBC, positive margins, and not receiving either chemotherapy, hormonal therapy or radiotherapy were independently associated with poor 5-year survival (p < 0.0001). In this analysis of IBC, categorized by biologic subtypes, we observed significant differential tumor, patient and treatment characteristics, and OS.
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Manthri, Sukesh, Muhammad Iqbal, Kathy Robinson, Robert S. Mocharnuk, and Meghna R. Desai. "Tumor biologic characteristics and clinical outcomes in geriatric patients with breast cancer." Journal of Clinical Oncology 35, no. 15_suppl (May 20, 2017): e21526-e21526. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.e21526.
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e21526 Background: The probability of dying from breast cancer increases from 0.2% to 2% annually for women once they reach 70 years of age. However there is limited age-related information available about tumor biologic characteristics (TBCs) and clinical outcomes among elderly patients (pts). The purpose of this study was to analyze the impact of TBCs on clinical outcomes in a single institution's geriatric breast cancer pts. Methods: An institutional database of a total of 269 patients with histologically confirmed invasive or in-situ breast cancer with age 65 years or older at the time of diagnosis was reviewed in an IRB approved fashion. Tumors were assessed for Nottingham grade, stage, ER/PR status, HER-2 status, tumor histology, lymphovascular invasion and nodal status. Kaplan-Meyer and Cox proportional hazards methods were used to calculate overall survival (OS). Results: Breast cancer was seen equally in both breasts: left n = 130 (48.3%), right n = 132 (49.1%). Most tumors were located in the upper outer quadrant (n = 122, 45.35%). TNM clinical stage Tlc was identified in 79 pts (29.36%), Tlb in 55 pts (20.44%), T2 in 54 pts (20.07%) and no nodal involvement in 146 pts (54.27%). Nottingham Grade 2 (n = 120, 44.60%) and invasive ductal carcinomas (n = 152, 56.50%) were diagnosed most often. Tumors were more frequently ER+ (n = 237, 88.10%), PR+ (n = 210, 78.06%), and HER2-negative (n = 219, 81.41%). There was no statistically significant increase in OS based on location of tumor (P = 0.9796) and tumor histology (invasive ductal vs invasive lobular cancers, P = 0.1143). Node negative breast cancers were associated with increased OS (P = 0.0014). Grade 2 tumors were associated with increased OS compared to Grade 3 tumors (P = 0.0112). ER+ and PR-negative tumors were associated with decreased OS in both short term and long term follow up (P = 0.0083 & P = 0.0254). Conclusions: In pts 65 years of age or older with newly diagnosed breast cancer, lack of nodal involvement is associated with increased OS. Prognosis for ER+ and PR-negative tumors is worse compared to ER+ and PR+ tumors. Nottingham Grade 2 tumors have better OS compared to Grade 3 tumors. Location of tumor and tumor histology are not associated with increased OS.
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Mercer, Louise K., Johan Askling, Pauline Raaschou, William G. Dixon, Lene Dreyer, Merete Lund Hetland, Anja Strangfeld, et al. "Risk of invasive melanoma in patients with rheumatoid arthritis treated with biologics: results from a collaborative project of 11 European biologic registers." Annals of the Rheumatic Diseases 76, no. 2 (June 15, 2016): 386–91. http://dx.doi.org/10.1136/annrheumdis-2016-209285.
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ObjectivesSome studies have reported a possible association between exposure to tumour necrosis factor (TNF) inhibitors and an increased risk of melanoma. The aim of this study was to investigate the incidence of invasive cutaneous melanomas in patients with rheumatoid arthritis (RA) treated with TNF inhibitors (TNFi), other biologic disease modifying drugs and non-biologic therapy.MethodsEleven biologic registers from nine European countries participated in this collaborative project. According to predefined exposure definitions, cohorts of patients with RA were selected. Using the country-specific general population of each register as reference, age, sex and calendar year standardised incidence ratios (SIRs) of invasive histology-confirmed cutaneous melanoma were calculated within each register. Pooled SIR and incidence rate ratios (IRRs) comparing biologic cohorts to biologic-naïve were calculated across countries by taking the size of the register into account.ResultsOverall 130 315 RA patients with a mean age of 58 years contributing 579 983 person-years were available for the analysis and 287 developed a first melanoma. Pooled SIRs for biologic-naïve, TNFi and rituximab-exposed patients were 1.1 (95% CI 0.9 to 1.4), 1.2 (0.99 to 1.6) and 1.3 (0.6 to 2.6), respectively. Incidence rates in tocilizumab and abatacept-exposed patients were also not significantly increased. IRR versus biologic-naïve patients were: TNFi 1.1 (95% CI 0.8 to 1.6); rituximab 1.2 (0.5 to 2.9).ConclusionsThis large European collaborative project did not confirm an overall increased risk of melanoma following exposure to TNFi.
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Anselmo, Aaron C., Yatin Gokarn, and Samir Mitragotri. "Non-invasive delivery strategies for biologics." Nature Reviews Drug Discovery 18, no. 1 (November 30, 2018): 19–40. http://dx.doi.org/10.1038/nrd.2018.183.
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Seror, R., B. Fautrel, A. Lafourcade, Y. De-Rycke, X. Mariette, and F. Tubach. "OP0124 RISK OF MALIGNANCIES ACROSS BIOLOGIC CLASSES IN RHEUMATOID ARTHRITIS: ANALYSIS OF A NATIONAL CLAIM DATABASE." Annals of the Rheumatic Diseases 79, Suppl 1 (June 2020): 81.2–82. http://dx.doi.org/10.1136/annrheumdis-2020-eular.3687.
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Background:Objectives:To estimate the incidence rate of malignancies in biologic-treated RA patients, and to compared it to the general population and across different classes of biologicsMethods:We conducted an historical cohort study within the French the national claim database, named SNDS. This database prospectively records individual health resource of 86% of the entire French population (65 million inhabitants) since 2007. RA adult patients were identified based on ICD-10 code (M05 or M06). Patients with cancer history were excluded. Treatment exposures focused on incident first use of biologics including all anti-TNF, rituximab, abatacept, tocilizumab, ustekinumab, anakinra. To identify incident treatment periods, only patients who did not receive any biologics in the 1-year period before the index date were selected. In the base case analysis, exposure was defined with a 90-day latency after treatment initiation and a 180-day carry-over period after drug discontinuation.To compare the risk of malignancies between biologic treated patients and general population, Standardized incidence ratio (SIR [95%CI]) were calculated using FRANCIM (“France Cancer Incidence et Mortalité”) estimations as reference.To compare the risk of malignancies between biologics, a propensity score (including age, sex, year of first occurrence of RA code, date of treatment initiation, number of previous DMARDs, Charlson comorbidity index, diagnosis of tobacco and/or alcohol-associated disorders, number of hospitalizations for RA, cumulative corticosteroid dose) was calculated for each comparison. Hazard Ratios (HRs) for risk of cancer were estimated using Cox proportional hazard model using inverse probability of treatment weighting (IPTW) with propensity score. Exposure was considered as a time-dependent variable and propensity scores were estimated dynamically using pooled logistic regression reassessed for each new exposure.Results:Between 2007 and 2016, 31,792 patients (112,802 patient-years)- were exposed to biologics. The annual incidence rate of overall malignancies was 0.865 per 100 patients-years. Malignancies occurred in 730 patients exposed to anti-TNF, 235 patients exposed to another biologic and 11 exposed to both.As compared to the general population, biologic treated patients had an increased risk of lung cancer (SIR=1.35 [1.14;1.60]), a decreased risk of pancreatic cancer (SIR=0.52[0.31-0.85]) and no significant increased risk of invasive melanoma (SIR=1.15 [0.82;1.61]). Results were similar for anti-TNF-treated patients. Other biologics were not analyzed separately due to small sample sizes.The overall risk of malignancies and risk of lymphoma did not differ between anti-TNF and other biologics (analysed all together), or abatacept. Within the anti-TNF class, the overall risk of malignancies and risk of lymphoma did not differ between etanercept and monoclonal anti-TNF (table).Type of malignanciesHR [95% CI]p-valueHR [95% CI]p-valueHR [95% CI]p-valueAnti-TNF (ref) vs. other biologicsAnti-TNF (ref) vs. AbataceptMonoclonal anti-TNF (ref) vs. EtanerceptP-Y exposure83256 vs. 2564991770 vs. 468149620 vs. 36790All malignancies (excl. non-melanoma skin cancer)0.97 [0.81;1.17]p=0.71.27 [0.89;1.81]p=0.21.11 [0.94;1.32]p=0.2Solid cancer (excl. non-melanoma skin cancer)0.98 [0.80;1.20]p=0.81.23 [0.84;1.82]p=0.41.10 [0.92;1.32]p=0.3Lymphoma0.69 [0.32;1.46]p=0.31.73 [0.55;5.48]p=0.50.87 [0.49;1.57]p=0.7Conclusion:Using a large nationwide healthcare database, representative of the French population, the overall risk of malignancies did not seem to differ across the different classes of biologic. Among anti-TNF, the risk of malignancies of lymphoma did not differ between etanercept and monoclonal antibodies. The risk of organ specific cancers, except lung cancer, did not differ from that of general population.Disclosure of Interests:Raphaèle Seror Consultant of: BMS, Medimmune, Novartis, Pfizer, GSK, Lilly, Bruno Fautrel Grant/research support from: AbbVie, Lilly, MSD, Pfizer, Consultant of: AbbVie, Biogen, BMS, Boehringer Ingelheim, Celgene, Lilly, Janssen, Medac MSD France, Nordic Pharma, Novartis, Pfizer, Roche, Sanofi Aventis, SOBI and UCB, Alexandre Lafourcade: None declared, yann de-rycke: None declared, Xavier Mariette Consultant of: BMS, Gilead, Medimmune, Novartis, Pfizer, Servier, UCB, Florence Tubach Grant/research support from: Florence TUBACH is head of the Centre de Pharmacoépidémiologie (Cephepi) of the Assistance Publique – Hôpitaux de Paris and of the Clinical Research Unit of Pitié-Salpêtrière hospital, both these structures have received research funding, grants and fees for consultant activities from a large number of pharmaceutical companies, that have contributed indiscriminately to the salaries of its employees. Florence Tubach didn’t receive any personal remuneration from these companies.
