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Al-Muqbel, Kusai M. "Bone Marrow Metastasis Is an Early Stage of Bone Metastasis in Breast Cancer Detected Clinically by F18-FDG-PET/CT Imaging." BioMed Research International 2017 (2017): 1–7. http://dx.doi.org/10.1155/2017/9852632.
Objective. To determine the value of 18F-FDG PET/CT in detection of bone marrow (BM) metastasis in breast cancer which is considered an early stage of bone metastasis. Patients and Methods. Retrospectively, breast cancer patients with bone metastasis were included. BM metastasis was considered if the lesion was PET positive/CT occult while bone metastasis was considered if the lesion was PET positive/ CT positive. BM metastases were observed sequentially on F18-FDG PET/CT. Results. We included 35 patients. Eighteen patients (51%) had BM metastases in addition to other bone metastases. BM metastases comprised 24% of all lesions. Posttreatment scan was performed on 26/35 patients. Twenty-three percent of BM metastases had resolved completely without causing bone destruction after treatment. Sixty-five percent of BM metastases had converted into bone metastases after treatment. Twelve percent of BM metastases had persisted after treatment. Conclusion. This retrospective study showed clinically by 18F-FDG PET/CT imaging that BM metastasis is an early stage of bone metastasis in breast cancer. Interestingly, 18F-FDG-PET/CT showed that early eradication of individual BM metastasis by systemic treatment precluded development of bone metastasis. However, more research is needed to study the impact of an early diagnosis of BM metastases on treatment outcome.
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Fidler, Isaiah J. "Melanoma Metastasis." Cancer Control 2, no. 5 (September 1995): 398–404. http://dx.doi.org/10.1177/107327489500200503.
Cancer metastasis requires a series of sequential steps, each of which is rate limiting. Neoplasms are biologically heterogeneous, and the process of metastasis is highly selective. Multiple metastases often differ in biologic characteristics and can change during the course of the disease. Clonal analysis of human melanoma suggest that systemic, physiologic signals can be recognized by neoplastic cells. Brain metastases are particularly common in patients with metastatic melanoma. The blood brain barrier does not prevent the invasion of the brain parenchyma by circulating metastatic cells, and its permeability varies among different experimental brain metastases.
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Ali, Kamran, Sukki Cho, Hyo Jun Jang, Kwhanmien Kim, and Sanghoon Jheon. "Predictive Factors of Thoracic Lymph Node Metastasis Accompanying Pulmonary Metastasis from Colorectal Cancer." Thoracic and Cardiovascular Surgeon 67, no. 08 (May 29, 2018): 683–87. http://dx.doi.org/10.1055/s-0038-1642602.
Background The aim of this study was to identify the factors predicting thoracic lymph node (LN) metastases for pulmonary resection from colorectal cancer (CRC). Methods The records of 160 patients who underwent pulmonary metastasectomy for CRC were retrospectively reviewed. Clinicopathologic factors were analyzed with chi-square test or t-test and logistic regression to identify predictable factors for LN metastases. Results Sixty patients (37.5%) underwent LN dissection during pulmonary metastasectomy, and LN metastases were found in five patients. Twenty-three patients had LN recurrence among the 100 patients (62.5%) without LN dissection during the follow-up period. Twenty-eight patients out of 160 (17.5%) had LN metastases. By multivariate analysis, the number of pulmonary metastasis and metastasis from colon cancers were independent factors predicting LN metastases. Conclusion The number of pulmonary metastasis and metastasis from colon cancers were independent factors predicting LN metastases. LN sampling should be performed especially in cases with strong predictive factors to improve staging and help guide further treatment.
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Pisani, P., G. Angeli, M. Krengli, and F. Pia. "Renal carcinoma metastasis to the parotid gland." Journal of Laryngology & Otology 104, no. 4 (April 1990): 352–54. http://dx.doi.org/10.1017/s0022215100112691.
AbstractMetastatic tumours in major salivary glands are uncommon with a higher incidence of primary sites from the head and neck. The lungs and breast are the common primary sites, while metastases from the kidney are very rarely found. The authors describe a case of renal clear-cell carcinoma with metastastis to the parotid gland. The incidence of a metastasis in the parotid gland from a primary renal carcinoma, even if rare, should not be overlooked in making a correct differential diagnosis with acinic cell carcinoma and monomorphic clear cell adenoma.
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Isidro, Ulysses, Liam M. O'Brien, and Ronnie Sebro. "Linear mixed-effects models for estimation of pulmonary metastasis growth rate: implications for CT surveillance in patients with sarcoma." British Journal of Radiology 93, no. 1114 (October 1, 2020): 20190856. http://dx.doi.org/10.1259/bjr.20190856.
Objectives: Sarcoma patients often undergo surveillance chest CT for detection of pulmonary metastases. No data exist on the optimal surveillance interval for chest CT. The aim of this study was to estimate pulmonary metastasis growth rate in sarcoma patients. Methods: This was a retrospective review of 95 patients with pulmonary metastases (43 patients with histologically confirmed metastases and 52 with clinically diagnosed metastases) from sarcoma treated at an academic tertiary-care center between 01 January 2000 and 01 June 2019. Age, sex, primary tumor size, grade, subtype, size and volume of the pulmonary metastasis over successive chest CT scans were recorded. Two metastases per patient were chosen if possible. Multivariate linear mixed-effects models with random effects for each pulmonary metastasis and each patient were used to estimate pulmonary metastasis growth rate, evaluating the impact of patient age, tumor size, tumor grade, chemotherapy and tumor subtype. We estimated the pulmonary metastasis volume doubling time using these analyses. Results: Maximal primary tumor size at diagnosis (LRT statistic = 2.58, df = 2, p = 0.275), tumor grade (LRT statistic = 1.13, df = 2, p = 0.567), tumor type (LRT statistic = 7.59, df = 6, p = 0.269), and patient age at diagnosis (LRT statistic = 0.735, df = 2, p = 0.736) were not statistically significant predictors of pulmonary nodule growth from baseline values. Chemotherapy decreased the rate of pulmonary nodule growth from baseline (LRT statistic = 7.96, df = 2, p = 0.0187). 95% of untreated pulmonary metastases are expected to grow less than 6 mm in 6.4 months. There was significant intrapatient and interpatient variation in pulmonary metastasis growth rate. Pulmonary metastasis volume growth rate was best fit with an exponential model in time. The volume doubling time for pulmonary metastases assuming an exponential model in time was 143 days (95% CI (104, 231) days). Conclusions: Assuming a 2 mm nodule is the smallest reliably detectable nodule by CT, the data suggest that an untreated pulmonary metastasis is expected to grow to 8 mm in 8.4 months (95% CI (4.9, 10.2) months). Tumor size, grade and sarcoma subtype did not significantly alter pulmonary metastasis growth rate. However, chemotherapy slowed the pulmonary metastasis growth rate. Advances in knowledge: CT surveillance intervals for pulmonary metastases can be estimated based on metastasis growth rate. There was significant variation in the pulmonary metastasis growth rate between metastases within patient and between patients. Pulmonary nodule volume growth followed an exponential model, linear in time.
