Journal articles: 'Tumor pathogenesis'

1

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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8

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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9

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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10

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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11

Look, A. Thomas. "Molecular Pathogenesis of MDS." Hematology 2005, no. 1 (January 1, 2005): 156–60. http://dx.doi.org/10.1182/asheducation-2005.1.156.

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Abstract Clonal disorders of hematopoiesis, such as myelodysplastic syndromes (MDS) and myeloproliferative diseases (MPD), affect both hematopoietic stem cells and progenitor cells within the erythroid, platelet and granulocytic lineages and can have devastating consequences in children and adults. The genetic features of these diseases often include clonal, nonrandom chromosomal deletions (e.g., 7q–, 5q–, 20q–, 6q–, 11q– and 13q–) that appear to inactivate tumor suppressor genes required for the normal development of myeloid cells (reviewed in Bench1 and Fenaux2). These putative tumor suppressors have proved to be much more difficult to identify than oncogenes activated by chromosomal translocations, the other major class of chromosomal lesions in MDS and MPD.3 Although MDS and MPD are almost certainly caused by mutations in stem/progenitor cells,4 the role of inactivated tumor suppressor genes in this process remains poorly understood. In a small portion of myeloid diseases, mutations have been identified in genes encoding factors known to be required for normal hematopoiesis, such as PU.1, RUNX1, CTNNA1 (α-catenin) and c/EBPα, and implicating these genes as tumor suppressors.5–7 Nonetheless, the identities of most deletion-associated tumor suppressors in these diseases remains elusive, despite complete sequencing of the human genome. The deleted regions detected by cytogenetic methods are generally very large, containing many hundreds of genes, thus making it hard to locate the critical affected gene or genes. It is also unclear whether dysfunctional myelopoiesis results from haploinsufficiency, associated with the deletion of one allele, or from homozygous inactivation due to additional point mutations or microdeletions of the retained wild-type allele. In general MDS have proved surprisingly resistant to conventional treatments. Targeted therapeutic advances in MDS will likely depend on a full comprehension of underlying molecular mechanisms, in particular the tumor suppressor genes lost through clonal, nonrandom chromosomal deletions, such as the 7q– and (del)5q.

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12

Tran Janco, Jo Marie, Purushottam Lamichhane, Lavakumar Karyampudi, and Keith L. Knutson. "Tumor-Infiltrating Dendritic Cells in Cancer Pathogenesis." Journal of Immunology 194, no. 7 (March 20, 2015): 2985–91. http://dx.doi.org/10.4049/jimmunol.1403134.

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13

Pluda, James M. "Tumor-associated angiogenesis: Pathogenesis and clinical implications." European Journal of Cancer 33 (June 1997): S47. http://dx.doi.org/10.1016/s0959-8049(97)89452-x.

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14

Adams, Seray, Nady Braidy, Alban Bessesde, Bruce J. Brew, Ross Grant, Charlie Teo, and Gilles J. Guillemin. "The Kynurenine Pathway in Brain Tumor Pathogenesis." Cancer Research 72, no. 22 (November 9, 2012): 5649–57. http://dx.doi.org/10.1158/0008-5472.can-12-0549.

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15

Ikeda, Fumiyo, and Ivan Dikic. "CYLD in Ubiquitin Signaling and Tumor Pathogenesis." Cell 125, no. 4 (May 2006): 643–45. http://dx.doi.org/10.1016/j.cell.2006.05.003.

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Chen, Dillon Y., Clark C. Chen, John R. Crawford, and Sonya G. Wang. "Tumor-related epilepsy: epidemiology, pathogenesis and management." Journal of Neuro-Oncology 139, no. 1 (May 24, 2018): 13–21. http://dx.doi.org/10.1007/s11060-018-2862-0.

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17

Ghezzi, P. "Tumor Necrosis Factor in the Pathogenesis of Human Diseases." International Journal of Immunopathology and Pharmacology 5, no. 2 (May 1992): 131–34. http://dx.doi.org/10.1177/039463209200500208.

