Relevant bibliographies by topics / Tumor pathogenesis

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Tumor pathogenesis'

Author: Grafiati
Published: 4 June 2021
Last updated: 12 February 2022

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Journal articles on the topic "Tumor pathogenesis"

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Shimon, I. "Pituitary Tumor Pathogenesis." Journal of Clinical Endocrinology & Metabolism 82, no. 6 (June 1, 1997): 1675–81. http://dx.doi.org/10.1210/jc.82.6.1675.

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Ellsworth, Rachel E., Jeffrey A. Hooke, Craig D. Shriver, and Darrell L. Ellsworth. "Genomic Heterogeneity of Breast Tumor Pathogenesis." Clinical medicine. Oncology 3 (January 2009): CMO.S2946. http://dx.doi.org/10.4137/cmo.s2946.

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Pathological grade is a useful prognostic factor for stratifying breast cancer patients into favorable (low-grade, well-differentiated tumors) and less favorable (high-grade, poorly-differentiated tumors) outcome groups. Under the current system of tumor grading, however, a large proportion of tumors are characterized as intermediate-grade, making determination of optimal treatments difficult. In an effort to increase objectivity in the pathological assessment of tumor grade, differences in chromosomal alterations and gene expression patterns have been characterized in low-grade, intermediate-grade, and high-grade disease. In this review, we outline molecular data supporting a linear model of progression from low-grade to high-grade carcinomas, as well as contradicting genetic data suggesting that low-grade and high-grade tumors develop independently. While debate regarding specific pathways of development continues, molecular data suggest that intermediate-grade tumors do not comprise an independent disease subtype, but represent clinical and molecular hybrids between low-grade and high-grade tumors. Finally, we discuss the clinical implications associated with different pathways of development, including a new clinical test to assign grade and guide treatment options.
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Tolstykh, Nadezhda V., Alexander F. Gurchin, Nadezhda Yu Koroleva, and Igor D. Stolyarov. "Modern conceptions about the pathogenesis of tumor-related epilepsy." Medical academic journal 19, no. 2 (September 18, 2019): 13–25. http://dx.doi.org/10.17816/maj19213-25.

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Tumor-related epilepsy is of interest among the symptomatic epilepsy, that develops in 75% of patients with gliomas low-grade (astrocytomas, oligodendrogliomas — Gr II) and more than 95% of patients with glioneuronal tumors (ganglioglioma — Gr I). Currently, the nature of epileptogenic activity in brain tumors is still controversial, and the search for epileptogenic foci that are part of the tumor zone presents certain difficulties. The authors described the structural changes and metabolism in the tumor and peritumoral zone, immunological status, and molecular genetic features of the tumor, which may explain the pathogenesis of tumor-related epilepsy. In turn, the clarification of the mechanisms of epileptogenesis is a prerequisite for the development of therapeutically effective anticonvulsants, and to improve the strategies of complex treatment of tumors associated with epilepsy.
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Sano, Keiji. "Pathogenesis of intracranial germ cell tumors reconsidered." Journal of Neurosurgery 90, no. 2 (February 1999): 258–64. http://dx.doi.org/10.3171/jns.1999.90.2.0258.

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Object. To determine the pathogenesis of intracranial germ cell tumors (GCTs), the author studied 153 cases of these tumors encountered through 1994, 62.7% of which showed monotypic histological patterns and 37.3% of which were shown to be mixed tumors.Methods. Six patients died soon after admission and underwent autopsy; the other patients underwent surgery followed by radio- and/or chemotherapy. One hundred thirty-four cases were followed through the end of 1997. All patients with a choriocarcinoma died within 1 year. Patients with a yolk sac tumor (endodermal sinus tumor) or an embryonal carcinoma also had poor outcomes. Patients with a mature teratoma had 5- and 10-year survival rates of 93% each. Patients with an immature teratoma had 5- and 10-year survival rates of 86% each, whereas patients who had a teratoma with malignant transformation had a 3-year survival rate of 50%. Patients with a germinoma had a 5-year survival rate of 96% and a 10-year survival rate of 93%. These results may bring into question the validity of the germ cell theory because germinoma, which should be the most undifferentiated tumor according to the theory, was the most benign and choriocarcinoma and yolk sac tumor (endodermal sinus tumor), which should be the most differentiated tumors, were the most malignant according to results obtained during the follow-up study.Conclusions. Germ cell tumors other than germinomas may not originate from one single type of cell (primordial germ cells). The embryonic cells of various stages of embryogenesis may perhaps be misplaced in the bilaminar embryonic disc at the time of the primitive streak formation, becoming involved in the stream of lateral mesoderm and carried to the neural plate area to become incorrectly enfolded into the brain at the time of neural tube formation. The author propounds the following hypothesis: tumors composed of cells resembling the cells that appear in the earlier stages of embryogenesis (ontogenesis) are more malignant than those composed of cells resembling the cells that appear in the later stages of embryogenesis.
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Vorobev, Alexander Viktorovich, Alexander Davidovich Makatsaria, Andrey Mikhailovich Chabrov, and Alexander Anatol’evich Savchenko. "Pathogenesis of Trousseau’s syndrome." Journal of obstetrics and women's diseases 64, no. 4 (September 15, 2015): 85–94. http://dx.doi.org/10.17816/jowd64485-94.

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Malignancies and thrombosis have common pathogenetic features that was shown by A. Trousseau in 1865. There is now no doubt that the cancer patients occur much more frequently thromboembolism, and migratory venous thrombosis is a manifestation of paraneoplastic syndrome in cancer patients. In general, any manifestation of thrombohemorrhagic complications in cancer patients called Trousseau’s syndrome. While thrombotic complications such as venous thromboembolism are most frequent in cancer patients, may also experience severe bleeding symptoms due to systemic coagulopathies, including disseminated intravascular coagulation, haemolytic thrombotic microangiopathy, and hyperfibrinolysis. The basis of the pathophysiology of Trousseau’s syndrome, except the classic triad of Virchow, is overproduction of tissue factor (TF), the main initiator of extrinsic coagulation pathway. Thus a significant release of microparticles from tumor cells bearing tissue factor is critical not only for the formation of a blood clot, but the growth and progression of tumors. Tumor cells activate the coagulation cascade or fibrinolysis system, providing conditions for its further spread, stimulation of angiogenesis, increased vascular permeability, which in turn promotes metastasis.
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BUDAY, L., and J. DOWNWARD. "Roles of cortactin in tumor pathogenesis." Biochimica et Biophysica Acta (BBA) - Reviews on Cancer 1775, no. 2 (June 2007): 263–73. http://dx.doi.org/10.1016/j.bbcan.2006.12.002.