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Choi, Hee Jun, Jai Min Ryu, Byung Joo Chae, Seok Jin Nam, Jonghan Yu, Se Kyung Lee, Jeong Eon Lee, and Seok Won Kim. "Is Sentinel Lymph Node Biopsy for Breast Cancer with Cytology-Proven Axillary Metastasis Safe? A Prospective Single-Arm Study." Journal of Clinical Medicine 10, no. 20 (October 16, 2021): 4754. http://dx.doi.org/10.3390/jcm10204754.
The purpose of this study was to evaluate pathologic lymph node metastasis in breast cancer with cytology-proven axillary metastasis. This study was designed prospectively. We performed axillary lymph node dissections (ALND) after lymphatic mapping by near-infrared (NIR) fluorescence imaging with Indocyanine Green (ICG). We evaluated 72 breast cancer patients with cytology-proven axillary metastasis by curative surgery at the Samsung Medical Center between May of 2016 and December of 2017. Among the 72 patients with cytology-proven axillary metastasis, 14 of 39 patients (35.9%) with one or two sentinel lymph nodes containing metastases were metastasized to post-sentinel lymph node. Thirteen of fourteen patients had additional non-sentinel lymph node metastases, seven of thirteen patients also had additional level II lymph node metastases, and one patient had only one additional level II lymph node metastasis. Of T1 or T2 stage patients, 10 of 33 patients (30.3%) with one or two sentinel lymph nodes containing metastases were metastasized to post-sentinel lymph node. Even in patients without SLN metastasis, 50% of the patients had at least three LN metastases, and 40% in the T1 or T2 stage patients. Sentinel lymph node biopsy without ALND might be not safe for patients with cytology-proven axillary metastasis.
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Park, Hyung Kyu, Joungho Han, Ghee Young Kwon, Min-Kyung Yeo, and Go Eun Bae. "Patterns of Extrathoracic Metastasis in Lung Cancer Patients." Current Oncology 29, no. 11 (November 16, 2022): 8794–801. http://dx.doi.org/10.3390/curroncol29110691.
Metastasis is a major cause of death in lung cancer patients. Therefore, a deeper understanding of the metastatic mechanisms is important for developing better management strategies for lung cancer patients. This study evaluated the patterns of extrathoracic metastases in lung cancer. We retrieved data for 25,103 lung cancer patients from an institutional database and then evaluated the impacts of clinicopathologic factors on metastasis patterns. We found that 36.5% of patients had extrathoracic metastasis. Younger patients had a significantly higher extrathoracic metastasis rate in most histologic subtypes. Metastases to the bone (58.3%), central nervous system (CNS) (44.3%), liver (26.6%) and adrenal gland (18.3%) accounted for 85.5% of all extrathoracic metastases. Patients with nonmucinous adenocarcinoma had significantly higher bone metastasis rate. Patients with small cell carcinoma and large cell neuroendocrine carcinoma (LCNEC) had significantly higher liver metastasis rates. Further, patients with LCNEC also had a significantly lower bone metastasis rate, and patients with squamous cell carcinoma had a significantly lower CNS metastasis rate. Patients with multiple cancers had similar patterns of metastasis compared to patients with only lung cancer. In conclusion, different histologic subtypes of lung cancer have different metastatic patterns. Our study might help clinicians decide on follow-up strategies.
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Li, Chuang, Zhao-zhong Meng, Jian-wu Qin, and Xin-guang Qiu. "Analysis of Risk Factors of Level V Lymphatic Metastasis for Papillary Thyroid Carcinoma with pN1b." Journal of Oncology 2021 (August 18, 2021): 1–5. http://dx.doi.org/10.1155/2021/5562065.
Objective. To explore the risk factors of level V lymphatic metastasis in papillary thyroid carcinoma (PTC) patients with pN1b. Methods. Patients were selected if they presented with a suspicious level III or IV lymph node metastasis and underwent surgery by hemi or total thyroidectomy with a lymph node dissection (levels III, IV, VI, and VII). For these patients, if frozen section showed a positive level III or IV node, then levels II and V nodes were resected. Univariate analysis was performed using the chi-square test for some factors, including age, sex, tumor location, multifocal lesions, tumor size, local invasion of primary focus, status of cervical lymphatic metastasis, TNM staging, tumor deposits (independent tumor nodules), and the metastasis to more than 5 central lymph nodes. Then, the factors with statistical significance indicated by the above univariate analysis underwent multivariate analysis. Results. Univariate analysis indicated that the level V lymphatic metastasis was significantly associated with simultaneous metastases to levels II, III, and IV, simultaneous metastases to levels III and IV, and tumor deposits (all p < 0.05 ), but it was not significantly associated with age, sex, tumor location, multifocal lesions, tumor size, local invasion of primary focus, other cervical lymphatic metastasis, TNM staging, and the metastases to more than 5 central lymph nodes (all p > 0.05 ). Multivariate analysis suggested that the simultaneous metastases to levels III and IV and tumor deposits were the risk factors of level V lymphatic metastasis. Conclusion. The simultaneous metastases to levels III and IV and tumor deposits are independent risk factors of level V lymphatic metastasis. The patients with pN1b PTC who have simultaneous metastases to levels III and IV or/and tumor deposits may have the risk of level V lymph node metastasis.