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This paper will deal with the role of tumor necrosis factor (TNF) in the pathogenesis of various diseases. However, it will be important to remember that originally TNF was characterized as an antitumor factor. In fact, it was known that endotoxin was able to induce hemorrhagic necrosis of some tumors in mice. In 1975 Carswell et al. demonstrated the presence of a tumor necrotizing activity (termed “tumor necrosis serum”) in the sera of mice primed with C. parvum or BCG, and subsequently injected with endotoxin (1). Later it was found that this factor was a macrophage product and was termed TNF. In vivo TNF induced hemorrhagic necrosis of Meth A sarcoma and in vitro demonstrated cytotoxic activity against various tumor cell lines (2). In 1984, TNF was purified and its cDNA was cloned, and the production of substantial amounts of recombinant TNF allowed the characterization of its various biological activities (3). In parallel to these studies on tumor necrosis, the group of Cerami, at the Rockefeller University in New York was studying the mechanisms of cachexia and wasting associated with infection. They found that infection or injection of endotoxin in laboratory animals resulted in a marked hypertrygliceridemia, which was associated with an inhibition of lipoprotein lipase. They hypothesized that a host-derived mediator was responsible for this and other metabolic derangements observed in infection. This factor, which was termed “cachectin”, was later found to be produced by macrophages, and once it was purified and sequenced it became clear that TNF and cachectin were identical (4).

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Staser, Karl, Feng-Chun Yang, and D. Wade Clapp. "Pathogenesis of Plexiform Neurofibroma: Tumor-Stromal/Hematopoietic Interactions in Tumor Progression." Annual Review of Pathology: Mechanisms of Disease 7, no. 1 (February 28, 2012): 469–95. http://dx.doi.org/10.1146/annurev-pathol-011811-132441.

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Noh, Byeong-Joo, and Yong-Koo Park. "Giant cell tumor of bone: updated molecular pathogenesis and tumor biology." Human Pathology 81 (November 2018): 1–8. http://dx.doi.org/10.1016/j.humpath.2018.06.017.

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Choi, S., and J. N. Myers. "Molecular Pathogenesis of Oral Squamous Cell Carcinoma: Implications for Therapy." Journal of Dental Research 87, no. 1 (January 2008): 14–32. http://dx.doi.org/10.1177/154405910808700104.

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The development of oral squamous cell carcinoma (OSCC) is a multistep process requiring the accumulation of multiple genetic alterations, influenced by a patient’s genetic predisposition as well as by environmental influences, including tobacco, alcohol, chronic inflammation, and viral infection. Tumorigenic genetic alterations consist of two major types: tumor suppressor genes, which promote tumor development when inactivated; and oncogenes, which promote tumor development when activated. Tumor suppressor genes can be inactivated through genetic events such as mutation, loss of heterozygosity, or deletion, or by epigenetic modifications such as DNA methylation or chromatin remodeling. Oncogenes can be activated through overexpression due to gene amplification, increased transcription, or changes in structure due to mutations that lead to increased transforming activity. This review focuses on the molecular mechanisms of oral carcinogenesis and the use of biologic therapy to specifically target molecules altered in OSCC. The rapid progress that has been made in our understanding of the molecular alterations contributing to the development of OSCC is leading to improvements in the early diagnosis of tumors and the refinement of biologic treatments individualized to the specific characteristics of a patient’s tumor.

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Xiong, Huimin, Ruiyao Wang, and Chao Zhang. "Research Progress on Inducible Nitric Oxide Synthase in the Pathogenesis of Pancreatic Malignancy." Proceedings of Anticancer Research 5, no. 4 (July 29, 2021): 27–29. http://dx.doi.org/10.26689/par.v5i4.2316.

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Pancreatic cancer is a common tumor of the digestive system. At present, the pathogenesis is still unclear, but current research on inducible nitric oxide synthase in relation to the pathogenesis of pancreatic malignant tumors is particularly extensive. Therefore, this article focuses on the research progress on inducible nitric oxide synthase in the pathogenesis of pancreatic cancer.