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Jones, Deborah P., Hazem Mahmoud, and Russell W. Chesney. "Tumor lysis syndrome: pathogenesis and management." Pediatric Nephrology 9, no. 2 (April 1995): 206–12. http://dx.doi.org/10.1007/bf00860751.

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Nagamine and Mikami. "Ovarian Seromucinous Tumors: Pathogenesis, Morphologic Spectrum, and Clinical Issues." Diagnostics 10, no. 2 (January 31, 2020): 77. http://dx.doi.org/10.3390/diagnostics10020077.

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Ovarian seromucinous tumors were introduced in the 2014 World Health Organization (WHO) classification as one of the seven types of ovarian epithelial tumors. They are characterized by frequent association with endometriosis and bilaterality, microscopic appearance of papillary architecture, and admixture of a variety of müllerian-type epithelium. They are considered to be endometriosis-related ovarian neoplasms, along with endometrioid and clear cell tumors; recent molecular studies suggest this particular tumor is a variant of endometrioid tumor. Discrepancies in nomenclature, definition, and morphology of seromucinous tumors appear to be a source of confusion, for both clinicians and general surgicalpathologists. This review summarizes the clinicopathological features of benign, borderline, and malignant seromucinous tumors, as well as controversies regarding these tumors.
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Sano, Keiji. "Pathogenesis of intracranial germ cell tumors reconsidered." Neurosurgical Focus 5, no. 1 (July 1998): E3. http://dx.doi.org/10.3171/foc.1998.5.1.4.

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The author studied 153 cases of intracranial germ cell tumors (GCTs) through 1994, 62.7% of which showed monotypic histological patterns and 37.3% of which were shown to be mixed tumors. All of these cases, except for six patients who died soon after admission and underwent autopsy, underwent surgery followed by radio- and/or chemotherapy. All patients with choriocarcinoma died within 2 years. Patients with yolk sac tumor (endodermal sinus tumor) and embryonal carcinoma also had poor outcomes. Patients with mature teratoma had 5- and 10-year survival rates of 92.9% each. Patients with immature teratoma and malignant teratoma had a 5- and 10-year survival rate of 70.7% each. Patients with germinoma had a 5-year survival rate of 95.4% and a 10-year survival rate of 92.7%. These results may bring into question the validity of the germ cell theory, because germinoma, which should be the most undifferentiated according to the theory, was the most benign and choriocarcinoma and yolk sac tumor (endodermal sinus tumor), which should be the most differentiated, were the most malignant according to results obtained during follow-up study. Therefore, GCTs other than germinoma may not originate from one single type of cell (primordial germ cells). The embryonic cells of various stages of embryogenesis may perhaps be misplaced in the bilaminar embryonic disc at the time of the primitive streak formation, becoming involved in the stream of lateral mesoderm and carried to the future cranial area to become incorrectly enfolded into the brain at the time of the neural tube formation. The authors propound the following law: tumors composed of cells resembling the cells that appear in the earlier stages of embryogenesis (ontogenesis) are more malignant than those composed of cells resembling the cells that appear in the later stages of embryogenesis.
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Zheng, Ruifang, and Debra S. Heller. "Borderline Brenner Tumor: A Review of the Literature." Archives of Pathology & Laboratory Medicine 143, no. 10 (February 19, 2019): 1278–80. http://dx.doi.org/10.5858/arpa.2018-0285-rs.

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Brenner tumors arise from ovarian epithelium, accounting for approximately 5% of benign ovarian epithelial tumors. The World Health Organization classification groups them into benign, borderline, and malignant on the basis of proliferation and invasiveness, and borderline Brenner tumor is defined as “displaying epithelial proliferation beyond that seen in benign Brenner's tumor, but lacking stromal invasion.” Borderline Brenner tumors are rare. Fewer than 60 cases have been reported. The more recent articles mostly focus on pathogenesis. We reviewed the literature on borderline Brenner tumor and have summarized the clinical and pathologic findings, as well as the treatment, differential diagnoses, and recent advances in histogenesis and molecular pathogenesis.
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Dissertations / Theses on the topic "Tumor pathogenesis"

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Lampa, Jon. "Studies of pharmacological interventions and pathogenesis of rheumatoid arthritis /." Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-372-4/.

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Lo, Kwok-pui, and 盧國培. "Tumor suppressive role of the α-isoform of transcriptional repressor PRDM1 in the pathogenesis of NK-cell malignancies." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B48421388.