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Suki, Dima, Rami Khoury Abdulla, Minming Ding, Soumen Khatua, and Raymond Sawaya. "Brain metastases in patients diagnosed with a solid primary cancer during childhood: experience from a single referral cancer center." Journal of Neurosurgery: Pediatrics 14, no. 4 (October 2014): 372–85. http://dx.doi.org/10.3171/2014.7.peds13318.
Object Metastasis to the brain is frequent in adult cancer patients but rare among children. Advances in primary tumor treatment and the associated prolonged survival are said to have increased the frequency of brain metastasis in children. The authors present a series of cases of brain metastases in children diagnosed with a solid primary cancer, evaluate brain metastasis trends, and describe tumor type, patterns of occurrence, and prognosis. Methods Patients with brain metastases whose primary cancer was diagnosed during childhood were identified in the 1990–2012 Tumor Registry at The University of Texas M.D. Anderson Cancer Center. A review of their hospital records provided demographic data, history, and clinical data, including primary cancer sites, number and location of brain metastases, sites of extracranial metastases, treatments, and outcomes. Results Fifty-four pediatric patients (1.4%) had a brain metastasis from a solid primary tumor. Sarcomas were the most common (54%), followed by melanoma (15%). The patients' median ages at diagnosis of the primary cancer and the brain metastasis were 11.37 years and 15.03 years, respectively. The primary cancer was localized at diagnosis in 48% of patients and disseminated regionally in only 14%. The primary tumor and brain metastasis presented synchronously in 15% of patients, and other extracranial metastases were present when the primary cancer was diagnosed. The remaining patients were diagnosed with brain metastasis after initiation of primary cancer treatment, with a median presentation interval of 17 months after primary cancer diagnosis (range 2–77 months). At the time of diagnosis, the brain metastasis was the first site of systemic metastasis in only 4 (8%) of the 51 patients for whom data were available. Up to 70% of patients had lung metastases when brain metastases were found. Symptoms led to the brain metastasis diagnosis in 65% of cases. Brain metastases were single in 60% of cases and multiple in 35%; 6% had only leptomeningeal disease. The median Kaplan-Meier estimates of survival after diagnoses of primary cancer and brain metastasis were 29 months (95% CI 24–34 months) and 9 months (95% CI 6–11 months), respectively. Untreated patients survived for a median of 0.9 months after brain metastasis diagnosis (95% CI 0.3–1.5 months). Those receiving treatment survived for a median of 8 months after initiation of therapy (95% CI 6–11 months). Conclusions The results of this study challenge the current notion of an increased incidence of brain metastases among children with a solid primary cancer. The earlier diagnosis of the primary cancer, prior to its dissemination to distant sites (especially the brain), and initiation of presumably more effective treatments may support such an observation. However, although the actual number of cases may not be increasing, the prognosis after the diagnosis of a brain metastasis remains poor regardless of the management strategy.
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Costa, Weruska Alcoforado, José Eleutério Jr., Paulo César Giraldo, and Ana Katherine Gonçalves. "Quality of life in breast cancer survivors." Revista da Associação Médica Brasileira 63, no. 7 (July 2017): 583–89. http://dx.doi.org/10.1590/1806-9282.63.07.583.
Summary Objective: To evaluate the influence of functional capacity (FC) and how it affects quality of life (QoL) in breast cancer survivors. Method: A total of 400 breast cancer survivors were studied - 118 without metastasis, 160 with locoregional metastasis and 122 with distant metastasis. The European Organization for Research and Treatment for Cancer Quality of Life Questionnaire--Core 30 (EORTC QLQ-C30), Breast Cancer-Specific (EORTC QLQ-BR23), and the Karnofsky Performance Scale (KPS) were used to evaluate FC and QoL. Results: Women with distant metastases presented lower KPS 75.3 (SD=12.5) (p<0.001). For QLQ-C30, the mean of the Functional Scale for patients with distant metastasis was 57 (SD=19) (p<0.001), and the mean of the Symptom Scale for patients with distant metastasis was 37 (SD=20) (p<0.001). Both the scales for pain and fatigue showed the highest mean in the groups. For the Global Health Scale, patients without metastasis scored a mean of 62 (SD=24) points, while those with locoregional metastases scored a mean of 63 (SD=21.4), and distant metastasis scored 51.3 (SD=24) points. In the group with distant metastases, 105 (87%) had pain, and the average KPS was 74 (SD=12.0) (p=0.001). Conclusion: Breast cancer was associated with decreased FC, compromised QoL in women with locoregional and distant metastases compared to those without metastasis.
The complex PI3K/mTOR pathway regulates tumor progression via effects on cellular proliferation, apoptosis, autophagy, and motility. New drugs that inhibit the catalytic site of both PI3K and mTOR have shown promise in clinical trials. Here, we report the first use of a novel, dual PI3K/mTOR catalytic site inhibitor (PF-04691502, PF1502) in a xenograft model of breast cancer metastasis to bone. Metastatic MDA-MB-1833 cells showed PI3K/mTOR activation relative to parental MDA-MB-231. Low-dose PF1502 significantly impaired tumor cell motility and invasion in vitro without causing cell cycle arrest, apoptosis, or reduced proliferation. Pre-treatment of tumor cells at this dose reduced bone metastatic outgrowth in vivo. The atypical tumor suppressor, p27KIP1, is phosphorylated in its C-terminal region by multiple AGC kinases downstream of PI3K/mTOR. These phosphorylation events promote cytoplasmic mislocalzation of p27 which, in turn, facilitates inhibition of the RhoA cytoskeletal regulatory protein. The resulting turnover of the actin cytoskeleton is thought to underlie the increased cellular motility attributed to cytoplasmic p27. In MDA-MB-1833 cells, PI3K/mTOR inhibition reduced p27 C-terminal phosphorylation at T157 and T198 and reduced cytoplasmic p27 levels. Overexpression of a p27T157D/T198D phospho-mimetic mutant conferred resistance to the anti-motility effects of PF1502 in vitro. MDA-MB-1833 cells demonstrate p27-dependent inhibition of RhoA-ROCK signaling, as well as p27-dependent motility and invasion in vitro, however, RhoA knockdown did not confer resistance to the anti-motility effects of PF1502. p27shRNA dramatically impaired the bone metastatic outgrowth of MDA-MB-1833 in vivo. In an effort to explore potentially novel RhoA-independent mechanisms whereby cytoplasmic p27 might drive tumor cell motility and metastasis, we turned to the process known as epithelial-to-mesenchymal transition (EMT). The EMT program has been implicated as a critical driver of tumor metastasis in a variety of cancer models. PI3K/mTOR inhibition and shRNA p27 treatment both reversed expression of EMT markers in MDA-MB-1833. Thus, PI3K/mTOR appears to drive p27-dependent motility and metastasis at least in part by induction of an EMT-like phenotype, a novel mechanism through which p27 might act to promote tumor progression. These results provide an important new clinical rationale supporting the use of PI3K/mTOR inhibitors as anticancer agents via their inhibition of tumor invasion and metastasis.