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Déchamp, C., and H. Méon. "Allergenic, Biologic Pollutant, Invasive… Do You Know Short Ragweed?" Epidemiology 17, Suppl (November 2006): S281. http://dx.doi.org/10.1097/00001648-200611001-00732.
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Sanders, Mary Ann, Jane E. Brock, Beth T. Harrison, Tad J. Wieczorek, Xuefei Hong, Anthony J. Guidi, Deborah A. Dillon, Leslie Max, and Susan C. Lester. "Nipple-Invasive Primary Carcinomas: Clinical, Imaging, and Pathologic Features of Breast Carcinomas Originating in the Nipple." Archives of Pathology & Laboratory Medicine 142, no. 5 (February 12, 2018): 598–605. http://dx.doi.org/10.5858/arpa.2017-0226-oa.
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Context Patients choosing to retain the nipple when undergoing therapeutic or prophylactic mastectomy are at risk for cancers arising at that site. Objective To identify cases of invasive carcinoma arising within the nipple and to investigate their clinical, imaging, biologic, and staging features. Design Carcinomas were identified by prospective review of surgical and consult cases at 4 hospitals. Results The 24 patients identified presented with symptoms related to the nipple. Mammography did not detect the cancer in most cases. Ten patients (42%) had skin changes from ductal carcinoma in situ involving nipple skin (Paget disease), with small foci of invasion into the dermis, and 6 of those 10 carcinomas (60%) stained positive for human epidermal growth factor receptor 2 (HER2). The remaining 14 patients (58%) presented with a nipple mass or with skin changes. These were larger invasive carcinomas of both ductal and lobular types. Only 2 of those 14 carcinomas (14%) were HER2+. Three of 15 patients (20%) undergoing lymph node biopsy had a single metastasis. No patients have had recurrent disease. Conclusions Rare, invasive, primary nipple carcinomas typically present as subtle nipple thickening or an exudative crust on the skin. Imaging studies are often nonrevealing. A variety of histologic and biologic types of carcinomas occur, similar to cancers arising deeper in the breast. Although the carcinomas invaded into the dermis, some with skin ulceration, the likelihood of lymph node metastasis was no higher than carcinomas of similar sizes. Patients who choose to preserve their nipple(s) should be aware of the possibility of breast cancer arising at that site and to bring any observed changes to the attention of their health care providers.
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Chung, Seung Woo, Taslim A. Hil-lal, and Youngro Byun. "Strategies for non-invasive delivery of biologics." Journal of Drug Targeting 20, no. 6 (May 28, 2012): 481–501. http://dx.doi.org/10.3109/1061186x.2012.693499.
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Schuler, Gerhard. "Equines Choriongonadotropin: Biologie und veterinärmedizinische Bedeutung." Tierärztliche Praxis Ausgabe G: Großtiere / Nutztiere 48, no. 05 (October 2020): 344–54. http://dx.doi.org/10.1055/a-1235-7973.
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ZusammenfassungDie hypophysären Gonadotropine follikelstimulierendes Hormon (FSH) und luteinisierendes Hormon (LH) spielen eine zentrale Rolle bei der Steuerung der Gonadenfunktionen. Daher ist ihr Einsatz in der Therapie von Fruchtbarkeitsstörungen (z. B. Azyklie) sowie in der Biotechnologie (z. B. Superovulation, Hormonprogramme zur Zyklussynchronisation) prinzipiell von hohem Interesse. Präparationen von FSH bzw. LH sind aufgrund der aufwendigen Gewinnung aus Hypophysengewebe relativ teuer und daher besonderen Anwendungen vorbehalten. Bei Primaten- und Equidenarten wurde die Expression eines LH-ähnlichen Moleküls im Chorionepithel nachgewiesen (Choriongonadotropin, CG). Equines CG (eCG) weist außer bei Equiden, bei denen es ausschließlich an LH-Rezeptoren bindet, bei allen bei uns üblichen Haussäugetierspezies neben seiner LH-Aktivität eine außerordentlich hohe FSH-Aktivität auf („duale Wirkung“). Seit seiner Markteinführung kommt ihm daher eine hohe Bedeutung als vergleichsweise kostengünstiges FSH-Analogon vorwiegend zur Anwendung bei Wiederkäuern und Schwein zu. Im Gegensatz zu dem als LH-Analogon eingesetzten humanen CG (hCG), das nicht invasiv aus dem Urin schwangerer Frauen isoliert werden kann, muss die Gewinnung von eCG aus dem Blut trächtiger Spenderstuten erfolgen, da im Urin nur minimale eCG-Konzentrationen vorliegen. Nach Berichten über Todesfälle und Leiden von Spenderstuten im Zusammenhang mit der eCG-Gewinnung in südamerikanischen Haltungen ist das derzeitige Verfahren der eCG-Produktion zunehmend in die öffentliche Kritik geraten, was zuletzt in Forderungen nach einem generellen Verbot mündete. Ziel dieses Beitrags ist daher, den aktuellen Kenntnisstand zu Eigenschaften und Biologie dieses auch aus Sicht der Grundlagenwissenschaft hochinteressanten Moleküls kurz zusammenzufassen.
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Bae, J., S. Lee, J. Lee, S. Woo, Y. Chae, K. Cho, and B. Koo. "P11 Biologic behavior of E-cadherin in invasive ductal carcinoma." Breast 16 (March 2007): S15—S16. http://dx.doi.org/10.1016/s0960-9776(07)70076-0.
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Damsky, C. H., C. Librach, K. H. Lim, M. L. Fitzgerald, M. T. McMaster, M. Janatpour, Y. Zhou, S. K. Logan, and S. J. Fisher. "Integrin switching regulates normal trophoblast invasion." Development 120, no. 12 (December 1, 1994): 3657–66. http://dx.doi.org/10.1242/dev.120.12.3657.
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Cells invade extracellular matrices in a regulated manner at specific times and places during normal development. A dramatic example is trophoblast invasion of the uterine wall. Previous studies have shown that differentiation of trophoblasts to an invasive phenotype is accompanied by temporally and spatially regulated switching of their integrin repertoire. In the first trimester human placenta, alpha 6 integrins are restricted to cytotrophoblast (CTB) stem cells and downregulated in invasive CTBs, whereas alpha 5 beta 1 and alpha 1 beta 1 integrins are upregulated in differentiating and invasive CTBs. The goal of the present study was to determine whether these changes have functional consequences for CTB invasiveness. Using an in vitro invasion model, we determined first that aggregates of invading first trimester CTBs in vitro undergo the same pattern of integrin switching as was observed in situ, thereby validating the utility of the model. We then showed that antibody perturbation of interactions involving laminin or collagen type IV and their integrin alpha 1/beta 1 receptor inhibited invasion by CTBs, whereas perturbing interactions between fibronectin and the alpha 5/beta 1 fibronectin receptor accelerated invasion. Finally, we report that later gestation CTBs, which display greatly decreased invasive capacity, are also unable to upregulate alpha 1 beta 1 complexes, providing further evidence that this integrin is critical for CTB invasion. This gestational regulation is transcriptional. These data indicate that integrin switching observed during differentiation in situ has significant functional consequences for CTB invasion. The data suggest further that differentiating CTBs upregulate counterbalancing invasion-accelerating and invasion-restraining adhesion mechanisms. We propose that this contributes to regulating the depth of CTB invasion during normal implantation.