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Murshid, Areen Abdulelah, and Hatim Q. Al-Maghraby. "Subsequent Development of Desmoid Tumor after a Resected Gastrointestinal Stromal Tumor." Case Reports in Pathology 2018 (2018): 1–5. http://dx.doi.org/10.1155/2018/1082956.

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Desmoid tumors (deep fibromatosis) of the mesentery are rare mesenchymal tumors. They are often misdiagnosed, especially with a previous history of resection for gastrointestinal stromal tumor (GIST). Immunohistochemistry can help differentiate between these two tumors. In this article, we present a case we had encountered: a Desmoid tumor developing in a patient with a history of GIST 3 years ago. It is the first case of GIST with subsequent development of Desmoid tumor to be reported in Saudi Arabia. We discuss the two entities of Desmoid tumor and GIST by comparing their definitions, clinical presentations, histological features, immunohistochemistry stains, molecular pathogenesis, prognosis, and treatment. We also discuss the relationship between GIST and the subsequent development of Desmoid tumors and compare our case with case reports in literature.

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23

Kapoor, Shailendra. "TROP2 expression and its evolving role in tumor pathogenesis in systemic tumors." Tumor Biology 34, no. 3 (November 13, 2012): 1967–68. http://dx.doi.org/10.1007/s13277-012-0586-x.

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Moore, Forrest O., Rafaat Z. Abdel-Misih, John D. Berne, Arthur W. Zieske, Nabeel R. Rana, and Jon G. Ryckman. "Poorly Differentiated Carcinoma Arising in a Warthin's Tumor of the Parotid Gland: Pathogenesis, Histopathology, and Surgical Management of Malignant Warthin's Tumors." American Surgeon 73, no. 4 (April 2007): 397–99. http://dx.doi.org/10.1177/000313480707300418.

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Warthin's tumor is a benign lymphoepithelial neoplasm representing 10 per cent of all parotid gland tumors. Malignant transformation of a Warthin's tumor is an extremely rare event. We report a case of a patient with poorly differentiated carcinoma arising from a Warthin's tumor, as well as review the pathogenesis, histopathology, and surgical management of malignant Warthin's tumors.

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Xiong, Huimin, Ruiyao Wang, and Chao Zhang. "A Review on the Research Progress of Inducible Nitric Oxide Synthase in the Pathogenesis of Pancreatic Malignancy." Journal of Clinical and Nursing Research 5, no. 4 (August 3, 2021): 151–53. http://dx.doi.org/10.26689/jcnr.v5i4.2281.

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Pancreatic cancer is a common tumor of the digestive system, at present, the pathogenesis is still unclear, but in the current research on the pathogenesis of pancreatic malignant tumors, the research on inducible nitric oxide synthase is particularly extensive. Therefore, this article focuses on the research progress of inducible nitric oxide synthase in the pathogenesis of pancreatic cancer. This is a review.

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Niinuma, Takeshi, Hiromu Suzuki, and Tamotsu Sugai. "Molecular characterization and pathogenesis of gastrointestinal stromal tumor." Translational Gastroenterology and Hepatology 3 (January 9, 2018): 2. http://dx.doi.org/10.21037/tgh.2018.01.02.

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27

Cantile, Monica, Giuseppe Palmieri, and Gerardo Botti. "Developmental Gene Markers in Tumor Pathogenesis and Progression." Disease Markers 2019 (July 8, 2019): 1–2. http://dx.doi.org/10.1155/2019/5462562.

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Heaney, Anthony P., Manory Fernando, and Shlomo Melmed. "Functional role of estrogen in pituitary tumor pathogenesis." Journal of Clinical Investigation 109, no. 2 (January 15, 2002): 277–83. http://dx.doi.org/10.1172/jci0214264.

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29

Sandgren, E. P., C. J. Quaife, A. G. Paulovich, R. D. Palmiter, and R. L. Brinster. "Pancreatic tumor pathogenesis reflects the causative genetic lesion." Proceedings of the National Academy of Sciences 88, no. 1 (January 1, 1991): 93–97. http://dx.doi.org/10.1073/pnas.88.1.93.