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Björndahl, Meit A. "Lymphangiogenesis and lymphatic metastasis /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-562-3/.
Chiang, Yan Ting. "Identification of metastasis-driving genes as potential therapeutic targets/ biomarkers for metastatic prostate cancer." Thesis/Dissertation, University of British Columbia, 2015. http://hdl.handle.net/2429/52901.
Metastatic prostate cancer is currently incurable. Metastasis is thought to result from changes in the expression of specific metastasis-driving genes, leading to a cascade of activated downstream genes setting the metastatic process in motion. As such, metastasis-driving genes could provide effective therapeutic targets and prognostic biomarkers for improved disease management. In search of potential metastasis-driving genes, genes with elevated expression in patient-derived metastatic LTL-313H prostate cancer tissues, as distinct from non-metastatic LTL-313B tissues, were identified. Among these genes, TIMELESS and DLX1 were promising. Unfortunately, their silencing and overexpression in prostate cancer cells did not lead to inhibition of metastatic properties, indicating that they were not metastasis-driving genes.
A different, novel approach was used based on the notion that metastasis-driving genes can activate genes in an amplification cascade fashion. Accordingly, I used the IPA’s Upstream Regulator Analysis tool to analyze the differential gene expression profile of the metastatic and non-metastatic tissues to predict the upstream master regulatory (metastasis-driving) genes accountable for the differential expression. Six candidate genes were identified, including GATA2, a pioneer factor-encoding gene. Elevated GATA2 expression in clinical metastatic prostate cancer specimens correlated with poor patient prognosis. Furthermore, GATA2 gene silencing in human prostate cancer LNCaP cells led to marked reduction in cell proliferation, cell migration, tissue invasion, focal adhesion disassembly and a dramatic change in transcriptional activity, indicating that GATA2 plays a critical role in prostate cancer metastasis. As such, GATA2 could represent a metastasis-driving gene and a potential therapeutic target for inhibiting the growth and metastasis development in prostate cancer.
Further analysis of GATA2-regulated genes led to the development of a GATA2-based metastatic gene signature. Its prognostic value was confirmed using two prostate cancer patient cohorts. In addition, it was shown to be a prognostic factor for risk assessment of metastasis development, independent of the widely used D’Amico prognostic classification system. However, a thorough validation is critical and, if successful, the GATA2-based gene signature could lead to a paradigm shift in the management of early prostate cancer.
In conclusion, the findings of this study appear to be potentially useful for improved management of metastatic prostate cancer. Medicine, Faculty of Graduate
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Nielsen, S. R. "Metastasis-associated macrophages orchestrate the formation of a hospitable metastatic niche in pancreatic cancer." Electronic Thesis or Diss., University of Liverpool, 2017. http://livrepository.liverpool.ac.uk/3007527/.
Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal cancers with an overall 5-year survival rate < 5%, a rate that has not improved for a long time. The dismal prognosis for PDAC is part due to late detection, often at advanced stages of the disease where patients have developed distant metastases, but also due to chemotherapeutical resistance. Patients eligible for surgical resection of the pancreatic tumour has the best prognosis, but even when resection is successful, patients often relapse with distant metastases within 2 years after surgery. Macrophages promote tumourigenesis and enhance metastasis in many cancer types; however, the role of macrophages in PDAC metastasis is poorly understood. Using an experimental mouse model of liver metastasis, we find that PDAC liver metastasis critically depends on the early recruitment of granulin-secreting metastasis-associated macrophages (MAMs) to the liver that promote metastatic colonisation. Mechanistically, we demonstrate that granulin secretion by MAMs activates resident hepatic stellate cells (HSTCs) into myofibroblasts that secrete extracellular matrix components, including periostin, resulting in a fibrotic microenvironment that sustains metastatic tumour growth. Disruption of MAM recruitment in PI(3)Kγ-deficient mice, chemical depletion of MAMs from established lesions or genetic ablation of granulin reduces HSTC activation and liver metastasis. Adjuvant CTX is standard for patients after surgical resection to eliminate any residual cancer cells, and it improves survival for patients after resection. We find that 45% of mice with metastatic lesions respond to gemcitabine treatment with a reduction in metastatic burden. The metastatic lesions in these mice are characterised by a reduction in αSMA+ myofibroblasts. HSTCs do not seem to promote cancer cell survival in the presence of chemotherapy, but rather constitutes a protective niche that promotes relapse by promoting the growth of pancreatic cancer cells after gemcitabine treatment.
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Yuzhalin, Arseniy. "Proteomic profiling of metastatic matrisome reveals citrullination as a marker of colorectal liver metastasis." Electronic Thesis or Diss., University of Oxford, 2018. http://ora.ox.ac.uk/objects/uuid:2612ba4b-b311-4802-84ae-ab60472bfe02.