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NK cell lymphoma is one of the cellular malignancies that arise from lymphocytes. Due to its rarity and aggressiveness the detailed molecular pathogenesis of NK cell lymphoma remains to be discovered. There are recent studies showing that the master regulator of B-cell differentiation into plasma cells, the Positive Regulatory Domain containing 1, with ZNF domain(PRDM1) has tumor suppressive function not only in diffuse large B-cell lymphoma (DLBCL), but also in NK cell lymphoma. The PRDM1 has two isoforms, αand β, where the former one is a functional isoform and the latter is a defective isoform with shortened and disrupted positive regulatory domain formed from transcription of internal promoter. By semi -quantitative RT-PCR, PRDM1-αexpression was found to be absent in 80% (4/5) NK cell lines while present in the normal NK cells. Loss of PRDM1 expression suggests its role as tumor suppressor. In order to study the tumor suppressive role of the αisoform of PRDM1, short-hairpin RNA (shRNA) with isoform specific sequence is used to knockdown the expression of PRDM1-αin NK cell lines. Western blot result showed about 40% decrease of PRDM1-αprotein after knockdown. Retroviral infection of the NK cell lines, NKYS and YT which have endogenous α-isoforms of expression, for the delivery of the shRNA was done and were subsequently subjected to in vitro functional analyses including MTS assay, colony formation assay, cell viability test and cell cycle analysis to determine potential effect of the loss of PRDM1-αon the NK cell lines. The PRDM1-αprotein isoform is expected to be able to repress excessive growth of NK cell line. When this isoform is inactivated, the NK cell lines are expected to proliferate significantly than the negative control counterpart in functional analyses. However in this study only YTcell line showed significant proliferation advantage in MTS and colony formation assay after the knockdown of PRDM1-α by shRNA. Cell viability assays and cell cycle analyses failed to show significant changes in both NK cell lines and yet even showed inhibitory effect after the knockdown of the gene. Ectopic expression of PRDM1-αby retroviral infection was done in KHYG cell line to further evaluate its tumor suppressive function. Apoptotic assay on the KHYG cells with ectopic expression of PRDM1-αwas performed and percentage of cells with late apoptosis was found to be significantly higher in this cell line. This suggests that one of the mechanisms for PRDM1-αto act as tumor suppressor is via the apoptosis pathway which in turn promotes the cell death. Future studies will be made to further investigate the effects of knockdown of PRDM-1αby designing another shRNA sequence which knockdown the expression of gene by at least 50% and to further investigate the role of PRDM1-αinthe pathogenesis NK cell lymphomaby proliferation assays, colony formation assay and cell cycle analysis.
published_or_final_version
Pathology
Master
Master of Medical Sciences
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Shan, Bing. "The novel sumoylation enhancer RSUME is implicated in pituitary tumor pathogenesis." Diss., lmu, 2010. http://nbn-resolving.de/urn:nbn:de:bvb:19-123612.

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Liu, Wen. "Functional Analysis of the Tumor Metastasis Suppressor, NDRG1." OpenSIUC, 2011. https://opensiuc.lib.siu.edu/dissertations/347.

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Metastasis suppressors regulate multiple steps during the process of dissemination of tumor cells from primary sites to distant organs, while they do not affect the growth of the primary tumor. Previously, we identified NDRG1 (N-myc downstream regulated gene 1) as a tumor metastasis suppressor gene and found that it is negatively involved in metastatic progression of prostate and breast cancers. To elucidate the molecular mechanism of NDRG1 function, we used the yeast two-hybrid system to identify proteins interacting with NDRG1. In the first part of this project, we demonstrate that NDRG1, interacts with the Wnt receptor, LRP6, followed by blocking of the Wnt signaling, and therefore, orchestrates a cellular network that impairs the metastatic progression of tumor cells in vitro and in animal model. We also found that restoring NDRG1 expression by a small molecule compound significantly suppressed the capability of otherwise highly metastatic tumor cells to thrive in circulation and distant organs in animal models. In addition, our analysis of clinical cohorts data indicate that Wnt+/NDRG-/LRP+ signature has a strong predictable value for recurrence-free survival of cancer patients. Collectively, we have identified NDRG1 as a negative master regulator of Wnt signaling during the metastatic progression, and therefore revealed a novel control mechanism of Wnt signaling in tumor progression. Previously, we identified the metastasis promoting transcription factor, ATF3, as a downstream target of NDRG1. Further analysis revealed that the KAI1 promoter contained a consensus binding motif of ATF3, suggesting a possibility that NDRG1 suppresses metastasis through inhibition of ATF3 expression followed by activation of KAI1 gene. In the second part of this project, we examine a possible link between two metastasis suppressor genes, NDRG1 and KAI1, through ATF3. We demonstrated that ectopic expression of NDRG1 was able to augment endogenous KAI1gene expression in prostate cancer cell lines, while silencing NDRG1 accompanied with significant decrease in KAI1 expression in vitro and in vivo. In addition, our results of ChIP analysis indicate that ATF3 indeed bound to the promoter of KAI1 gene. Importantly, our promoter-based analysis revealed that ATF3 modulated KAI1 transcription through cooperation with other endogenous transcription factor as co-activator (ATF3-JunB) or co-repressor (ATF3-NFêB). Moreover, loss of KAI1 expression significantly abrogated NDRG1-mediated metastatic suppression in vitro as well as in a spontaneous metastasis animal model, indicating that KA11 is a functional down-stream target of NDRG1 pathway. Our result of immunohistochemical analysis showed that loss of NDRG1 and KAI1 occurs in parallel as prostate cancer progresses. We also found that a combined expression status of these two genes serves as a strong independent prognostic marker to predict metastasis-free survival of prostate cancer patients. Taken together, our result revealed a novel regulatory network of two metastasis suppressor genes, NDRG1 and KAI1, which together concerted metastasis-suppressive activities through intrinsic transcriptional cascade.
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Li, Jun. "Role of tumor suppressor ing4 in human cutaneous melanoma pathogenesis and progression." Thesis, University of British Columbia, 2010. http://hdl.handle.net/2429/30234.

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ING4 was identified as a tumor suppressor in 2003 and shown to diminish colony-forming efficiency, induce p53-dependent apoptosis, and arrest cell cycle at G2/M phase. To investigate the role of ING4 in human cutaneous melanoma, we examined ING4 expression using tissue microarray and found that ING4 expression was significantly decreased in malignant melanoma compared with dysplastic nevi and reduced ING4 expression was correlated with melanoma thickness, ulceration and poor 5-year survival of melanoma patients. Multivariate analysis revealed that ING4 expression is an independent prognostic marker in melanoma patients. In melanoma cells, we found that overexpression of ING4 suppressed melanoma cell migration through RhoA-ROCK pathway and cell invasion by inhibiting MMP-2 and MMP-9 activity. We also demonstrated that ING4 inhibits endothelial cell growth and tube formation in vitro through suppressing NF- κB/IL-6 pathway. In vivo model revealed that ING4 inhibited blood vessel formation and recruitment of endothelial cells in matrigel plugs. Strikingly, we found that ING4 is induced by BRMS1. Further experiments showed that BRMS1 expression was significantly decreased in metastatic melanoma compared with primary melanoma or dysplastic nevi, and reduced BRMS1 staining was correlated with AJCC stages and worse 5-year survival of melanoma patients. Moreover, we demonstrated that BRMS1 overexpression inhibited endothelial cell growth and tube formation in vitro through suppressing NF-κB/IL-6 pathway and this BRMS1-mediated IL-6 expression is dependent on NF-κB. In vivo studies indicated that BRMS1 inhibited supportive blood vessel formation in matrigel plugs. Furthermore, we demonstrated that ING4 knockdown abrogated the suppressive effect of BRMS1 on HUVECs growth, while ING4 overexpression inhibited BRMS1 knockdown-induced angiogenesis, indicating BRMS1 as upstream regulator of ING4 in regulating tumor angiogenesis. Finally, we found that the integrate score of six-biomarker system, including ING4, BRMS1 together with other four biomarkers, showed higher variations between melanoma with and without metastasis, and predicted melanoma patients outcome more accurately than individual biomarker. In summary, reduced ING4 expression in melanoma results in deficient suppression of melanoma cell migration and invasion. With BRMS1 as the upstream regulator, ING4 inhibits NF-κB/IL-6 to modulate melanoma angiogenesis. ING4 expression can be a prognostic marker and novel target for human melanoma treatment.
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Avecilla, Vincent E. "ID3, Estrogenic Chemicals, and the Pathogenesis of Tumor-Like Proliferative Vascular Lesions." FIU Digital Commons, 2017. https://digitalcommons.fiu.edu/etd/3519.