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N. Goltsev, Anatoliy, Olga A. Diabina, Maksim V. Ostankov, Nikolay A. Bondarovich, and Ekaterina Ye. Yampolskaya. "Cancer stem cells in tumor pathogenesis after cryoablation." Problems of Cryobiology and Cryomedicine 25, no. 3 (September 25, 2015): 205–18. http://dx.doi.org/10.15407/cryo25.03.205.

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31

Minematsu, Takeo, Shunsuke Miyai, Hanako Kajiya, Masanori Suzuki, Naoko Sanno, Susumu Takekoshi, Akira Teramoto, and Robert Y. Osamura. "Recent Progress in Studies of Pituitary Tumor Pathogenesis." Endocrine 28, no. 1 (2005): 037–42. http://dx.doi.org/10.1385/endo:28:1:037.

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Ellert-Miklaszewska, Aleksandra, Katarzyna Poleszak, Maria Pasierbinska, and Bozena Kaminska. "Integrin Signaling in Glioma Pathogenesis: From Biology to Therapy." International Journal of Molecular Sciences 21, no. 3 (January 30, 2020): 888. http://dx.doi.org/10.3390/ijms21030888.

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Integrins are a large family of transmembrane adhesion receptors, which play a key role in interactions of a cell with the surrounding stroma. Integrins are comprised of non-covalently linked α and β chains, which form heterodimeric receptor complexes. The signals from integrin receptors are combined with those originating from growth factor receptors and participate in orchestrating morphological changes of cells, organization of the cytoskeleton, stimulation of cell proliferation and rescuing cells from programmed cell death induced by extracellular matrix (ECM) detachment. Upon binding to specific ligands or ECM components, integrin dimers activate downstream signaling pathways, including focal adhesion kinase, phosphoinositide-3-kinase (PI3K) and AKT kinases, which regulate migration, invasion, proliferation and survival. Expression of specific integrins is upregulated in both tumor cells and stromal cells in a tumor microenvironment. Therefore, integrins became an attractive therapeutic target for many cancers, including the most common primary brain tumors—gliomas. In this review we provide an overview of the involvement of integrin signaling in glioma pathogenesis, formation of the tumor niche and brain tissue infiltration. We will summarize up-to-date therapeutic strategies for gliomas focused on interference with integrin ligand-receptor signaling.

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Cherepanov, S. A., V. P. Baklaushev, A. N. Gabashvili, I. I. Shepeleva, and V. P. Chekhonin. "Hedgehog signaling in the pathogenesis of neuro-oncology diseases." Biomeditsinskaya Khimiya 61, no. 3 (2015): 332–42. http://dx.doi.org/10.18097/pbmc20156103332.

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The review summarizes current knowledge on the Hedgehog signaling pathway, its role in normal embryogenesis and/or initiation and progression of neuro-oncological diseases, especially of high-grade gliomas, the most malignant neuroepithelial tumors. The main proteins forming the Hedgehog signaling pathway include Shh, PTCH1, SMO, HHIP, SUFU and GLI1 isoforms. Effects of other signaling pathways on the family of transcription factors GLI and other proteins are described. The review summarizes modern data about the impact of the Hedgehog signaling pathway on proliferation, migration activity and invasiveness, and also on tumor neoangiogenesis and tumor cell chemoresistance. The role of the Hedgehog signaling pathway in origin of cancer stem cells and epithelial-mesenchymal transition is also analyzed. Some prospects for new anticancer drugs acting on components of the Hedgehog signaling pathway inhibitors are demonstrated.

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Gültekin, Sibel Elif, Burcu Sengüven, Reemitcha Aziz, Carina Heydt, and Reinhard Buettner. "Molecular Profiling of Odontogenic Tumors - Pilot Study." Balkan Journal of Dental Medicine 21, no. 2 (July 26, 2017): 112–15. http://dx.doi.org/10.1515/bjdm-2017-0017.