Colorectal cancer is one of the most frequently occurring malignancies and a major cause of cancer death. Distant metastases in this disease most commonly develop in the liver and are often untreatable. Here, we use proteomics to characterise, qualitatively and quantitatively, extracellular matrix (ECM) from colorectal cancer liver metastases. We show that citrullination of the ECM by cancer cell derived peptidyl arginine deiminase 4 (PAD4) is important for the growth of liver metastases. Citrullination of proteins, a posttranslational conversion of arginine residues to citrulline, is well recognised in rheumatoid arthritis, but largely undocumented in cancer. PAD4, a key enzyme responsible for catalysing citrullination, is produced by metastatic colorectal cancer cells and found at higher levels in human liver metastases than in normal liver. Functional significance for citrullination in metastatic growth was evident in murine models where inhibition of citrullination, either globally by pharmacologic inhibition of PADs or specifically in colorectal cancer cells by PAD4 knockdown reduced liver metastatic burden by 3- to 4-fold (P < 0.05). Additionally, citrullination of key extracellular matrix (ECM) component collagen type I in vitro led to greater adhesion and 25-30% decreased migration of colorectal cancer cells (P < 0.05) along with increased expression of characteristic epithelial markers, indicating a role for citrullination in promoting mesenchymal-to-epithelial transition (MET). Overall, our study revealed PAD4- dependent citrullination of the ECM altering mesenchymal-epithelial plasticity in colorectal cancer cells and the progression of liver metastasis. These data indicate that inhibition of citrullination could be exploited to potentially prevent the development of liver metastases in colorectal cancer.
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Stitzlein, Russell Neil. "The role of ezrin in osteosarcoma metastasis and its potential use in early identification of metastases." Text, Miami University Honors Theses / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=muhonors1177692826.
Clark, S. R. "The investigation of tumour metastasis." Electronic Thesis or Diss., University of Oxford, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.370241.
Liu, Hui Ph D. Massachusetts Institute of Technology. "Identification of a novel metastasis enhancer, CDCP1, and analysis of its functions during melanoma metastasis." Thesis, Massachusetts Institute of Technology, 2009. http://hdl.handle.net/1721.1/47881.
Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Biology, 2009. Includes bibliographical references. Nearly 90% of cancer mortality from solid tumors is due to metastasis of malignant cells to the distant vital organs. It is now well established that a plethora of stromal cells are present within the tumor, and contribute in various ways to tumor initiation and progression, and plasma membrane proteins are the mediators for tumor-stromal communications. In this thesis, I focused on plasma membrane proteins that may contribute to tumor metastasis. I applied quantitative mass spectrometry technology to first identify plasma proteins that are expressed at different levels in melanoma cells with high versus low metastatic abilities. Using SILAC (stable isotope labeling with amino acids in culture) coupled with nano-spray tandem mass spectrometry, this work led to the discovery of C̲ub Ḏomain C̲ontaining Protein 1 (CDCP1) as one of those differentially expressed transmembrane proteins. We found that CDCP1 is not only a surface marker for cells with higher metastatic potential, it is also functionally engaged in enhancing tumor metastasis. When searching for the underlying mechanisms, we found that CDCP1 is important for soft agar colony-forming abilities, suggesting that CDCP1 might regulate the balance between cell proliferation and anoikis. Making use of 3D Matrigel culture system, we found that CDCP1 also regulates scattered growth of melanoma cells. We speculate these two factors may contribute to enhanced-metastatic ability observed in mice. (cont.) When investigating signaling pathways that may mediate the functions of CDCP1, we found that overexpression of CDCP1 correlates with hyper-activation of Src family kinases. While wild-type CDCP1 enhances SFK activation, point mutation that abolished CDCP1 functions (in scattered growth and in metastasis) also abolished SFK hyper-activation, suggesting that CDCP1 might function through the activation of SFKs. Such notion was further supported since pharmacological reagents PP2 and Dasatinib, which are two SFK inhibitors, blocked in vitro functions of CDCP1 in scattered growth. Thus the work in this thesis has identified a novel metastasis enhancer, CDCP1, and has gained insight into the mechanisms by which CDCP1 functions. by Hui Liu. Ph.D.
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Onder, Tamer T. "Role of e-cadherin in tumor metastasis and discovery of compounds targeting metastasis cancer cells." Thesis, Massachusetts Institute of Technology, 2008. http://hdl.handle.net/1721.1/43226.
Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Biology, 2008. Includes bibliographical references. The epithelial cell adhesion molecule E-cadherin is often downregulated during carcinoma progression and metastatic spread of tumors. However, the precise mechanism and molecular basis of metastasis promotion by E-cadherin loss is not completely understood. To investigate its role in metastasis, I utilized two distinct methods of E-cadherin inhibition that distinguish between E-cadherin's cell-cell adhesion and intracellular signaling functions. While the disruption of cell-cell contacts alone does not enable metastasis in vivo, the loss of E-cadherin protein does, through induction of an epithelial-to-mesenchymal transition (EMT), invasiveness and anoikis-resistance. E-cadherin binding partner f3-catenin is necessary but not sufficient for these phenotypes. In addition, gene expression analysis shows that E-cadherin loss results in the induction of multiple transcription factors, at least one of which, Twist, is necessary for E-cadherin loss-induced metastasis. These findings indicate that E-cadherin loss in tumors contributes to metastatic dissemination by inducing wide-ranging transcriptional and functional changes. In addition to promoting metastasis, loss of E-cadherin and the accompanying EMT renders cells resistant to conventional chemotherapeutic drugs. As the cells that have undergone an EMT represent the pool of cancer cells most competent to metastasize and lead to tumor recurrence, it is of vital importance to find therapies that effectively target such cells. Paired cell lines that differ in their differentiation state were utilized to discover compounds with selective toxicity against cells that have undergone an EMT. High-throughput screening of small molecule libraries resulted in a number of compounds that specifically affect the viability of cells that have undergone an EMT while having minimal cytotoxic effects on control epithelial cells. These studies establish a proof-of-principle for discovering compounds that target highly metastatic and otherwise chemotherapy resistant cancer cells. by Tamer T. Onder. Ph.D.
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Gooding, Alex Joseph. "Characterizing a Role for the lncRNA BORG during Breast Cancer Progression and Metastasis." Text, Case Western Reserve University School of Graduate Studies / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=case1528462540265762.