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Arnold, Tamra M., Catherine R. Sears, and Chadi A. Hage. "Invasive Fungal Infections in the Era of Biologics." Clinics in Chest Medicine 30, no. 2 (June 2009): 279–86. http://dx.doi.org/10.1016/j.ccm.2009.02.007.
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Ramshekar, Aniket, Haibo Wang, and M. Hartnett. "Regulation of Rac1 Activation in Choroidal Endothelial Cells: Insights into Mechanisms in Age-Related Macular Degeneration." Cells 10, no. 9 (September 14, 2021): 2414. http://dx.doi.org/10.3390/cells10092414.
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Age-related macular degeneration (AMD) is one of the leading causes of blindness worldwide. Vision loss from the neovascular form is associated with the invasion of choroidal endothelial cells into the neural retina to form vision-threatening macular neovascularization (MNV). Anti-angiogenic agents are the current standard of care but are effective in only ~50% of AMD cases. The molecular mechanisms involved in invasive MNV point to the importance of regulating signaling pathways that lead to pathologic biologic outcomes. In studies testing the effects of AMD-related stresses, activation of the Rho GTPase, Rac1, was found to be important for the choroidal endothelial cell invasion into the neural retina. However, current approaches to prevent Rac1 activation are inefficient and less effective. We summarize active Rac1-mediated mechanisms that regulate choroidal endothelial cell migration. Specifically, we discuss our work regarding the role of a multidomain protein, IQ motif containing GTPase activating protein 1 (IQGAP1), in sustaining pathologic Rac1 activation and a mechanism by which active Rap1, a Ras-like GTPase, may prevent active Rac1-mediated choroidal endothelial cell migration.
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Lichtenstein, L., B. Koslowsky, I. Avni-Biron, B. Ovadia, O. Ben-Bassat, T. Naftali, U. Kopylov, et al. "P275 Course of COVID-19 in patients with Inflammatory Bowel Diseases treated with biologics: the Israeli experience." Journal of Crohn's and Colitis 15, Supplement_1 (May 1, 2021): S307—S308. http://dx.doi.org/10.1093/ecco-jcc/jjab076.400.
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Abstract Background Biologic treatments are inherently associated with an increased risk of infections, and recipients are intuitively considered at-risk for a more severe course of COVID-19. However, the actual risks are not fully described, neither are the appropriate adjustments needed to mitigate such risks. Methods Nation-wide registry was set up by Israeli IBD Section, to characterize course of COVID-19 in IBD patients who contacted SARS-CoV-2 infection while on biologics. We prospectively collected demographic and clinical data, and analyzed COVID-19 outcomes with regard to the specific treatments. Results Between Apr and Oct 2020, 144 patients with an established IBD diagnosis and confirmed COVID-19 were enrolled at 20 IBD referral centers. The majority of patients was under the age of 40 (113, 78%), 9 (6%) were younger than 18, only 4 patients (3%) over the age of 70. 94 patients received biologics, as monotherapy (76, 52.8%), combined with immunomodulators (9, 10%) or concomitant corticosteroids (9, 10%). 37 patients (26%) were reported with moderate and severe COVID-19 course, third of them (13) on biologics. 24 patents (17%) were admitted for hospitalization, the rest managed in home setting (114, 79%) and hotels converted into makeshift healthcare facilities (6, 4%). Fifteen patients (10%) required non-invasive ventilation and oxygen support, 3 patients (2%) went on mechanical ventilation. All patients recovered uneventfully, with no mortalities reported. Age was the most significant factor associated with moderate and severe disease. We found no correlation between bowel disease activity and the severity of COVID-19 course. The rate of serious COVID-19 for the 94 patients who had received biologics was significantly lower than that of 50 patients who were not treated with biologics (13/94 vs 24/50; RR 0.29 [95% CI, 0.161–0.515]; p < 0.0001). On adjusting for age, gender, comorbidities, IBD phenotype and activity, the surprising ameliorating effect associated with biologics was profound and significant (OR, 0.082 [95% CI 0.009-0.621], p =0.013) in all age categories. Conclusion Our results are reassuring and encouraging, and do not suggest that therapeutic immune suppression renders IBD patients particularly vulnerable for more severe course of the COVID-19. Adjusted odds for severe COVID-19 course actually decreased significantly in patients treated with biologics. It could be speculated that cytokine inhibition may mitigate progression of the infection to a devastating hyperinflammatory state. Continuing necessary maintenance immune suppression seems to be appropriate and safe approach, despite the COVID-19 pandemic.
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Porter, Andrew, Taryn Youngstein, Enrico Tombetti, and Justin C. Mason. "Biologic therapy in supra-aortic Takayasu arteritis can improve symptoms of cerebral ischaemia without surgical intervention." Rheumatology 59, Supplement_3 (April 29, 2020): iii28—iii32. http://dx.doi.org/10.1093/rheumatology/kez616.
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Abstract Objectives Takayasu arteritis commonly results in severe arterial injury with stenoses, occlusions and occasionally aneurysms. Arterial disease may compromise organ blood flow and result in significant cardiovascular morbidity and premature mortality. Involvement of the supra-aortic arteries is common, and in its most severe form may compromise cerebral blood supply, resulting in signs of cerebral ischaemia including visual impairment, dysphasia, transient hemiparesis, loss of consciousness and stroke. In addition to combination immunosuppression, the management paradigm for symptomatic cerebral ischaemia includes revascularization. The invasive nature of this surgery, the risk of complications and the relatively high rate of re-stenosis is of concern to patients and their physicians alike. The aim of this study was to determine whether combined immunosuppression with early escalation to biologic therapy improved outcomes and reduced the need for high risk surgical intervention. Methods A retrospective review of 145 Takayasu arteritis patients attending Imperial College Healthcare between 2010–2018 was conducted to identify those with cerebral ischaemia secondary to supra-aortic disease and to analyse their treatment and outcomes. Results Eight patients (5.5%) were identified. Seven patients received long-term combined immunosuppressive therapy and six were prescribed biologics. The data revealed a higher than expected comprehensive response to therapy, with significant falls in disease activity, the cerebral ischaemia score and the prednisolone dose required, over a median follow-up of 37 months. Serial imaging analysis detected no arterial disease progression after the initiation of optimal therapy. Only one patient required surgical intervention for persistent neurological symptoms. Conclusion Early use of biologic therapy in those with supra-aortic Takayasu arteritis presenting with cerebral ischaemia may reduce the numbers of patients requiring surgical intervention and improve outcomes.
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Rocourt, Dorothy, and Travis Hoover. "MINIMAL INVASIVE MANAGEMENT OF PEDIATRIC CROHN’S ANORECTAL STRICTURE, LESS IS MORE." Inflammatory Bowel Diseases 27, Supplement_1 (January 1, 2021): S16. http://dx.doi.org/10.1093/ibd/izaa347.039.