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Summary Background/Aim: In the pathogenesis of odontogenic tumors which arise from the rests of the dental apparatus in the jaw, several molecular pathways have been shown to play critical roles such as genetic alterations in the hedgehog, BRAF/Ras/MAPK, epidermal growth factor receptor. Next generation genomic sequencing has identified gene mutations in many different tumors. Materials and Methods: Here we report four types of odontogenic tumor including six cases in which five had mutation according to next generation sequencing analysis from archival paraffin blocks that diagnosed previously as ameloblastoma (solid), amloblastoma (unicystic-mural), ameloblastic fibroma, squamous odontogenic tumor, and adenomatoid odontogenic tumor. Results: All ameloblastomatic tumors were shown BRAF mutation and adenomatoid odontogenic tumors were KRAS mutation. Conclusion: This evidence may highlight the poorly understood pathogenesis of odontogenic tumors. Further comparisons need to be made with other benign and malignant odontogenic tumors so that unique odontogenic features may be found.

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Bachir, Suha, Sanjit Shah, Scott Shapiro, Abigail Koehler, Abdelkader Mahammedi, Ravi N. Samy, Mario Zuccarello, Elizabeth Schorry, and Soma Sengupta. "Neurofibromatosis Type 2 (NF2) and the Implications for Vestibular Schwannoma and Meningioma Pathogenesis." International Journal of Molecular Sciences 22, no. 2 (January 12, 2021): 690. http://dx.doi.org/10.3390/ijms22020690.

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Patients diagnosed with neurofibromatosis type 2 (NF2) are extremely likely to develop meningiomas, in addition to vestibular schwannomas. Meningiomas are a common primary brain tumor; many NF2 patients suffer from multiple meningiomas. In NF2, patients have mutations in the NF2 gene, specifically with loss of function in a tumor-suppressor protein that has a number of synonymous names, including: Merlin, Neurofibromin 2, and schwannomin. Merlin is a 70 kDa protein that has 10 different isoforms. The Hippo Tumor Suppressor pathway is regulated upstream by Merlin. This pathway is critical in regulating cell proliferation and apoptosis, characteristics that are important for tumor progression. Mutations of the NF2 gene are strongly associated with NF2 diagnosis, leading to benign proliferative conditions such as vestibular schwannomas and meningiomas. Unfortunately, even though these tumors are benign, they are associated with significant morbidity and the potential for early mortality. In this review, we aim to encompass meningiomas and vestibular schwannomas as they pertain to NF2 by assessing molecular genetics, common tumor types, and tumor pathogenesis.

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Du, Qiu, De-shan Yao, You-wei Wang, and Cheng Cheng. "Research Progress on lncRNA Functions and Mechanisms in Pituitary Adenomas." Hormone and Metabolic Research 52, no. 05 (May 2020): 280–88. http://dx.doi.org/10.1055/a-1142-8815.

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AbstractDespite being the most common human neuroendocrine tumor, the pathogenesis of pituitary adenomas (PAs) is still unclear. Long non-coding RNA (lncRNA) is involved in a variety of physiological and pathological processes, and has been shown to play a key role in the process of tumor instigation and development by affecting the proliferation, migration, invasiveness, and metastasis of tumor cells. Therefore, lncRNAs may be used as diagnostic and prognostic markers of tumors. In this paper, the effect of lncRNA on the onset and progression of PAs is reviewed so as to provide a profound understanding of its pathogenesis and clinical reference for the early diagnosis of PAs.

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Lutsenko, A. S., Z. E. Belaya, E. G. Przhiyalkovskaya, and G. A. Mel'nichenko. "MICRORNA: ROLE IN GH-SECRETING PITUITARY ADENOMA PATHOGENESIS." Annals of the Russian academy of medical sciences 72, no. 4 (July 7, 2017): 290–98. http://dx.doi.org/10.15690/vramn856.