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Tumor-like proliferative vascular lesions manifest in several diseases such as peripheral arterial disease (PAD) and atherosclerosis (AS) after arterial injury. The cause of the vascular cell dysfunction in PAD patients is not known. Our recent novel discovery shows that inhibitor of differentiation 3 (ID3) is highly expressed in intimal lesions of clinical vascular disease samples. The central hypothesis of our study is: estrogenic chemical induced dysregulation of ID3 target genes is involved in the development of vascular disease. NHANES data analysis demonstrated higher geometric levels of all 6 PCB congeners in both PAD diagnosed participants and participants at risk of AS when compared to the rest of the population. Adjusted models showed association between higher exposure of PCBs, phthalates, BPA, and increased risk of PAD. Furthermore PCB153 was shown to have the highest geometric mean amongst all PCB congeners in both participants diagnosed with PAD and at risk of AS. Gene expression of ID3 & ID3 candidate targets in blood & tissue studies identified ID3 & ID3 candidate target genes as a driver of vascular disease. Overlapping ID3 & ID3 candidate target genes included: ABCB6, ACP1, BYSL, CAD, CDH15, DCBLD2, DHRS3, DNMT1, ID3, MCM4, and NDUFA7. The ID3 target genes involved in the: focal adhesion pathway were ACTN1, COL1A2, COL3A1, COL6A1, CTNNB1, IBSP, ID3, ITGA8, and MYL2; ECM-receptor interaction were COL1A2, COL3A1, COL6A1, IBSP, ID3, and ITGA8; oxidative phosphorylation pathway ATP5D, ATP5H, ATP6V0B, ATP6V0D1, ATP6V1B2, COX5A, COX7C, COX8A, CYC1, ID3, NDUFA1, NDUFA7, NDUFS4, NDUFV1, NDUFV2; and cell cycle pathway ANAPC10, ATM, CDKN2B, E2F5, MCM3, and MCM4. In summary our results showed an association between exposure to PCBs, phthalates, BPA, and increased risk of PAD and AS, and possible molecular mechanisms of interaction of ID3 target genes and estrogenic chemicals involved in PAD and AS.
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Zewdu, Abeba. "Novel Insights into Dedifferentiated Liposarcoma Pathogenesis: Evaluating the Tumor-Promoting Role of IL6/GP130 Signaling via MDM2 Upregulation." The Ohio State University, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=osu15320904714479.

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Riding, Rebecca L. "The Role of Type I Interferon in Vitiligo Pathogenesis and Melanoma Immunotherapy." eScholarship@UMMS, 2020. https://escholarship.umassmed.edu/gsbs_diss/1065.