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Abstract Background Anorectal stricture (ARS) is an uncommon but potentially disabling manifestation of perianal Crohn disease (CD) in pediatric patients. Various treatment options are available but there is little data regarding their efficacy, particularly in the pediatric population. We present three case reports of patients with symptomatic ARS treated with serial dilation and biologic therapy. Methods An institutional review board-approved retrospective review was performed using electronic health records. Three patients with ileocolonic CD and perianal involvement with symptomatic ARS were identified. All patients were treated with serial rectal dilations under general anesthesia using Hegar dilators. Results All patients are currently asymptomatic at follow-ups ranging from 1 to 3.5 years since the last dilation. Patient demographics and details of ARS management are presented in Table 1. All patients tolerated the procedures well and did not experience complications such as perforation, sepsis, or fecal incontinence. Rectal biopsy in each patient showed active inflammation, suggesting type 1 stricture according to the Hughes-Cardiff Classification (vs. type 2 fibrotic stricture). Patient 1 experienced 6 recurrences, each managed with an average of 2 dilations until disease control was established with ustekinumab (USK) and eventually vedolizumab (VDZ). She underwent ileocecal resection three years after the final dilation. Patient 2 underwent ileocecal resection immediately following the first series of dilations. He later experienced one stricture recurrence at 2 years, which was managed with one dilation and increased USK dosing frequency. Patient 3 received steroid suppositories prior to dilation and has been self-dilating at home. He has had no recurrences requiring operative dilation. Self-dilation was not feasible in patients 1 and 2. Conclusion Inflammatory anorectal stricture associated with perianal Crohn disease in pediatric patients can be managed successfully with dilation until disease control with biologic therapy. Recurrences of stricture can also be managed with dilation and modification of biologic therapy. If tolerated, self-dilation may reduce recurrence. Background Anorectal stricture (ARS) is an uncommon but potentially disabling manifestation of perianal Crohn disease (CD) in pediatric patients. Various treatment options are available but there is little data regarding their efficacy, particularly in the pediatric population. We present three case reports of patients with symptomatic ARS treated with serial dilation and biologic therapy. Crohn’s rectal stricture pre and post dilation
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Seror, R., A. Lafourcade, Y. De-Rycke, B. Fautrel, X. Mariette, and F. Tubach. "THU0151 RISK OF MALIGNANCIES ASSOCIATED WITH CS DMARDS IN RHEUMATOID ARTHRITIS: COMPARISON WITH GENERAL POPULATION AND BIOLOGIC TREATED PATIENTS (ANALYSIS OF A NATIONAL CLAIM DATABASE)." Annals of the Rheumatic Diseases 79, Suppl 1 (June 2020): 291.1–291. http://dx.doi.org/10.1136/annrheumdis-2020-eular.3656.
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Background:Objectives:To estimate the incidence rate of malignancies in csDMARD-treated RA patients and to compare it to that of general population and to biologic-treated RA patientsMethods:We conducted an historical cohort study within the national claim database that prospectively records individual health resource use of 86% of the French population (65 million inhabitants). RA adult patients were identified based on ICD-10 code (M05 or M06) between 2007-2016. Patients with previous cancer history were excluded. Treatment exposures were incident first use of any treatment: csDMARD (methotrexate, leflunomide, sulfasalazine, azathioprine, hydroxychloroquine) or biologics (anti-TNF, rituximab, abatacept, tocilizumab, ustekinumab, anakinra). To identify incident treatment periods, only patients who did not receive any treatment in the 1-year period before the index date were selected. Exposure was defined with a 90-day latency after treatment initiation and a 180-day carry-over period after drug discontinuation.To compare the risk of malignancies between csDMARD-treated patients and general population, standardized incidence ratio (SIR [95%CI]) were calculated using FRANCIM (“France Cancer Incidence et Mortalité”) estimations as reference.To compare the risk of malignancies between csDMARD and biologics treated patients, a dynamically propensity score (including age, sex, year of first occurrence of RA code, date of treatment initiation, number of previous DMARDs, Charlson’s comorbidity index, diagnosis of tobacco and/or alcohol-associated disorders, number of hospitalizations for RA, cumulative corticosteroid dose) was constructed using pooled logistic regression. Hazard Ratios (HRs) for risk of cancer were estimated using Cox proportional hazards model after dynamically propensity score matching. Exposure was considered as a time-dependent variable.Results:Between 2007 and 2016, 83,706 RA patients exposed to csDMARD (n=63,837) and/or biologics (n=19,727) were identified.As compared to the general population, csDMARDs treated patients had an increased risk of lung cancer (SIR=1.29 [1.14; 1.45]), invasive melanoma (SIR=1.52 [1.24; 1.86]) and a borderline increased risk of breast cancer (SIR=1.11 [1.01;1.22]). By contrast, they had a decreased risk of pancreatic cancer (SIR=0.68[0.51-0.9]) and liver cancer (SIR=0.43 [0.27; 0.67]). This later is due to a protopathic bias.After propensity score matching, analyses the risk of malignancies between csDMARD and biologics treated patients were conducted on 19727 patients in each group (mean age: 51 ±14 yrs; female: 74.6%). Malignancies occurred in 435 patients exposed to biologics and 332 patients exposed to csDMARD. The overall risk of malignancies (figure), risk of solid cancer (excluding non-melanoma skin cancer), lymphoma, and other hematologic malignancies did not differ significantly between csDMARD and all biologics (table). Regarding organ specific cancer, no difference was observed. Results were similar for biologic in monotherapy or associated with csDMARD.Type of malignanciesHR [95%CI] csDMARD (ref) vs. all biologicsp-valueAll malignancies (excl. non-melanoma skin cancer)0.99 [0.86;1.14]p=0.9Solid cancer (excl. non-melanoma skin cancer)0.95 [0.82;1.11]p=0.5Lymphoma1.35 [0.72;2.53]p=0.3Other hematologic malignancies1.18 [0.56;2.49]p=0.7Conclusion:Using a large nationwide representative healthcare database, the overall risk of malignancies and the risk of organ-specific cancers and hematologic malignancies in biologic treated RA patients did not differ from that of patients treated with csDMARD. Compared to general population, patients treated with csDMARD had an increased risk of lung cancer and melanoma, but a decreased risk of pancreatic cancer.Disclosure of Interests:Raphaèle Seror Consultant of: BMS, Medimmune, Novartis, Pfizer, GSK, Lilly, Alexandre Lafourcade: None declared, yann de-rycke: None declared, Bruno Fautrel Grant/research support from: AbbVie, Lilly, MSD, Pfizer, Consultant of: AbbVie, Biogen, BMS, Boehringer Ingelheim, Celgene, Lilly, Janssen, Medac MSD France, Nordic Pharma, Novartis, Pfizer, Roche, Sanofi Aventis, SOBI and UCB, Xavier Mariette Consultant of: BMS, Gilead, Medimmune, Novartis, Pfizer, Servier, UCB, Florence Tubach Grant/research support from: Florence TUBACH is head of the Centre de Pharmacoépidémiologie (Cephepi) of the Assistance Publique – Hôpitaux de Paris and of the Clinical Research Unit of Pitié-Salpêtrière hospital, both these structures have received research funding, grants and fees for consultant activities from a large number of pharmaceutical companies, that have contributed indiscriminately to the salaries of its employees. Florence Tubach didn’t receive any personal remuneration from these companies.
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Ossowski, L. "In vivo invasion of modified chorioallantoic membrane by tumor cells: the role of cell surface-bound urokinase." Journal of Cell Biology 107, no. 6 (December 1, 1988): 2437–45. http://dx.doi.org/10.1083/jcb.107.6.2437.
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The ability of the chick embryo chorioallantoic membrane (CAM) to withstand invasion by tumor cells can be intentionally compromised by altering its morphological integrity. Using a newly developed quantitative assay of invasion we showed that intact CAMs were completely resistant to invasion by tumor cells, wounded CAMs did not pose a barrier to penetration, and CAMs that were wounded and then allowed to reseal displayed partial susceptibility to invasion. The invasion of resealed CAMs required catalytically active plasminogen activator (PA) of the urokinase type (uPA); the invasive efficiency of tumor cells was reduced by 75% when tumor uPA activity or tumor uPA production was inhibited. The invasive ability of human tumor cells, which have surface uPA receptors but which do not produce the enzyme, could be augmented by saturating their receptors with exogenous uPA. The mere stimulation of either uPA or tissue plasminogen activator production, in absence of binding to cell receptors, did not result in an enhancement of invasiveness. These findings suggest that the increased invasive potential of tumor cells is correlated with cell surface-associated proteolytic activity stemming from the interaction between uPA and its surface receptor.
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Stojadinovic, Alexander, Ronald A. Ghossein, Axel Hoos, Marshall J. Urist, Ronald H. Spiro, Jatin P. Shah, Murray F. Brennan, Ashok R. Shaha, and Bhuvanesh Singh. "Hürthle Cell Carcinoma: A Critical Histopathologic Appraisal." Journal of Clinical Oncology 19, no. 10 (May 15, 2001): 2616–25. http://dx.doi.org/10.1200/jco.2001.19.10.2616.