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MicroRNA presents small (19–25 nucleotides long) non-coding RNA molecules which regulate gene expression on post-transcriptional level. Numerous studies revealed microRNA’s important role in physiological processes. Moreover, its aberrant expression has been described in many pathological conditions including pituitary tumors. Pituitary adenomas are benign intracranial tumors with various clinical presentations depending on the type of hormone secretion. Prediction of the pituitary adenoma aggressive level and treatment response is challenging due to the lack of reliable clinical predictors or non-invasive biomarkers. MicroRNAs in body fluids could potentially be a minimally invasive biomarker for tumor diagnosis and a predictor of treatment response and prognosis. Some studies reveal that microRNA is specific for a different pituitary adenoma subtypes. In the article, we review existing evidence on microRNA expression in GH-secreting tumors and its possible involvement in pathogenesis of somatotroph tumors.

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Yang, Chenjie, and Paul D. Robbins. "The Roles of Tumor-Derived Exosomes in Cancer Pathogenesis." Clinical and Developmental Immunology 2011 (2011): 1–11. http://dx.doi.org/10.1155/2011/842849.

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Exosomes are endosome-derived, 30–100 nm small membrane vesicles released by most cell types including tumor cells. They are enriched in a selective repertoire of proteins and nucleic acids from parental cells and are thought to be actively involved in conferring intercellular signals. Tumor-derived exosomes have been viewed as a source of tumor antigens that can be used to induce antitumor immune responses. However, tumor-derived exosomes also have been found to possess immunosuppressive properties and are able to facilitate tumor growth, metastasis, and the development of drug resistance. These different effects of tumor-derived exosomes contribute to the pathogenesis of cancer. This review will discuss the roles of tumor-derived exosomes in cancer pathogenesis, therapy, and diagnostics.

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Wu, Meng-Yu, Chia-Jung Li, Giou-Teng Yiang, Yeung-Leung Cheng, Andy Po-Yi Tsai, Yueh-Tseng Hou, Yu-Chieh Ho, Ming-Feng Hou, and Pei-Yi Chu. "Molecular Regulation of Bone Metastasis Pathogenesis." Cellular Physiology and Biochemistry 46, no. 4 (2018): 1423–38. http://dx.doi.org/10.1159/000489184.

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Distant metastases are the major cause of mortality in cancer patients. Bone metastases may cause bone fractures, local pain, hypercalcemia, bone marrow aplasia, and spinal cord compression. Therefore, the management of bone metastases is important in cancer treatment. Normal bone remodeling is regulated by osteoprotegerin ligand (OPGL), receptor activator of NF-κB ligand (RANKL), parathyroid hormone-related protein (PTHrP), and other cytokines. In the tumor microenvironment, tumor cells induce a vicious cycle that promotes osteoblastic and osteolytic lesions. Studies support the idea that distant metastases may occur due to the immunosuppressive function of myeloid-derived suppressor cells (MDSCs). These cells inhibit T cells and natural killer (NK) cells and differentiate into tumor-associating macrophages (TAMs), monocytes, and dendritic cells (DCs). In this review, we summarize studies focusing on the role of MDSCs in bone metastasis and provide a strong foundation for developing anticancer immune treatments and anticancer therapies, in general.

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Sun, Chuan-ce, Li-chuan Zhang, Cheng-long Gao, Hao-ran Zhang, Ri-lei Yu, and Cong-min Kang. "Design and screening of SGK1, Src dual inhibitors using pharmacophore models, molecular docking, and molecular dynamics simulation." New Journal of Chemistry 44, no. 41 (2020): 17815–20. http://dx.doi.org/10.1039/d0nj02249g.

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Serum and glucocorticoid-regulated protein kinase 1 that can promote the growth of tumor cells is highly expressed in many tumors. Sarcoma gene plays an important role in the pathogenesis of cancer and is an important kinase in tumor cell expression pathways.

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Unachukwu, Uchenna, Kiran Chada, and Jeanine D’Armiento. "High Mobility Group AT-Hook 2 (HMGA2) Oncogenicity in Mesenchymal and Epithelial Neoplasia." International Journal of Molecular Sciences 21, no. 9 (April 29, 2020): 3151. http://dx.doi.org/10.3390/ijms21093151.