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Vitiligo is an autoimmune skin disease in which the pigment producing cells of the epidermis, melanocytes, are targeted for destruction by CD8+ T cells specific for melanocyte/melanoma-shared antigens. Previous work has identified IFNg as the central cytokine driving disease pathogenesis in both human patients and in our mouse model of vitiligo. IFNg signaling induces production of the chemokines CXCL9 and CXCL10, which trigger autoreactive T cell migration into the epidermis where effector T cells can target and destroy melanocytes. However, both IFNg and type I IFN signaling through activation of STAT1 proteins can induce transcription of the chemokines CXCL9 and CXCL10. Therefore, it seems reasonable that type I IFN signaling may also contribute to disease pathogenesis. The role of type I IFN in vitiligo is still unclear. Genome wide association studies identified multiple genes within the type I IFN pathway including TICAM1 and IFIH1 as susceptibility loci in vitiligo. One additional study reported increased epidermal staining of CD123, a marker expressed by pDCs, and the type I IFN induced gene MX1 in vitiligo patient skin. However, this study did not show any functional data to support the role of type I IFN signaling in vitiligo pathogenesis. Since the role of type I IFN in vitiligo is ill-defined, we used two different mouse models of vitiligo to functionally determine the role of type I IFN in disease by inducing vitiligo in hosts which lack the type I IFN receptor (IFNaR). In the first model, we induced vitiligo by adoptive transfer of melanocyte-specific CD8 T cells, which are activated in vivo by infection with recombinant vaccinia virus (VACV) expressing their cognate antigen. Vitiligo induction in IFNaR-deficient mice led to the development of severe disease compared to wild type mice. Acceleration and severity of disease was characterized by increased early recruitment of melanocyte-specific CD8 T cells to the skin, increased production of effector cytokines TNFa and IFNg, and reduced PD-1 expression. Increased production of IFNg by CD8 T cells in the skin of IFNaR-deficient mice led to increased expression of the chemokines CXCL9 and CXCL10 driving disease progression. IFNaR-deficient mice also displayed significantly increased VACV titters compared to wild type hosts. This data reveals a role of type I IFN in the clearance of recombinant VACV. This data also suggests that persistent VACV infection and prolonged antigen exposure in IFNaR deficient hosts is likely driving enhanced activation of melanocyte specific CD8 T cells and the subsequent development of severe vitiligo. Since melanocytes and melanoma cells express shared antigens that can be recognized by CD8 T cells, and because the development of vitiligo after melanoma immunotherapy is a positive prognostic factor for patients, we asked whether VACV vaccine therapy in IFNaR deficient mice would enhance the anti-tumor response to melanoma. B16-F10 inoculated wild type and IFNaR-deficient mice received adoptive transfer of melanocyte-specific CD8 T cells in combination with vaccinia virus expressing their cognate antigen to activate the cells in vivo. Treatment of adoptive T cell transfer and infection with VACV in IFNaR-deficient mice revealed significantly reduced tumor burden compared to wild type mice. Improved tumor regression in IFNaR-deficient hosts was characterized by increased infiltrating cytotoxic T lymphocytes and reduced PD-1 expression. These results further demonstrate that in the absence of type I IFN, hosts mount a robust cytotoxic CD8 T cell response against melanocyte/melanoma antigens and this is likely a result of persistent VACV that leads to prolonged CD8 T cell priming. As a result, IFNaR deficient hosts kill tumor cells more efficiently. To determine whether type I IFN regulates disease pathogenesis in the absence of virus infection, we generated a model of vitiligo in which bone marrow derived dendritic cells (BMDCs) pulsed with the cognate antigen were used to prime melanocyte-specific T cells in place of the viral vector. Induction of vitiligo in IFNaR-deficient hosts using BMDCs revealed no significant differences in disease score compared to wild type hosts. This data clearly demonstrates that type I IFN, in contrast to IFNg, is not required during the effector stage of vitiligo pathogenesis in mice. However, since we intentionally activate transferred melanocyte-specific CD8 T cells with VACV or BMDCs expressing their cognate antigen, our mouse models may circumvent the role of type I IFNs in initiating activation of autoreactive cells and driving autoimmunity. Type I IFN is critical for providing innate immune signals that drive the priming of autoreactive T cells through maturation of DCs by inducing antigen presentation, co-stimulatory molecule expression, and migration to the lymph nodes to encounter naïve T cells. Our mouse models of vitiligo may not capture this process. We have addressed this question by using a TLR ligand to activate BMDCs before transfer into hosts. In fact, activation of BMDCs before transfer leads to significantly enhanced vitiligo in mice and this is partially a result of type I IFN signaling on host cells. Thus, we provide evidence that type I IFNs can enhance the activation of melanocyte-specific CD8 T cells and drive autoimmunity. Collectively, our results show that type I IFN signaling has disparate effects on autoreactive T cell priming in a context dependent manner. We reveal that although type I IFN is not required for the effector phase of vitiligo in mice, maturation of DCs and subsequent type I IFN production can enhance the priming of autoreactive T cells and enhance vitiligo severity. Our studies also reveal that type I IFN is required to clear recombinant attenuated VACV infection and vaccine administration in IFNaR deficient hosts led to a robust autoreactive and anti-tumor response. These insights describing the role of type I IFN in autoimmunity and tumor immunology could have important implications for T cell dependent tumor immunotherapy.
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Tang, Jun. "The tumor microenvironment in lung cancer pathogenesis: A hint to therapeutic agents and the influence of chronic obstructive pulmonary disease." Doctoral thesis, Universitat Autònoma de Barcelona, 2021. http://hdl.handle.net/10803/672510.