Schirrmacher, Volker, and Reinhard Schwartz-Albiez, eds. Cancer Metastasis. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74236-1.
Lyden, David, Danny R. Welch, and Bethan Psaila, eds. Cancer Metastasis. Cambridge: Cambridge University Press, 2009. http://dx.doi.org/10.1017/cbo9780511976117.
Popper, Helmut, and Bruno Murer. "Metastasis." In Essentials of Diagnostic Pathology, 275–96. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-22664-0_19.
Armstrong, Carol L. "Metastasis." In Encyclopedia of Clinical Neuropsychology, 1586. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-0-387-79948-3_129.
Armstrong, Carol L. "Metastasis." In Encyclopedia of Clinical Neuropsychology, 1. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56782-2_129-2.
Armstrong, Carol L. "Metastasis." In Encyclopedia of Clinical Neuropsychology, 2163. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-57111-9_129.
Muschel, Ruth J. "Metastasis." In Encyclopedia of Cancer, 1–3. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_3671-2.
Brockhausen, Inka, and William Kuhns. "Metastasis." In Glycoproteins and Human Disease, 221–26. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-662-21960-7_26.
Davis, Barbara J. "Metastasis." In Encyclopedia of Systems Biology, 1300. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-9863-7_1587.
Costa, Rafael Everton Assunção Ribeiro da, Fergus Tomás Rocha de Oliveira, Eduarda Norberto Siqueira, Ana Lúcia Nascimento Araújo, and Sabas Carlos Vieira. "CUTANEOUS AND BONE METASTASIS OF OCCULT BREAST CANCER: CASE REPORT." In Abstracts from the Brazilian Breast Cancer Symposium - BBCS 2021. Mastology, 2021. http://dx.doi.org/10.29289/259453942021v31s2078.
Introduction: Occult breast cancer (OBC) is defined as a metastatic carcinoma that occurs mainly in the axillary lymph nodes, derived from a primary malignant breast tumor undetectable by clinical and radiological analyses. OBC is a rare disease accounting for 0.3%–1.0% of all breast cancers, which occurs more commonly at the age of around 55 years. The OBC represents a rare event (especially with the manifestation of systemic metastases) and a major diagnostic challenge. Thus, the aim of this study was to report a case of OBC with the primary manifestation of cutaneous metastases and the subsequent detection of bone metastasis. Case report: A 70-year-old female patient, G1P0A0, nonsmoker, nonalcoholic, with hypertension, and sedentary lifestyle, exhibited multiple metastatic cutaneous lesions in the left cervical region (2 cm), of the left breast (3 cm), left axilla (0.5 cm), left subscapular region (3 cm), and in the second and fifth left chirodactyls (using anastrozole for 1 month). Mammography, ultrasonography, and magnetic resonance imaging of the breast were performed, and no structural alterations were detected in any of these tests. Biopsy of the skin lesion of the left cervical region and immunohistochemistry also indicated positive estrogen receptors (ER), progesterone receptors (PR), and GATA-binding protein 3 (GATA-3; compatible with breast cancer metastasis), establishing the diagnosis of occult breast cancer with cutaneous metastasis. The use of anastrozole was maintained. The scintigraphy was performed, indicating bone metastasis in the right coastal arcs 8 and 9 considered stable in a new test performed 8 months later. All cutaneous metastatic lesions disappeared 2 years later, with the exception of a lesion in the left cervical region, where surgical resection was indicated. The study was approved by a Research Ethics Committee, under CAAE No 30154720.0.0000.5209. Conclusion: The patient exhibited an excellent response to anastrozole and is in excellent general condition with the stability of bone metastasis.
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Singh, Gajender, Sant Parkash Kataria, and Rajeev Sen. "Carcinoma uterine cervix metastasis to the skin: A rare case report." In 16th Annual International Conference RGCON. Thieme Medical and Scientific Publishers Private Ltd., 2016. http://dx.doi.org/10.1055/s-0039-1685280.
Introduction: Most common site of metastasis from carcinoma cervix is lung, liver, bone and brain. Cutaneous metastasis is rare occurrence in carcinoma cervix. Incidence reported ranges from 0.1 to 2%. Common morphological pattern of skin metastases are nodules, plaques and inflammatory telangiectatic lesions. Materials and Methods: A 68 years old postmenopausal female diagnosed as squamous cell carcinoma of cervix stage III B. She was given chemotherapy and radiotherapy and on regular follow up without no evidence of disease locally. After two years she presented with a sub cutaneous nodule of approximately 5x4 cm size just below the left scapula of one month duration. There was no similar swelling in any other region. It was rapidly increased in size and painful. The FNAC of the nodule showed metastatic from squamous cell carcinoma. PET scan showed metastases in bilateral lung and pelvic lymph node with no evidence of local disease. Excision biopsy of the nodule confirmed the diagnosis. Conclusion: Cutaneous metastases from carcinoma cervix are rare. Differential diagnoses include benign dermatitis, subcutaneous phycomycosis, and plaque like mycosis fungoides.
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Tang, Xin, and Taher Saif. "In Vitro Cancer Metastasis Induced by Mechanical Force." In ASME 2013 2nd Global Congress on NanoEngineering for Medicine and Biology. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/nemb2013-93130.
Based on the American Cancer Society’s report at 2004, after 50-year’s efforts in bio-chemical medicine development, the U.S.A. cancer mortality is 193.9 per 100,000 persons, which is not significantly reduced from that at 1950, 185.8 per 100,000 persons. One critical reason for the clinical inefficacy is that it is not identified what signals trigger the onset of metastasis. 90% of cancer deaths are caused by metastases (1–6). During metastasis, malignant cancer cells detach from the parent cancer tumor to invade new organs (5–7). Although the primary tumor can be readily removed by surgery if detected in time, metastasis cannot be cured effectively due to the presence of numerous secondary tumors. Here we present, for the first time, that cancer cells can exhibit metastasis like phenotype (MLP) in vitro when they are experiencing appropriate mechanical stimuli.