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High mobility group AT-hook 2 (HMGA2) has been associated with increased cell proliferation and cell cycle dysregulation, leading to the ontogeny of varied tumor types and their metastatic potentials, a frequently used index of disease prognosis. In this review, we deepen our understanding of HMGA2 pathogenicity by exploring the mechanisms by which HMGA2 misexpression and ectopic expression induces mesenchymal and epithelial tumorigenesis respectively and distinguish the pathogenesis of benign from malignant mesenchymal tumors. Importantly, we highlight the regulatory role of let-7 microRNA family of tumor suppressors in determining HMGA2 misexpression events leading to tumor pathogenesis and focused on possible mechanisms by which HMGA2 could propagate lymphangioleiomyomatosis (LAM), benign mesenchymal tumors of the lungs. Lastly, we discuss potential therapeutic strategies for epithelial and mesenchymal tumorigenesis based on targeting the HMGA2 signaling pathway.

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Noureldine, H. A., W. Nour-Eldine, M. H. Hodroj, M. H. A. Noureldine, A. Taher, and I. Uthman. "Hematological malignancies in connective tissue diseases." Lupus 29, no. 3 (January 14, 2020): 225–35. http://dx.doi.org/10.1177/0961203319899986.

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Chronic inflammation has profound tumor-promoting effects. Inflammatory cells are the key players in immunosurveillance against tumors, and immunosuppression is known to increase the risk of tumors. Autoimmune diseases, which manifest as loss of self-tolerance and chronic immune dysregulation, provide a perfect environment for tumor development. Aside from managing the direct inflammatory consequences of autoimmune pathogenesis, cancer risk profiles should be considered as a part of a patient's treatment. In this review, we describe the various associations of malignancies with autoimmune diseases, specifically systemic lupus erythematosus, rheumatoid arthritis, systemic sclerosis, and Sjögren's syndrome, as well as discuss the mechanisms contributing to the pathogenesis of both disorders.

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Biserova, Karina, Arvids Jakovlevs, Romans Uljanovs, and Ilze Strumfa. "Cancer Stem Cells: Significance in Origin, Pathogenesis and Treatment of Glioblastoma." Cells 10, no. 3 (March 11, 2021): 621. http://dx.doi.org/10.3390/cells10030621.

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Cancer stem cells (CSCs), known also as tumor-initiating cells, are quiescent, pluripotent, self-renewing neoplastic cells that were first identified in hematologic tumors and soon after in solid malignancies. CSCs have attracted remarkable research interest due to their role in tumor resistance to chemotherapy and radiation treatment as well as recurrence. Extensive research has been devoted to the role of CSCs in glioblastoma multiforme (GBM), the most common primary brain tumor in adults, which is characterized by a dismal prognosis because of its aggressive course and poor response to treatment. The aim of the current paper is to provide an overview of current knowledge on the role of cancer stem cells in the pathogenesis and treatment resistance of glioblastoma. The six regulatory mechanisms of glioma stem cells (GSCs)—tumor microenvironment, niche concept, metabolism, immunity, genetics, and epigenetics—are reviewed. The molecular markers used to identify GSCs are described. The role of GSCs in the treatment resistance of glioblastoma is reviewed, along with future treatment options targeting GSCs. Stem cells of glioblastoma thus represent both a driving mechanism of major treatment difficulties and a possible target for more effective future approaches.

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Adams, Gregory N., Dusty Waltz, Leah Rosenfeldt, Malinda Frederick, Whitney Miller, Alexey S. Revenko, Brett P. Monia, and Joseph S. Palumbo. "Thrombin Drives Colorectal Cancer Pathogenesis at the Level of Primary Tumor Growth, Tumor Invasion and Metastasis." Blood 124, no. 21 (December 6, 2014): 2812. http://dx.doi.org/10.1182/blood.v124.21.2812.2812.