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PURPOSE: Controversy exists over the ability of morphology to predict the biologic behavior of Hürthle cell carcinoma. The aim of this study was to conduct a critical histopathologic review of Hürthle cell carcinoma and to correlate morphologic parameters with clinical outcome. PATIENTS AND METHODS: Patients with histologically confirmed Hürthle cell carcinoma treated between 1940 and 2000 form the basis of this study. Adenomas were excluded. Tumors of unknown malignant behavior ([UMB] n = 17) had solid growth pattern, incomplete capsular invasion (Ci), or both but no vascular invasion (Vi). Minimally invasive carcinomas ([MIC] n = 23) had one focus of intra- or extracapsular Vi, one focus of complete Ci, or both. Widely invasive carcinomas ([WIC] n = 33) demonstrated more than one focus of Vi, more than one focus of Ci, or both. The primary end points were relapse-free survival (RFS) and disease-specific survival (DSS). Rates of recurrence/death were estimated by Kaplan-Meier method. The univariate influence of prognostic factors on end points was analyzed by log-rank test, and multivariate analysis was performed by Cox regression. RESULTS: Median follow-up was 8 years. No patients with UMB or MIC relapsed or died of disease. Of WIC, 73% relapsed and 55% died of disease. Age, size, and extent of resection did not influence outcome. Adverse predictors of RFS and DSS among WIC were extrathyroidal extension, nodal metastasis, positive margin, and solid growth pattern (P < .05). Both Ci and Vi were associated with worse DSS (P < .05). On multivariate analysis, extrathyroidal extension and nodal metastases were independent predictors of outcome (P < .05). CONCLUSION: Patients with Hürthle cell carcinoma have a prognosis that is predicted by well-defined histomorphologic characteristics. Unlike differentiated thyroid cancer, nodal metastases predict a worse outcome in widely invasive Hürthle cell carcinoma, as does extrathyroidal extension.
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Yiu, Gary K., Aura Kaunisto, Y. Rebecca Chin, and Alex Toker. "NFAT promotes carcinoma invasive migration through glypican-6." Biochemical Journal 440, no. 1 (October 27, 2011): 157–66. http://dx.doi.org/10.1042/bj20110530.
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Invasive migration of carcinoma cells is a prerequisite for the metastatic dissemination of solid tumours. Numerous mechanisms control the ability of cancer cells to acquire a motile and invasive phenotype, and subsequently degrade and invade the basement membrane. Several genes that are up-regulated in breast carcinoma are responsible for mediating the metastatic cascade. Recent studies have revealed that the NFAT (nuclear factor of activated T-cells) is a transcription factor that is highly expressed in aggressive breast cancer cells and tissues, and mediates invasion through transcriptional induction of pro-invasion and migration genes. In the present paper we demonstrate that NFAT promotes breast carcinoma invasion through induction of GPC (glypican) 6, a cell-surface glycoprotein. NFAT transcriptionally regulates GPC6 induction in breast cancer cells and binds to three regulatory elements in the GPC6 proximal promoter. Expression of GPC6 in response to NFAT signalling promotes invasive migration, whereas GPC6 silencing with shRNA (small-hairpin RNA) potently blocks this phenotype. The mechanism by which GPC6 promotes invasive migration involves inhibition of canonical β-catenin and Wnt signalling, and up-regulation of non-canonical Wnt5A signalling leading to the activation of JNK (c-Jun N-terminal kinase) and p38 MAPK (mitogen-activated protein kinase). Thus GPC6 is a novel NFAT target gene in breast cancer cells that promotes invasive migration through Wnt5A signalling.
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Rajagopal, S., G. van der Velde, B. G. P. Paffen, F. W. B. van den Brink, and A. Bij de Vaate. "Life history and reproductive biology of the invasive amphipod Corophium curvispinum (Crustacea: Amphipoda) in the Lower Rhine." Fundamental and Applied Limnology 144, no. 3 (March 5, 1999): 305–25. http://dx.doi.org/10.1127/archiv-hydrobiol/144/1999/305.
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Albores-Saavedra, Jorge, Matthew Tuck, Bernadette K. McLaren, Kelley S. Carrick, and Donald Earl Henson. "Papillary Carcinomas of the Gallbladder: Analysis of Noninvasive and Invasive Types." Archives of Pathology & Laboratory Medicine 129, no. 7 (July 1, 2005): 905–9. http://dx.doi.org/10.5858/2005-129-905-pcotga.
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Abstract Context.—Although papillary carcinomas have been recognized as distinct morphologic variants of gallbladder neoplasms, they have been lumped together in a single group despite the recognition of noninvasive and invasive types. As a result, the biologic behavior of each type remains undescribed. Objective.—To compare the biologic behavior of noninvasive and invasive papillary carcinomas of the gallbladder. Design.—The clinical and morphologic features of 16 noninvasive papillary carcinomas (>1 cm) of the gallbladder were analyzed, and their clinical behavior was compared with that of 370 invasive papillary carcinomas recorded in the Survey Epidemiology and End Results (SEER) Program of the National Cancer Institute from 1973 through 2001. The biologic behavior of invasive papillary carcinomas was compared with that of invasive nonpapillary carcinomas of the gallbladder recorded in SEER. Hematoxylin-eosin–stained sections were available for review in the 16 noninvasive papillary carcinomas. The number of slides examined per case varied from 3 to 16, with an average of 7. Results.—The 16 patients with noninvasive papillary carcinomas included 11 women and 5 men, aged 34 to 83 years (mean age, 61 years). Thirteen patients had cholelithiasis. Laparoscopic cholecystectomy was performed on 12 patients and open cholecystectomy on 4. The tumors measured from 1.3 to 8.6 cm and were well to moderately differentiated. Fourteen noninvasive papillary carcinomas showed biliary phenotype, and 2 showed intestinal phenotype. Follow-up was obtained in 11 patients; 6 were asymptomatic 5 to 11 years after surgery, 2 were symptom free 9 months to 4 years following cholecystectomy, and 3 died of unrelated causes 2 to 3 years after surgery. Three hundred seventy cases of invasive papillary carcinomas were recorded in SEER. The 10-year relative survival rate for 225 patients with invasive papillary carcinomas confined to the gallbladder wall was 52%, while the 10-year relative survival rate for 83 patients with papillary carcinomas that had spread to the lymph nodes was less than 10%. Of the remaining 62 invasive papillary carcinomas, 58 had distant metastases and 4 were not staged. The 10-year relative survival rate for invasive nonpapillary carcinomas confined to the gallbladder wall was 30%. Conclusion.—Noninvasive papillary carcinomas of the gallbladder—regardless of size, cell phenotype, and degree of differentiation—do not metastasize, and a simple cholecystectomy appears to be a curative procedure. In contrast, invasive papillary carcinomas do metastasize and are associated with a poor prognosis (10-year relative survival rate for tumors confined to the gallbladder wall was 52%, while the 10-year relative survival rate for tumors with lymph node metastasis was <10%). The separation of papillary carcinomas into noninvasive and invasive types is clinically relevant and therefore fully justified.
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Mukhopadhyay, Utpal K., Patrick Mooney, Lilly Jia, Robert Eves, Leda Raptis, and Alan S. Mak. "Doubles Game: Src-Stat3 versus p53-PTEN in Cellular Migration and Invasion." Molecular and Cellular Biology 30, no. 21 (August 23, 2010): 4980–95. http://dx.doi.org/10.1128/mcb.00004-10.
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ABSTRACT We have recently shown that Src induces the formation of podosomes and cell invasion by suppressing endogenous p53, while enhanced p53 strongly represses the Src-induced invasive phenotype. However, the mechanism by which Src and p53 play antagonistic roles in cell invasion is unknown. Here we show that the Stat3 oncogene is a required downstream effector of Src in inducing podosome structures and related invasive phenotypes. Stat3 promotes Src phenotypes through the suppression of p53 and the p53-inducible protein caldesmon, a known podosome antagonist. In contrast, enhanced p53 attenuates Stat3 function and Src-induced podosome formation by upregulating the tumor suppressor PTEN. PTEN, through the inactivation of Src/Stat3 function, also stabilizes the podosome-antagonizing p53/caldesmon axis, thereby further enhancing the anti-invasive potential of the cell. Furthermore, the protein phosphatase activity of PTEN plays a major role in the negative regulation of the Src/Stat3 pathway and represses podosome formation. Our data suggest that cellular invasiveness is dependent on the balance between two opposing forces: the proinvasive oncogenes Src-Stat3 and the anti-invasive tumor suppressors p53-PTEN.
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Lee, Seung Geun, Jeoung Won Bae, Jong Han Kim, Yang Suk Chae, Kyu Ran Cho, Jae Bok Lee, Gil Soo Son, and Bum Hwan Koo. "Biologic Behavior of E-cadherin in Invasive Ductal Carcinoma of the Breast." Journal of Breast Cancer 9, no. 2 (2006): 105. http://dx.doi.org/10.4048/jbc.2006.9.2.105.