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Moreno, Marcelo, Amauri de Oliveira, Tália Cássia Boff, Gabriela Nogueira Matschinski, and Izadora Czarnobai. "SQUAMOUS CELL CARCINOMA METASTASIS OF THE MAMMARY GLAND: CASE REPORT." In Scientifc papers of XXIII Brazilian Breast Congress - 2021. Mastology, 2021. http://dx.doi.org/10.29289/259453942021v31s1007.
Introduction: Primary squamous cell carcinoma (SCC) of the breast is a rare neoplasm, which represents less than 0.1% of invasive breast cancers. Therefore, it is essential to discriminate between a primary SCC and a metastatic SCC. In order to be considered a primary carcinoma of the breast, a histological examination of the lesion must show more than 90% of squamous neoplastic cells, in addition to the absence of cutaneous SCC or other anatomical sites. Extra-mammary neoplasm metastases are uncommon, representing 0.5% to 2% of breast malignancies. Metastatic SCC in the mammary gland is an uncommon event. To date, only three cases were reported in the literature of secondary involvement of vulvar SCC in the mammary gland. The objective of this work is to report the case of a patient with secondary mammary metastasis to a vulva SCC. Case report: A 74-year-old female patient who underwent radical modified vulvectomy 10 years before. Her pathological stage was characterized as IIIB. For this reason, she was also submitted to adjuvant treatment with chemotherapy associated with radiotherapy to the vulvar region, inguinal lymph node chains and pelvic arteries. On the ninth year of cancer follow-up, she presented recurrence in the vaginal wall. In the complementary image exams, an extentension of neoplasia to pelvic organs was identified, but no distant metastatic lesions were found. She underwent monobloc resection of pelvic organs, with reconstruction of the urinary and intestinal transits. The patient showed a good clinical evolution, with no pelvic complaints. After one year, the patient returned complaining of a nodule in the right breast. On physical examination, a lesion was observed at the junction of the lateral quadrants of the breast, measuring +/- 3.5 cm, with associated inflammatory signs and imprecise limits, with a central region showing a fistulous orifice through which the necrotic material passed. On the mammography, a dense, rounded and partially delimited lesion was identified. She underwent a core biopsy that described a SCC. According to her clinical history, it was considered a remote relapse of the vulvar SCC. The patient was submitted to a quadrantectomy with an ipsilateral axillary lymphadenectomy and reconstruction with a lateral thoracic flap. On an anatomopathological examination there was a description that the neoplasm would invade the underlying muscle tissue; and the resection margins were free. Four out of the fourteen isolated axillary lymph nodes had metastases, without perinodal soft tissue invasion. Six months after breast surgery, the patient evolved metastases to both lungs and soon after she died without response to the systemic treatment employed. This report was approved by the Research Ethics – UFFS (Universidade Federal da Fronteira Sul) (number 4.034.565).
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Shareef, Sarah J., Mihai Nita-Lazar, and Maria A. Kukuruzinska. "E-cadherin N-glycosylation Modulates the Strength of Adherens Junctions." In ASME 2010 First Global Congress on NanoEngineering for Medicine and Biology. ASMEDC, 2010. http://dx.doi.org/10.1115/nemb2010-13013.
Metastasis, the spread of cancer cells throughout the body, claims 90% of solid tumor deaths. During metastasis, cancer cells undergo discohesion. An understanding of how to control and strengthen cell adhesion through junction formation could lead to methods for decreasing metastatic tendencies.
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Kraning-Rush, Casey M., Shawn P. Carey, and Cynthia A. Reinhart-King. "Molded Collagen Microchannels for the Study of Cancer Cell Invasion." In ASME 2012 10th International Conference on Nanochannels, Microchannels, and Minichannels collocated with the ASME 2012 Heat Transfer Summer Conference and the ASME 2012 Fluids Engineering Division Summer Meeting. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/icnmm2012-73093.
Metastasis is the cause of 90% of cancer-related deaths and yet the precise mechanism of metastasis is poorly understood[1]. To metastasize, cells break free from the primary tumor, migrate through the surrounding tissue, and enter the vascular system to move to a secondary site. To migrate through the stroma, cell can both degrade the tissue and use physical force to move the tissue from its path. However, the relative roles of matrix degradation and cellular force are not well-understood. Previous work has shown that as cell move through the matrix, they create channels that other cells can then use to more easily escape from the primary tumor [2, 3]. To investigate the mechanisms by which metastatic cells move through 3D matrices, we fabricated microchannels from collagen that simulate the paths that are made and used by cells during metastasis. Here, we will present our method for molding channels in compliant collagen gels to investigate cell migration. The channels dimensions approximate the size of a cell and permit cell migration without the need for matrix degradation. We demonstrate that the channels cause persistent, unidirectional cell migration that is significantly faster than the migration observed in 3D matrices without channels. These channels provide a unique platform to probe 3D cellular migration and permit the dissection of the relative roles of matrix degradation and force generation in facilitating cell invasion.
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Hoskins, Meghan H., Shile Liang, Payal Khanna, Robert F. Kunz, and Cheng Dong. "Cytokine Convection Affects Cancer Metastasis by a Shear Rate Dependent Mechanism." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192904.
Hoskins, Meghan H., Shile Liang, Robert F. Kunz, and Cheng Dong. "Cellular Mechanics and Biology of Tumor Cell-Leukocyte Interactions in the Near Wall Region Under Shear Flow Conditions." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176376.
Malignant melanoma has a high propensity for metastatic spread, making it the most deadly form of skin cancer. Currently, no effective treatment exists to prevent melanoma metastasis or to inhibit metastatic tumors growing in distant organs [1,2].
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Gupta, Vivek, Amita Mishra, Namit Kalra, and Bhawna Narula. "A rare case report of incidental solitary uterine metastasis in primary invasive lobular carcinoma of breast." In 16th Annual International Conference RGCON. Thieme Medical and Scientific Publishers Private Ltd., 2016. http://dx.doi.org/10.1055/s-0039-1685401.