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Introducció: La malaltia pulmonar obstructiva crònica (MPOC) és un factor de risc independent per el desenvolupament de càncer de pulmó (CP) en els pacients. Els mecanismes encara s’han de dilucidar per a comprendre les relacions entre MPOC i CP. Hipòtesi: Els components del microambient tumoral poden diferir en els tumors de pacients amb CP amb i sense MPOC. La immunoteràpia també pot reduir la càrrega tumoral a través de diversos mecanismes biològics. Objectius: 1) Pacients: estudiar el paper del microambient tumoral, les cèl·lules immunitàries, les característiques de l’estroma i la sobreactivació de PARP en el procés de tumorigènesi en pacients amb CP amb i sense MPOC. 2) Ratolins: avaluar els efectes de la immunoteràpia en la grandària tumoral mitjançant l’anàlisi de diversos mecanismes biològics com l’estrès oxidatiu, l’apoptosi i l’autofàgia. Mètodes: 1) Pacients: es van reclutar 90 pacients amb MPOC-CP i 43 pacients només amb CP procedents de la cohort Càncer de Pulmó Mar (Barcelona) des de l’any 2008 fins al 2019. Es van obtenir mostres pulmonars tumorals i no tumorals en els pacients mitjançant toracotomia/cirurgia toracoscòpica assistida per vídeo (VATS), sempre previ a la quimioteràpia i/o radioteràpia. 2) Ratolins: dos grups de ratolins Balb/c amb CP induït mitjançant la inoculació subcutània de cèl·lules d’adenocarcinoma pulmonar LP07: ratolins tractats i no tractats, n = 9/grup. Al grup tractat se li va administrar un còctel d’anticossos monoclonals (anti-PD-L1, anti-CTLA-4, anti-CD19 i anti-CD137) i una solució tampó (PBS) als ratolins control. Es van obtenir els tumors en tots els ratolins per dur a terme l’estudi (30 dies). Anàlisi biològic: es van utilitzar Western-blot, immunohistoquímica, ELISA, cultius cel·lulars, i immunofluorescència per avaluar els marcadors biològics objecte d’estudi en cada model i tipus de mostres. Resultats: 1) Pacients: els tumors pulmonars de pacients amb MPOC van mostrar nivells més baixos d’estructures limfoides terciàries (ETLs) i centres germinals (CG) respecte dels pacients sense MPOC. Els nivells més baixos de ETLs i cèl·lules B en els tumors pulmonars es van associar amb una pitjor supervivència a 10 anys, especialment en aquells amb MPOC. En l’estroma tumoral, la presència de MPOC no es va associar a diferències en els components de l’estroma com ara la matriu extracel·lular, els fibroblasts associats al càncer o les cèl·lules endotelials. A més, els nivells de dany de l’ADN i la consegüent activació de PARP estaven més elevats només en els tumors pulmonars dels pacients amb MPOC, mentre que l’expressió dels enzims PARP-1 i PARP-2 estaven disminuïdes en els tumors pulmonars respecte de les no tumorals, independentment de la presència de MPOC. 2) Ratolins: la immunoteràpia va reduir la càrrega tumoral a través de l’augment dels nivells de l’estrès oxidatiu, apoptosi, autofàgia i de vies de senyalització com NF-kB i sirtuin-1 en tumors dels ratolins tractats comparant amb els ratolins amb CP sense immunoteràpia. Conclusions: El microambient immunològic tumoral, els components de l’estroma i l’activitat de PARP s’expressen de forma clarament diferenciada en els tumors pulmonars de pacients amb CP amb MPOC respecte dels pacients sense MPOC. La reducció en la formació de ELTs i CGs, l’augment en el dany de l’ADN i la sobreactivació de PARP probablement contribueixin a la major susceptibilitat per desenvolupar CP en pacients amb MPOC. En ratolins tractats amb la immunoteràpia, l’augment dels nivells d’estrès oxidatiu juntament amb l’activació d’apoptosi i autofàgia poden ser part dels mecanismes mitjançant els quals la immunoteràpia redueix la càrrega tumoral. En resum, la presència de MPOC s’ha de tenir en compte en el disseny de teràpies per al CP, incloses la immunoteràpia i la inhibició de l’activació de PARP.
Introducción: La enfermedad pulmonar obstructiva crónica (EPOC) es un factor de riesgo independiente para el desarrollo de cáncer de pulmón (CP) en los pacientes. Los mecanismos aún se quedan por dilucidar a comprender las relaciones entre EPOC y CP. Hipótesis: Los componentes del microambiente tumoral pueden diferir en los tumores de pacientes con CP con y sin EPOC. La inmunoterapia también puede reducir la carga tumoral a través de varios mecanismos biológicos. Objetivos: 1) Pacientes: estudiar el papel del microambiente tumoral, las células inmunes, las características del estroma y la sobreactivación de PARP en el proceso de tumorigénesis en pacientes con CP con y sin EPOC. 2) Ratones: evaluar los efectos de la inmunoterapia en el tamaño tumoral mediante el análisis de varios mecanismos biológicos como el estrés oxidativo, la apoptosis y la autofagia. Métodos: 1) Pacientes: se reclutaron 90 pacientes con EPOC-CP y 43 pacientes solo con CP procedentes de la Cohorte Cáncer de Pulmón Mar, Barcelona, desde el año 2008 hasta el 2019. Se obtuvieron muestras pulmonares tumorales y no tumorales en los pacientes mediante toracotomía/cirugía toracoscópica asistida por video (VATS), siempre previo a la quimioterapia y/o radioterapia. 2) Ratones: dos grupos de ratones BALB /c con CP inducido mediante la inoculación subcutánea de células de adenocarcinoma pulmonar LP07: ratones tratados y no tratados, n= 9/grupo. Al grupo tratado se le administró un cóctel de anticuerpos monoclonales (anti-PD-L1, anti-CTLA-4, anti-CD19 y anti-CD137) y una solución tampón (PBS) a los ratones control. Se obtuvieron los tumores en todos los ratones al final del estudio (30 días). Análisis biológico: se utilizaron Western-blot, inmunohistoquímica, ELISA, cultivos celulares, y inmunofluorescencia para evaluar los marcadores biológicos objeto de estudio en cada modelo y tipos de muestras. Resultados: 1) Pacientes: los tumores pulmonares de pacientes con EPOC mostraron niveles más bajos de estructuras linfoides terciarias (ETLs) y centros germinales (CG) respecto de los pacientes sin EPOC. Los niveles más bajos de ELTs y células B en los tumores pulmonares se asociaron con una peor supervivencia a 10 años, especialmente en aquéllos con EPOC. En el estroma tumoral, la presencia de EPOC no se asoció a diferencias en los componentes del estroma tales como la matriz extracelular, los fibroblastos asociados al cáncer o las células endoteliales. Además, los niveles de daño del ADN y la consiguiente activación de PARP estaban más elevados solamente en los tumores pulmonares de los pacientes con EPOC, mientras que la expresión de las enzimas PARP-1 y PARP-2 estaban disminuidas en los tumores pulmonares respecto de las no tumorales, independientemente de la presencia de EPOC. 2) Ratones: la inmunoterapia redujo la carga tumoral a través del aumento de los niveles del estrés oxidativo, apoptosis, autofagia y de vías de señalización como NF-kB y sirtuin-1 en tumores de los ratones tratados comparando con los ratones con CP sin inmunoterapia. Conclusiones: El microambiente inmunológico tumoral, los componentes del estroma y la actividad de PARP se expresan de forma claramente diferenciada en los tumores pulmonares de pacientes con CP con EPOC respecto de los pacientes sin EPOC. La reducción en la formación de ELTs y CGs, el aumento en el daño del ADN y la sobreactivación de PARP probablemente contribuyan a la mayor susceptibilidad para desarrollar CP en pacientes con EPOC. En ratones tratados con la inmunoterapia, el aumento de los niveles de estrés oxidativo junto con la activación de apoptosis y autofagia pueden ser parte de los mecanismos mediante los cuales la inmunoterapia reduce la carga tumoral. En resumen, la presencia de EPOC debe tenerse en cuenta en el diseño de terapias para el CP, incluidas la inmunoterapia y la inhibición de la activación de PARP.
Background: Lung cancer (LC) is a leading cause of death worldwide. Chronic obstructive pulmonary disease (COPD) is a highly prevalent lung disease. COPD has been well established as an independent risk factor for lung tumorigenesis in patients. However, the biological mechanisms that explain the possible associations between lung cancer and COPD remain to be fully elucidated. Hypothesis: The tumor microenvironment components (immune profile, stroma, cytokines, and PARP activation) may differ in tumors of lung cancer patients with and without COPD. Immunotherapy may also reduce tumor burden through several biological events. Objectives: 1) Studies in patients: to elucidate the role of the biological events: tumor microenvironment, immune cell composition, stroma characteristics, and PARP overactivation in the process of tumorigenesis in tumors of patients with and without underlying COPD; 2) Mouse study: to evaluate the effects of immunotherapy on tumor burden through the analyses of several biological mechanisms such as oxidative stress, apoptosis, and autophagy. Methods: Two models were used: 1) Studies in patients: 90 LC patients with underlying COPD and 43 LC-only patients were recruited from 2008 to 2019 from the Lung Cancer Mar Cohort, Barcelona. Lung tumor and the surrounding non-tumor lung specimens were obtained from all study patients through thoracotomy or video-assisted thoracoscopic surgery (VATS) prior to chemotherapy and/or radiotherapy; 2) Mouse study: Two groups of wild-type BALB/C mice with experimental lung cancer (subcutaneous inoculation of LP07 adenocarcinoma cells in the left flank of mice) were established: treated and non-treated mice, n=9/group. In the treatment group, lung cancer mice were treated with a cocktail of monoclonal antibodies (intraperitoneal injection, anti-PD-L1, anti-CTLA-4, anti-CD19, and anti-CD137). Lung tumors were obtained from all mice. Biological analysis: laboratory techniques such as western-blot, immunohistochemistry, ELISA, cell culture, and immunofluorescence were used to assess the target biological markers in each study. Results: 1) Studies in patients: lung tumors of patients with underlying COPD showed lower levels of tertiary lymphoid structures (TLSs) compared to lung cancer only patients. Moreover, lower levels of TLS and B cells in lung tumors were associated with poorer 10-year overall survival rates of patients, especially in those with underlying COPD. In tumor stroma, the presence of COPD did not elicit any significant difference in levels of extracellular matrix, cancer-associated fibroblasts or endothelial cells. In addition, DNA damage and PARP activation levels were higher only in lung tumors of patients with underlying COPD, while PARP-1 and PARP-2 enzyme expression levels were lower in lung tumors compared to non-tumor specimens irrespective of the presence of COPD. 2) Mouse study: treatment with immunotherapy reduced tumor burden through increased levels of oxidative stress, apoptosis, autophagy, and signaling pathways such as NF-kB and sirtuin-1 in tumors of the treated mice compared to tumors of non-treated animals. Conclusions: Tumor immune microenvironment, stroma components, and PARP are differentially expressed in lung tumors of lung cancer patients with underlying COPD. The reduction in TLS and GC formation, the rise in DNA damage, and PARP overactivation probably contribute to the greater susceptibility of COPD patients to develop lung tumors. In mice treated with the combination of monoclonal antibodies, increased levels of oxidative stress along with activated apoptosis and autophagy may be part of the mechanisms whereby immunotherapy may reduce tumor burden. In conclusion, the presence of COPD should be considered when designing therapeutic strategies of lung cancer including immunotherapy as well as PARP activity inhibition.
Universitat Autònoma de Barcelona. Programa de Doctorat en Medicina
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Marshall, Aiden Christopher James 1976. "The role of Fas and TNFα in experimental autoimmune gastritis." Monash University, Dept. of Pathology and Immunology, 2003. http://arrow.monash.edu.au/hdl/1959.1/9413.