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Kim, Jin You, Hyun Jung Kang, Jong Ki Shin, Nam Kyung Lee, You Seon Song, Kyung Jin Nam, and Ki Seok Choo. "Biologic Profiles of Invasive Breast Cancers Detected Only With Digital Breast Tomosynthesis." American Journal of Roentgenology 209, no. 6 (December 2017): 1411–18. http://dx.doi.org/10.2214/ajr.17.18195.
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Sasaki, Maiko, and Jan-Michael A. Klapproth. "W1198 Genetic and Biologic Characterization of Invasive E. coli in Crohn's Disease." Gastroenterology 134, no. 4 (April 2008): A—653. http://dx.doi.org/10.1016/s0016-5085(08)63049-8.
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Nieman, Marvin T., Ryan S. Prudoff, Keith R. Johnson, and Margaret J. Wheelock. "N-Cadherin Promotes Motility in Human Breast Cancer Cells Regardless of Their E-Cadherin Expression." Journal of Cell Biology 147, no. 3 (November 1, 1999): 631–44. http://dx.doi.org/10.1083/jcb.147.3.631.
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E-cadherin is a transmembrane glycoprotein that mediates calcium-dependent, homotypic cell–cell adhesion and plays a role in maintaining the normal phenotype of epithelial cells. Decreased expression of E-cadherin has been correlated with increased invasiveness of breast cancer. In other systems, inappropriate expression of a nonepithelial cadherin, such as N-cadherin, by an epithelial cell has been shown to downregulate E-cadherin expression and to contribute to a scattered phenotype. In this study, we explored the possibility that expression of nonepithelial cadherins may be correlated with increased motility and invasion in breast cancer cells. We show that N-cadherin promotes motility and invasion; that decreased expression of E-cadherin does not necessarily correlate with motility or invasion; that N-cadherin expression correlates both with invasion and motility, and likely plays a direct role in promoting motility; that forced expression of E-cadherin in invasive, N-cadherin–positive cells does not reduce their motility or invasive capacity; that forced expression of N-cadherin in noninvasive, E-cadherin–positive cells produces an invasive cell, even though these cells continue to express high levels of E-cadherin; that N-cadherin–dependent motility may be mediated by FGF receptor signaling; and that cadherin-11 promotes epithelial cell motility in a manner similar to N-cadherin.
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Hira, Vashendriya VV, Barbara Breznik, Cornelis JF Van Noorden, Tamara Lah, and Remco J. Molenaar. "2D and 3D in vitro assays to quantify the invasive behavior of glioblastoma stem cells in response to SDF-1α." BioTechniques 69, no. 5 (November 2020): 339–46. http://dx.doi.org/10.2144/btn-2020-0046.
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Invasion is a hallmark of cancer and therefore in vitro invasion assays are important tools in cancer research. We aimed to describe in vitro 2D transwell assays and 3D spheroid assays to quantitatively determine the invasive behavior of glioblastoma stem cells in response to the chemoattractant SDF-1α. Matrigel was used as a matrix in both assays. We demonstrated quantitatively that SDF-1α increased invasive behavior of glioblastoma stem cells in both assays. We conclude that the 2D transwell invasion assay is easy to perform, fast and less complex whereas the more time-consuming 3D spheroid invasion assay is physiologically closer to the in vivo situation.
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Yom, Cha Kyong, Kyung-Min Lee, Wonshik Han, Sung-Won Kim, Hyeong-Gon Moon, Hee-Chul Shin, Eunyoung Kang, and Dong-Young Noh. "The role and significance of FoxM1 in invasive breast cancer." Journal of Clinical Oncology 30, no. 15_suppl (May 20, 2012): 1056. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.1056.
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1056 Background: The Forkhead Box protein M1 (FoxM1) is known to regulate a variety of biologic processes in mammalian cells including cell growth and survival, angiogenesis, DNA damage response, chemotherapeutic drug resistance, and cancer cell migration and invasion. We evaluate the role and significance of Fox M1 in primary breast cancer in vitro and analyzed the relation with FoxM1 expression and clinicopathologic features. Methods: Immunohistochemical staining was used for evaluation of cytoplasmic expression of FoxM1 with TMA of invasive breast cancer. In various breast cancer cell lines, we evaluated FoxM1 expression and treated docetaxel/cisplatin in combination with Siomycin A (FoxM1 inhibitor) for BT20 cell line. Results: From Nov 1995 to Jul 2007, in 84 patients with stage 1-3 invasive breast cancer, FoxM1 expression was noted in 58.7%. Median follow-up duration was 85.1 months. Lymphovascular invasion was positively correlated with FoxM1 expression (p=0.040). In multivariate analysis, FoxM1 expression (p=0.005), HR negativity (p=0.002), high histologic grade (p=0.023), hign nuclear grade (p=0.045), lymphovascular invasiveness (p=0.017), and stage 3 cancer (p=0.015) matched poor disease-free survival. In vitro study, FoxM1 was expressed BT474, JIMT-1, BT20, HCC-1937, and MDA-MB-231 cell lines. The inhibition of FoxM1 had synergistic effect on cisplatin treatment, not docetaxel in BT20 cell. Conclusions: FoxM1 expression was noted in triple negative breast cancer cell lines and its inhibition had synergistically cytotoxic effect on BT20 cell line in combination with cisplatin. Although the further in vivo and clinical study should be needed to draw the solid conclusions, FoxM1 could be both a promising target of treatment for triple negative breast cancer and a independent prognostic factor.
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Cho, Samuel Y., and Richard L. Klemke. "Extracellular-Regulated Kinase Activation and Cas/Crk Coupling Regulate Cell Migration and Suppress Apoptosis during Invasion of the Extracellular Matrix." Journal of Cell Biology 149, no. 1 (April 3, 2000): 223–36. http://dx.doi.org/10.1083/jcb.149.1.223.
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Regulation of cell migration/invasion is important for embryonic development, immune function, and angiogenesis. However, migratory cells must also coordinately activate survival mechanisms to invade the extracellular matrix and colonize foreign sites in the body. Although invasive cells activate protective programs to survive under diverse and sometimes hostile conditions, the molecular signals that regulate these processes are poorly understood. Evidence is provided that signals that induce cell invasion also promote cell survival by suppressing apoptosis of migratory cells. Extracellular-regulated kinase (ERK) activation and molecular coupling of the adaptor proteins p130 Crk-associated substrate (CAS) and c-CrkII (Crk) represent two distinct pathways that induce cell invasion and protect cells from apoptosis in a three-dimensional collagen matrix. CAS/Crk-mediated cell invasion and survival requires activation of the small GTPase Rac, whereas ERK-induced cell invasion, but not survival requires myosin light chain kinase activation and myosin light chain phosphorylation. Uncoupling CAS from Crk or inhibition of ERK activity prevents migration and induces apoptosis of invasive cells. These findings provide molecular evidence that during invasion of the extracellular matrix, cells coordinately regulate migration and survival mechanisms through ERK activation and CAS/Crk coupling.
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Wong, Alice S. T., and Barry M. Gumbiner. "Adhesion-independent mechanism for suppression of tumor cell invasion by E-cadherin." Journal of Cell Biology 161, no. 6 (June 16, 2003): 1191–203. http://dx.doi.org/10.1083/jcb.200212033.
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Loss of E-cadherin expression or function in tumors leads to a more invasive phenotype. In this study, we investigated whether the invasion suppressor activity of E-cadherin is mediated directly by tighter physical cell adhesion, indirectly by sequestering β-catenin and thus antagonizing β-catenin/T cell factor (TCF) signaling, or by other signaling pathways. To distinguish mechanisms, we expressed wild-type E-cadherin and various E-cadherin mutants in invasive E-cadherin–negative human breast (MDA-MB-231) and prostate (TSU-Pr1) epithelial carcinoma cell lines using a tetracycline-inducible system. Our data confirm that E-cadherin inhibits human mammary and prostate tumor cell invasion. We find that adhesion is neither necessary nor sufficient for suppressing cancer invasion. Rather, the invasion suppressor signal is mediated through the β-catenin–binding domain of the E-cadherin cytoplasmic tail but not through the p120ctn-binding domain. β-catenin depletion also results in invasion suppression. However, alteration in the β-catenin/TCF transcriptional regulation of target genes is not required for the invasion suppressor activity of E-cadherin, suggesting the involvement of other β-catenin–binding proteins.
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Kuhl, C. K., S. Schrading, E. Wardelmann, M. Braun, W. Kuhn, and H. H. Schild. "Magnetic resonance imaging versus mammography for diagnosing ductal carcinoma in situ." Journal of Clinical Oncology 25, no. 18_suppl (June 20, 2007): 1504. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.1504.