Introduction: Infiltrating Lobular carcinoma (ILC) of the breast is second most common cancer of breast next only to Infiltrating ductal carcinoma (IDC). It has a different metastatic pattern as compared to the IDC. Breast cancer is the most frequent primary site which spreads to gynaecologic organs. Case Presentation: A 40 yrs old Iraqi lady presented as a diagnosed case of lobular carcinoma of left breast. She had already undergone a lumpectomy at Iraq a month back and now had come for completion of treatment. On metastatic workup with PETCT scan, we found a multicentric residual disease in the left breast along with some ipsilateral axillary LN with significant uptake. The concurrent CECT done showed a uterine leiomyomam also. As she was strongly hormone receptor positive, had completed her family and was having mennorhagia probably attributable to uterine fibroids. She was offered hysterectomy with B/L salpingo-oophorectomy. She was keen for breast preservation but in view of her multicentricity of disease on the left breast she was counselled for mastectomy with upfront whole breast reconstruction with TRAM flap. She underwent left modified radical mastectomy with hysterectomy with BSO and TRAM flap reconstruction. The histopathological examination revealed a multicentric, multifocal ILC, grade II with heavy nodal involvement including extracapsular extension. The leiomyoma of uterus also showed tumor deposits from lobular carcinoma breast. Conclusion: We report a very rare case of metastatic pattern of carcinoma of breast. On literature review we found that it is common for the lobular carcinomas of breast to metastasise to gynaecologic organs. Uterine corpus is a very rare site of metastasis for extragenital cancers including breast. All the patients of primary lobular carcinoma of breast should be screened for gynaecologic secondaries in the preoperative workup with high degree of suspicion.
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Sharma, Puja, Brian Koons, and Amrinder S. Nain. "Blebbing Dynamics, Single Cell Force Measurements, and the Influence of Cytochalasin D on Glioblastoma Multiforme Cells Using STEP Fibers." In ASME 2013 2nd Global Congress on NanoEngineering for Medicine and Biology. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/nemb2013-93105.
Classified as a grade IV tumor of the central nervous system, Glioblastoma multiforme (GBM) arises from the glia. A poor understanding of tumor metastasis and limited treatment options have led to increase in deaths of patients suffering from GBM. Studying glioma behavior using aligned structures that mimic native glioblastoma metastatic path is challenging. In this study, we utilize a previously described non-electrospinning platform to manufacture aligned 3D structures called STEP nanonets that not only allows the study of individual cell-nanofiber interaction, but also allows the calculation of migratory forces using beam mechanics. In particular, the blebbing dynamics, force generation, and the effect of an actin disruptor, Cytochalasin D have been investigated on a glioma cell line (DBTRG, Denver Based Tumor Research Group). It was observed that cell pulled onto the nanofibers causing measurable deflections when they were in spread and non-blebbing conditions. In non-spread configurations while attached to fibers, the cells acquired spherical configurations and resumed blebbing. The average migratory force generated by cells exposed to DMSO (control, 1:1000 dilution) using nanonets of 2μm by 400nm fibers was 0.58±0.06nN. Actin disruptor, Cytochalasin D severely compromised the ability of the glioma cells to migrate causing no deflection of the fibers. Forces exerted by tumor cells on their native microenvironment affects their ability to metastasize, invade and proliferate. While the result presents actin disruptor as a potential target to minimize metastasis, the influence of other cytoskeleton disruptors can also be studied using the platform. Moreover, the results obtained from the study can be utilized to better understand the individual cell – nanofibers interaction which can shed light on how cells interact with their native environment during metastasis.
Reports on the topic "Metastasis":
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Zhao, Hao, Chunhao Liu, Yanlong Li, and Xiaoyi Li. Prognostic factors for survival in differentiated thyroid cancer with pulmonary metastases: a protocol of systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, February 2022. http://dx.doi.org/10.37766/inplasy2022.2.0026.
Pulmonary metastasis (PM) is the most common form of distance metastasis in differentiated thyroid cancer (DTC), which has a poor prognosis. However, the prognostic risk factors are not yet well identified and analyzed. This systematic review and meta-analysis aims to fill this blank though identifying and discussing survival prognostic risk factors systematically for DTC patients with PM. Pulmonary metastasis (PM) is the most common form of distance metastasis in differentiated thyroid cancer (DTC), which has a poor prognosis. However, the prognostic risk factors are not yet well identified and analyzed. This systematic review and metastases aims to fill this blank though identifying and discussing survival prognostic risk factors systematically of DTC patients with PM. Condition being studied: differentiated thyroid cancer with pulmonary metastases.
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Welch, Danny R. Metastasis Genes in Breast Cancer Metastasis to Bone. Fort Belvoir, VA: Defense Technical Information Center, June 2004. http://dx.doi.org/10.21236/ada427647.
Teng, Yong. Targeting Prostate Cancer Metastasis. Fort Belvoir, VA: Defense Technical Information Center, September 2015. http://dx.doi.org/10.21236/ada621823.
Pettaway, Curtis A. Angiogenesis Regulates Prostate Cancer Metastasis. Fort Belvoir, VA: Defense Technical Information Center, March 2001. http://dx.doi.org/10.21236/ada398034.
Wang, Weigang. Hypoxia in Invasion and Metastasis. Fort Belvoir, VA: Defense Technical Information Center, August 2007. http://dx.doi.org/10.21236/ada485743.
Massague, Joan. Dissecting and Targeting Latent Metastasis. Fort Belvoir, VA: Defense Technical Information Center, September 2013. http://dx.doi.org/10.21236/ada605186.
Keller, Evan. Novel Aptamers to Target Metastasis. Fort Belvoir, VA: Defense Technical Information Center, September 2010. http://dx.doi.org/10.21236/ada534850.
Zhang, Yan. Antibody Microchips to Study Metastasis. Fort Belvoir, VA: Defense Technical Information Center, July 2003. http://dx.doi.org/10.21236/ada418683.
Keller, Evan, and Greg Shelley. Novel Aptamers to Target Metastasis. Fort Belvoir, VA: Defense Technical Information Center, November 2012. http://dx.doi.org/10.21236/ada569358.
Pettaway, Curtis A. Angiogenesis Regulates Prostate Cancer Metastasis. Fort Belvoir, VA: Defense Technical Information Center, September 1999. http://dx.doi.org/10.21236/ada378066.