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Books on the topic "Tumor pathogenesis"

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Nose and viral cancer: Etiology, pathogenesis and treatment. New York: Nova Science Publishers, 2010.

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Mercier, Isabelle, Jean-François Jasmin, and Michael P. Lisanti. Caveolins in cancer pathogenesis, prevention and therapy. New York, NY: Springer, 2012.

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M, Howley Peter, Broker Thomas R, Burroughs Wellcome Company, and University of California, Los Angeles., eds. Papillomaviruses: Proceedings of a Burroughs-Wellcome-UCLA Symposium held at Taos, New Mexico, March 11-18, 1989. New York, N.Y: Wiley-Liss, 1990.

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Primary central nervous system tumors: Pathogenesis and therapy. New York: Humana Press, 2011.

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1943-, Eng Kenneth, and Coppa Gene Francis, eds. Anorectal, presacral, and sacral tumors: Anatomy, physiology, pathogenesis, and management. Philadelphia: Saunders, 1987.

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Glioblastoma: Molecular mechanisms of pathogenesis and current therapeutic strategies. Dordrecht: Springer, 2010.

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Khurana, Jasvir S. Essentials in Bone and Soft-Tissue Pathology. Boston, MA: Springer Science+Business Media, LLC, 2010.

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(Editor), Giuseppe Barbanti-Brodano, Mauro Bendinelli (Editor), and Herman Friedman (Editor), eds. DNA Tumor Viruses: Oncogenic Mechanisms (Infectious Agents and Pathogenesis). Springer, 1996.

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Aloisio, Medeiros, and Veloso Carlitos, eds. Nose and viral cancer: Etiology, pathogenesis, and treatment. Hauppauge, N.Y: Nova Science Publishers, 2009.

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Mercier, Isabelle, Michael P. Lisanti, and Jean-François Jasmin. Caveolins in Cancer Pathogenesis, Prevention and Therapy. Springer, 2011.

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Book chapters on the topic "Tumor pathogenesis"

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Bernard, Hans-Ulrich. "Papillomaviruses: Biology, Diversity, and Pathogenesis." In DNA Tumor Viruses, 127–43. New York, NY: Springer US, 2008. http://dx.doi.org/10.1007/978-0-387-68945-6_6.

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Liebowitz, David. "Pathogenesis of Epstein-Barr Virus." In Human Tumor Viruses, 175–99. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555818289.ch5.

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Wiestler, Otmar D., and Andreas von Deimling. "A Model for the Molecular Pathogenesis of Astrocytic Gliomas." In Brain Tumor, 173–86. Tokyo: Springer Japan, 1996. http://dx.doi.org/10.1007/978-4-431-66887-9_18.

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Hansen, Hans. "Serologic Approaches to Tumor Diagnosis." In Lymphoproliferative Diseases: Pathogenesis, Diagnosis, Therapy, 107–13. Dordrecht: Springer Netherlands, 1985. http://dx.doi.org/10.1007/978-94-009-5016-0_9.

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Mischel, Paul S., and Harry V. Vinters. "Neuropathology and Molecular Pathogenesis of Primary Brain Tumors." In Brain Tumor Immunotherapy, 3–45. Totowa, NJ: Humana Press, 2001. http://dx.doi.org/10.1007/978-1-59259-035-3_1.

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Sowa, Grzegorz. "Caveolins in Tumor Angiogenesis." In Caveolins in Cancer Pathogenesis, Prevention and Therapy, 75–90. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4614-1001-0_6.