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1504 Background: Mammographic screening is considered the mainstay for diagnosing pre-invasive breast cancer (DCIS). However, (over)diagnosis of DCIS has become a major concern. We investigated the sensitivities of high-resolution MRI and of state-of-the-art mammography (Mx) for diagnosing pure DCIS, and compared the biologic profile of MRI-detected versus Mx-detected DCIS. Methods: Prospective study on 5960 consecutive women who were referred to a dedicated breast unit for screening or for diagnostic assessment. Women underwent bilateral mammography with at least 2 views, plus spot compression views where appropriate, and high-resolution bilateral MRI. A total 137 women received the final pathologic diagnosis of having DCIS (no invasion). Of these, 108 (79%) had been referred for regular screening, 14 (10%) for high risk screening, 10 (7%) for follow up after breast cancer, and 5 (4%) for clinical symptoms. We investigated the mode of detection, and the biologic profile of the DCIS (size, nuclear grading, ER/PR and HER2-receptor status). Results: Overall, Mx was positive in 79/137 patients (58%), MRI was positive in 123/137 (90%). In 68/137 (50%), Mx and MRI were concordantly positive. In 3/137 (2%), Mx and MRI were both false-negative. In 11/137 (8%), only Mx was positive, MRI was false- negative. In 55/137 (40%), only MRI was positive, Mx was false negative. Of the 11 DCIS which were only detected by Mx, 1 was high grade, none was ER negative or HER2 positive. Mean VNPI was 4.2. Of the 55 DCIS which were only MRI detected, 41 (78%) were high grade, 14 (27%) were ER negative, 17(33%) HER-2 positive. Mean VNPI was 6.5. Conclusions: Compared to mammography, MRI offers a significantly higher sensitivity for DCIS, in particular for DCIS with adverse biologic profile: Half of the high grade or HER2-positive DCIS were only MRI detected. In turn, DCIS which was only mammography detected had a relatively benign biologic profile. We propose that MRI is helpful for diagnosing biologically (i.e. possibly prognostically) relevant DCIS [Table: see text] No significant financial relationships to disclose.
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Basu, Moitri, Isha Sengupta, Md Wasim Khan, Dushyant Kumar Srivastava, Partha Chakrabarti, Siddhartha Roy, and Chandrima Das. "Dual histone reader ZMYND8 inhibits cancer cell invasion by positively regulating epithelial genes." Biochemical Journal 474, no. 11 (May 19, 2017): 1919–34. http://dx.doi.org/10.1042/bcj20170223.
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Enhanced migratory potential and invasiveness of cancer cells contribute crucially to cancer progression. These phenotypes are achieved by precise alteration of invasion-associated genes through local epigenetic modifications which are recognized by a class of proteins termed a chromatin reader. ZMYND8 [zinc finger MYND (myeloid, Nervy and DEAF-1)-type containing 8], a key component of the transcription regulatory network, has recently been shown to be a novel reader of H3.1K36Me2/H4K16Ac marks. Through differential gene expression analysis upon silencing this chromatin reader, we identified a subset of genes involved in cell proliferation and invasion/migration regulated by ZMYND8. Detailed analysis uncovered its antiproliferative activity through BrdU incorporation, alteration in the expression of proliferation markers, and cell cycle regulating genes and cell viability assays. In addition, performing wound healing and invasion/migration assays, its anti-invasive nature is evident. Interestingly, epithelial–mesenchymal transition (EMT), a key mechanism of cellular invasion, is regulated by ZMYND8 where we identified its selective enrichment on promoters of CLDN1/CDH1 genes, rich in H3K36Me2/H4K16Ac marks, leading to their up-regulation. Thus, the presence of ZMYND8 could be implicated in maintaining the epithelial phenotype of cells. Furthermore, syngeneic mice, injected with ZMYND8-overexpressed invasive breast cancer cells, showed reduction in tumor volume and weight. In concert with this, we observed a significant down-regulation of ZMYND8 in invasive ductal and lobular breast cancer tissues compared with normal tissue. Taken together, our study elucidates a novel function of ZMYND8 in regulating EMT and invasion of cancer cells, possibly through its chromatin reader function.
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Gonzalez-Angulo, Ana Maria, Aysegul Sahin, Savitry Krishnamurthy, Ying Yang, Shu-Wan Kau, Gabriel N. Hortobagyi, and Massimo Cristofanilli. "Biologic Markers in Axillary Node-Negative Breast Cancer: Differential Expression in Invasive Ductal Carcinoma Versus Invasive Lobular Carcinoma." Clinical Breast Cancer 7, no. 5 (December 2006): 396–400. http://dx.doi.org/10.3816/cbc.2006.n.056.
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Jacquemet, Guillaume, David M. Green, Rebecca E. Bridgewater, Alexander von Kriegsheim, Martin J. Humphries, Jim C. Norman, and Patrick T. Caswell. "RCP-driven α5β1 recycling suppresses Rac and promotes RhoA activity via the RacGAP1–IQGAP1 complex." Journal of Cell Biology 202, no. 6 (September 9, 2013): 917–35. http://dx.doi.org/10.1083/jcb.201302041.
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Inhibition of αvβ3 or expression of mutant p53 promotes invasion into fibronectin (FN)-containing extracellular matrix (ECM) by enhancing Rab-coupling protein (RCP)–dependent recycling of α5β1 integrin. RCP and α5β1 cooperatively recruit receptor tyrosine kinases, including EGFR1, to regulate their trafficking and downstream signaling via protein kinase B (PKB)/Akt, which, in turn, promotes invasive migration. In this paper, we identify a novel PKB/Akt substrate, RacGAP1, which is phosphorylated as a consequence of RCP-dependent α5β1 trafficking. Phosphorylation of RacGAP1 promotes its recruitment to IQGAP1 at the tips of invasive pseudopods, and RacGAP1 then locally suppresses the activity of the cytoskeletal regulator Rac and promotes the activity of RhoA in this subcellular region. This Rac to RhoA switch promotes the extension of pseudopodial processes and invasive migration into FN-containing matrices, in a RhoA-dependent manner. Thus, the localized endocytic trafficking of α5β1 within the tips of invasive pseudopods elicits signals that promote the reorganization of the actin cytoskeleton, protrusion, and invasion into FN-rich ECM.
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Menier, Jean J., and Marcel Jouan. "Biologie et description d'Aethina tumida Murray, 1867, espèce invasive déprédatrice de l'Abeille mellifère (Coleoptera, Nitidulidae)." Bulletin de la Société entomologique de France 108, no. 3 (2003): 323–28. http://dx.doi.org/10.3406/bsef.2003.16974.
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Mikkelsen, Tom. "Cytostatic Agents in the Management of Malignant Gliomas." Cancer Control 5, no. 2 (March 1998): 150–62. http://dx.doi.org/10.1177/107327489800500206.
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Background: Cytotoxic therapy for malignant gliomas is limited by poor delivery and drug resistance, and local therapy is ineffective in managing migratory cells. However, recent developments in malignant glioma therapy involve trials of cytostatic rather than conventional cytotoxic agents. Methods: The biology of the brain extracellular matrix, tumor invasion, and angiogenesis are reviewed, and the cytostatic agents that inhibit matrix metalloproteinases, angiogenesis, cell proliferation, and signal transduction are discussed, as well as studies of the angiogenic and migratory capacity of malignant brain tumors. Results: Two specific and interrelated areas, anti-invasion (migration) and anti-angiogenesis, are potential areas to develop new treatment strategies. Tumor invasion and angiogenesis are important components of the spread and biologic effects of malignant gliomas. Several proteinase inhibitors are in clinical trial, as well as anti-angiogenic agents and signal transduction cascade inhibitors. Conclusions: Biologic control of brain tumor cell populations may offer a new management approach to add to currently available management options for malignant brain tumors.
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Lochter, André, Marc Navre, Zena Werb, and Mina J. Bissell. "α1 and α2 Integrins Mediate Invasive Activity of Mouse Mammary Carcinoma Cells through Regulation of Stromelysin-1 Expression." Molecular Biology of the Cell 10, no. 2 (February 1999): 271–82. http://dx.doi.org/10.1091/mbc.10.2.271.
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Tumor cell invasion relies on cell migration and extracellular matrix proteolysis. We investigated the contribution of different integrins to the invasive activity of mouse mammary carcinoma cells. Antibodies against integrin subunits α6 and β1, but not against α1 and α2, inhibited cell locomotion on a reconstituted basement membrane in two-dimensional cell migration assays, whereas antibodies against β1, but not against α6 or α2, interfered with cell adhesion to basement membrane constituents. Blocking antibodies against α1 integrins impaired only cell adhesion to type IV collagen. Antibodies against α1, α2, α6, and β1, but not α5, integrin subunits reduced invasion of a reconstituted basement membrane. Integrins α1 and α2, which contributed only marginally to motility and adhesion, regulated proteinase production. Antibodies against α1 and α2, but not α6 and β1, integrin subunits inhibited both transcription and protein expression of the matrix metalloproteinase stromelysin-1. Inhibition of tumor cell invasion by antibodies against α1 and α2 was reversed by addition of recombinant stromelysin-1. In contrast, stromelysin-1 could not rescue invasion inhibited by anti-α6 antibodies. Our data indicate that α1 and α2 integrins confer invasive behavior by regulating stromelysin-1 expression, whereas α6 integrins regulate cell motility. These results provide new insights into the specific functions of integrins during tumor cell invasion.
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Genna, Alessandro, Stefanie Lapetina, Nikola Lukic, Shams Twafra, Tomer Meirson, Ved P. Sharma, John S. Condeelis, and Hava Gil-Henn. "Pyk2 and FAK differentially regulate invadopodia formation and function in breast cancer cells." Journal of Cell Biology 217, no. 1 (November 13, 2017): 375–95. http://dx.doi.org/10.1083/jcb.201702184.
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The nonreceptor tyrosine kinase Pyk2 is highly expressed in invasive breast cancer, but the mechanism by which it potentiates tumor cell invasiveness is unclear at present. Using high-throughput protein array screening and bioinformatic analysis, we identified cortactin as a novel substrate and interactor of proline-rich tyrosine kinase 2 (Pyk2). Pyk2 colocalizes with cortactin to invadopodia of invasive breast cancer cells, where it mediates epidermal growth factor–induced cortactin tyrosine phosphorylation both directly and indirectly via Src-mediated Abl-related gene (Arg) activation, leading to actin polymerization in invadopodia, extracellular matrix degradation, and tumor cell invasion. Both Pyk2 and the closely related focal adhesion kinase (FAK) regulate tumor cell invasion, albeit via distinct mechanisms. Although Pyk2 regulates tumor cell invasion by controlling invadopodium-mediated functions, FAK controls invasiveness of tumor cells by regulating focal adhesion–mediated motility. Collectively, our findings identify Pyk2 as a unique mediator of invadopodium formation and function and also provide a novel insight into the mechanisms by which Pyk2 mediates tumor cell invasion.
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Chen, W. C., and B. Obrink. "Cell-cell contacts mediated by E-cadherin (uvomorulin) restrict invasive behavior of L-cells." Journal of Cell Biology 114, no. 2 (July 15, 1991): 319–27. http://dx.doi.org/10.1083/jcb.114.2.319.
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L-cells were cotransfected with plasmids coding for mouse E-cadherin (uvomorulin) and the neophosphotransferase gene, and stable transfectants expressing E-cadherin at the cell surface were selected and cloned. Control transfection was done with the neophosphotransferase gene alone. The invasive migration of transfected and untransfected L-cells into three-dimensional collagen gels was then analyzed. L-cells not expressing E-cadherin migrated efficiently into the gels, whereas invasion of the E-cadherin-expressing L-cells was restricted in a cell density dependent manner. At sparse density, when the cells exhibited little cell-cell contacts, no difference was observed between the level of invasion of the cadherin-expressing cells and the control cells. However, with increasing cell density, decreasing amounts of the cadherin-expressing cells but increasing amounts of the control cells migrated into the gels. At confluent density hardly any cadherin-expressing cells were able to migrate into the gels. The inhibition of the invasion of the cadherin-expressing cells could be reverted if confluent cells were cultured in the presence of monoclonal antibodies against E-cadherin. Since the expression of E-cadherin did not influence the invasive mobility of single cells, these results indicate that E-cadherin-mediated cell-cell contacts inhibited invasive cellular migration. Time-lapse videoscopy and studies of cell migration from a monolayer into a cell-free area demonstrated that the restricted invasion could be explained by contact inhibition of cell movement of the cadherin-expressing cells.
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Hsia, Datsun A., Satyajit K. Mitra, Christof R. Hauck, Daniel N. Streblow, Jay A. Nelson, Dusko Ilic, Shuang Huang, et al. "Differential regulation of cell motility and invasion by FAK." Journal of Cell Biology 160, no. 5 (March 3, 2003): 753–67. http://dx.doi.org/10.1083/jcb.200212114.
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Cell migration and invasion are fundamental components of tumor cell metastasis. Increased focal adhesion kinase (FAK) expression and tyrosine phosphorylation are connected with elevated tumorigenesis. Null mutation of FAK results in embryonic lethality, and FAK−/− fibroblasts exhibit cell migration defects in culture. Here we show that viral Src (v-Src) transformation of FAK−/− cells promotes integrin-stimulated motility equal to stable FAK reexpression. However, FAK−/− v-Src cells were not invasive, and FAK reexpression, Tyr-397 phosphorylation, and FAK kinase activity were required for the generation of an invasive cell phenotype. Cell invasion was linked to transient FAK accumulation at lamellipodia, formation of a FAK–Src-p130Cas–Dock180 signaling complex, elevated Rac and c-Jun NH2-terminal kinase activation, and increased matrix metalloproteinase expression and activity. Our studies support a dual role for FAK in promoting cell motility and invasion through the activation of distinct signaling pathways.
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Alexander, C. M., and Z. Werb. "Targeted disruption of the tissue inhibitor of metalloproteinases gene increases the invasive behavior of primitive mesenchymal cells derived from embryonic stem cells in vitro." Journal of Cell Biology 118, no. 3 (August 1, 1992): 727–39. http://dx.doi.org/10.1083/jcb.118.3.727.
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The metalloproteinase family of proteolytic enzymes can degrade extracellular matrix and facilitate invasive migration. This class of enzymes is specifically inhibited by the tissue inhibitor of metalloproteinases (TIMP-1). Using homologous recombination, we have disrupted the gene encoding TIMP-1 in pluripotent embryonic stem cells. Because the TIMP-1 gene is X linked and is hemizygous in embryonic stem cells, we have been able to study the effect of this mutation in culture. Using a basement membrane invasion assay, we found that the mutant cells, differentiated in low concentrations of serum with retinoic acid, were more invasive than their normal cell counterparts, and that this was specifically reversed by adding exogenous TIMP-1 protein. The invasive cell population had characteristics of an early population of primitive mesenchymal cells, including expression of vimentin and a transient period of invasiveness from 4-8 d after initiation of differentiation. Therefore, metalloproteinase activity can be rate limiting for cell invasion.
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Olazcuaga, Laure, Anne Loiseau, Hugues Parrinello, Mathilde Paris, Antoine Fraimout, Christelle Guedot, Lauren M. Diepenbrock, et al. "A Whole-Genome Scan for Association with Invasion Success in the Fruit Fly Drosophila suzukii Using Contrasts of Allele Frequencies Corrected for Population Structure." Molecular Biology and Evolution 37, no. 8 (April 17, 2020): 2369–85. http://dx.doi.org/10.1093/molbev/msaa098.
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Abstract Evidence is accumulating that evolutionary changes are not only common during biological invasions but may also contribute directly to invasion success. The genomic basis of such changes is still largely unexplored. Yet, understanding the genomic response to invasion may help to predict the conditions under which invasiveness can be enhanced or suppressed. Here, we characterized the genome response of the spotted wing drosophila Drosophila suzukii during the worldwide invasion of this pest insect species, by conducting a genome-wide association study to identify genes involved in adaptive processes during invasion. Genomic data from 22 population samples were analyzed to detect genetic variants associated with the status (invasive versus native) of the sampled populations based on a newly developed statistic, we called C2, that contrasts allele frequencies corrected for population structure. We evaluated this new statistical framework using simulated data sets and implemented it in an upgraded version of the program BayPass. We identified a relatively small set of single-nucleotide polymorphisms that show a highly significant association with the invasive status of D. suzukii populations. In particular, two genes, RhoGEF64C and cpo, contained single-nucleotide polymorphisms significantly associated with the invasive status in the two separate main invasion routes of D. suzukii. Our methodological approaches can be applied to any other invasive species, and more generally to any evolutionary model for species characterized by nonequilibrium demographic conditions for which binary covariables of interest can be defined at the population level.