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Zimmermann, Arthur. "Etiology and Pathogenesis of Hepatocellular Carcinoma: Epigenetic Mechanisms." In Tumors and Tumor-Like Lesions of the Hepatobiliary Tract, 1–13. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-26587-2_168-1.

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Zimmermann, Arthur. "Etiology and Pathogenesis of Hepatocellular Carcinoma: Epigenetic Mechanisms." In Tumors and Tumor-Like Lesions of the Hepatobiliary Tract, 3029–40. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-26956-6_168.

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Kerzerho, Jerome, Florence Anne Castelli, and Bernard Maillère. "Midkine as a Tumor-Shared Antigen." In Midkine: From Embryogenesis to Pathogenesis and Therapy, 247–58. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-4234-5_22.

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Alouf, Joseph E. "Immunomodulating Toxins and Tumor Necrosis Factors." In Pathogenesis of Wound and Biomaterial-Associated Infections, 101–5. London: Springer London, 1990. http://dx.doi.org/10.1007/978-1-4471-3454-1_12.

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Conference papers on the topic "Tumor pathogenesis"

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Aggarwal, Sadhna, Suresh C. Sharma, and Satya N. Das. "Abstract PO082: Significance of Treg cells in pathogenesis of oral squamous cell carcinoma." In Abstracts: AACR Virtual Special Conference: Tumor Immunology and Immunotherapy; October 19-20, 2020. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/2326-6074.tumimm20-po082.

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Kegelman, Timothy P., Swadesh K. Das, Bin Hu, Mitchell Menezes, Luni Emdad, Santanu Dasgupta, Albert S. Baldwin, et al. "Abstract B85: MDA-9/syntenin is a key regulator of glioma pathogenesis." In Abstracts: AACR Special Conference on Tumor Invasion and Metastasis - January 20-23, 2013; San Diego, CA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.tim2013-b85.

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Hess, J., S. Homann, N. Koerich Laureano, B. Tawk, M. Bieg, X. Pastor Hostenech, K. Freier, W. Weichert, K. Zaoui, and J. Hess. "Tumor cell plasticity in the pathogenesis and prognosis of head and neck cancer." In Abstract- und Posterband – 89. Jahresversammlung der Deutschen Gesellschaft für HNO-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn – Forschung heute – Zukunft morgen. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1640039.

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Phi, Ji Hoon, Seung Ah Choi, Yong Hwy Kim, Young-Hoon Kim, Chul-Kee Park, Kyu-Chang Wang, and Seung-Ki Kim. "Abstract 3107: The role of LIN28 in atypical teratoid rhabdoid tumor (ATRT) pathogenesis." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-3107.

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Bartek, Jiri, and Jirina Bartkova. "Abstract IA13: Replication stress in cancer pathogenesis: Mechanisms and treatment opportunities." In Abstracts: AACR Special Conference on DNA Repair: Tumor Development and Therapeutic Response; November 2-5, 2016; Montreal, QC, Canada. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1557-3125.dnarepair16-ia13.

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Zhao, Shuying, Lyazat Kurenbekova, Lawrence A. Donehower, and Jason T. Yustein. "Abstract A85: Novel mouse models to investigate the molecular pathogenesis of metastatic osteosarcoma." In Abstracts: AACR Special Conference on Tumor Invasion and Metastasis - January 20-23, 2013; San Diego, CA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.tim2013-a85.

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Taylor, Holly, Jaroslav Slamecka, Alla Musiyenko, Elaine Gavin, Tiffany S. Norton, Ileana Aragon, Taylor Young, et al. "Abstract B31: Tumor-intrinsic B7-H3 regulates drug resistance, metabolism, and pathogenesis in ovarian cancer." In Abstracts: AACR Special Conference: Addressing Critical Questions in Ovarian Cancer Research and Treatment; October 1-4, 2017; Pittsburgh, PA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1557-3265.ovca17-b31.

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Chan, Lok Hei, Kai Yu Ng, and Stephanie Ma. "Abstract 2333: The tumor suppressive role of PRMT6 in regulating the pathogenesis of hepatocellular carcinoma." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-2333.

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Hu, Wei-Xin, Sai-Qun Luo, Yan Zhong, Xiu-Feng Bu, and Yang Zhou. "Abstract LB-070: The studies of tumor-associated gene C1orf35 in pathogenesis of human multiple myeloma." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-lb-070.

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Mitra, Sheetal A., Anirban P. Mitra, Yang Liu, Jonathan D. Buckley, and Timothy J. Triche. "Abstract 2066: The functional noncoding genome in childhood sarcomas plays important regulatory roles in tumor pathogenesis." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-2066.

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Reports on the topic "Tumor pathogenesis"

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Asgharzadeh, Shahab. Studies of the Tumor Microenvironment in Pathogenesis of Neuroblastoma. Fort Belvoir, VA: Defense Technical Information Center, July 2012. http://dx.doi.org/10.21236/ada568118.

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Asgharzadeh, Shahab. Studies of the Tumor Microenvironment in Pathogenesis of Neuroblastoma. Fort Belvoir, VA: Defense Technical Information Center, July 2013. http://dx.doi.org/10.21236/ada591449.

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Shao, Rong, and Xiao-Fan Wang. Functional Characterization of TPF (Tumor Promoting Factor), a Novel Angiogenic Factor in Breast Cancer Pathogenesis. Fort Belvoir, VA: Defense Technical Information Center, June 2003. http://dx.doi.org/10.21236/ada418988.

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Shao, Rong, and Xiao-Fan Wang. Functional Characterization of TPF (Tumor Promoting Factor), A Novel Angiogenic Factor in Breast Cancer Pathogenesis. Fort Belvoir, VA: Defense Technical Information Center, June 2004. http://dx.doi.org/10.21236/ada426921.

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Kurman, Robert J., and Ie-Ming Shih. Pathogenesis of Ovarian Serous Carcinoma as the Basis for Immunologic Directed Diagnosis and Treatment. Project 1 - Molecular Characterization of Ovarian Serous Tumors Developing Along Different Pathways. Fort Belvoir, VA: Defense Technical Information Center, August 2003. http://dx.doi.org/10.21236/ada420920.

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