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Abstract Cell-associated and circulating hemostatic factors have been identified as powerful determinants of tumor cell metastatis, primarily by supporting the early survival of newly formed micrometastases. However, despite substantial evidence that procoagulants and related signaling molecules can control cell proliferation, angiogenesis and other reparative processes, multiple prior studies unexpectedly demonstrated that hemostatic factors were often dispensable for the growth of established tumors. Here, we report that colorectal cancer represents at least one important exception where hemostatic factors control multiple aspects of cancer pathogenesis. Consistent with clinical findings that patients with prothrombotic mutations (homozygosity for the fVLeiden) have a ~6-fold increased risk of developing colorectal cancer, we have shown previously that mice with even a relatively modest 50% genetically-imposed diminution in circulating prothrombin exhibit a dramatically decreased tumor incidence in a murine model of inflammation-driven colon cancer. In order to determine if thrombin supports the growth of established colorectal cancer, we compared the subcutaneous growth of an aggressive C57Bl/6-derived colonic adenocarcinoma (MC38) in cohorts of wildtype mice and fIILox/- mice carrying just ~10% the normal level of circulating prothrombin. Colon cancer growth was significantly diminished in fIILox/- mice relative to control animals, resulting in a ~3-fold difference in tumor mass between cohorts at the end of the 3 week study period. Complementary studies in which hepatic prothrombin expression and circulating prothrombin levels were diminished using a specific prothrombin antisense oligonucleotide “gapmer” resulted in a similar reduction in colorectal cancer primary tumor growth. Furthermore, prothrombin “gapmer” treatment also slowed the growth of an aggressive, human-derived colorectal adenocarcinoma cell line transplanted into immunodeficient nude mice. Detailed histological analyses revealed no significant prothrombin-dependent differences in angiogenesis, tumor cell apoptosis or the numbers of tumor-associated macrophages. However, histological analyses of colonic adenocarcinoma tumors revealed a significantly lower mitotic index as well as significantly less migration of tumor cells through the panniculus muscle in tumors harvested from fIILox/- mice relative to control mice, suggesting that thrombin promotes tumor cell proliferation and local migration through tissue barriers. Complementary studies of pulmonary metastatic foci formed following intravenous injection of MC38 cells into fIILox/- and control mice further revealed that lowering prothrombin essentially eliminated pulmonary metastases, whereas numerous pulmonary foci were present in animals with normal prothrombin levels. To further characterize the role of thrombin in colorectal cancer growth, we analyzed the potential of a-thrombin to promote MC38 proliferation and invasion in vitro. Here, brief exposure to a-thrombin induced the proliferation of MC38 cells and acted as a chemoattractant when added to the lower chamber in a Boyden chamber assay. Together, these findings suggest thrombin significantly contributes to multiple stages of colon cancer pathogenesis, including tumor growth, invasion, and metastatic seeding, and emphasize the potential utility of targeting prothrombin, thrombin generation or thrombin activity as novel adjunct therapeutic strategies to impede the growth and progression of colorectal carcinoma. Disclosures No relevant conflicts of interest to declare.

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VAUPEL, P. "Oxygenation status of malignant tumors: Pathogenesis of hypoxia and significance for tumor therapy." Seminars in Oncology 28 (April 2001): 29–35. http://dx.doi.org/10.1016/s0093-7754(01)90210-6.

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Vaupel, Peter, Debra K. Kelleher, and Michael H[ouml ]ckel. "Oxygenation status of malignant tumors: Pathogenesis of hypoxia and significance for tumor therapy." Seminars in Oncology 28, no. 2F (April 2001): 29–35. http://dx.doi.org/10.1053/sonc.2001.25398.

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Caperton, Caitlin, and Aime T. Franco. "Macrophage-Tumor Crosstalk in the Pathogenesis of Follicular Thyroid Cancer." Journal of the Endocrine Society 5, Supplement_1 (May 1, 2021): A864. http://dx.doi.org/10.1210/jendso/bvab048.1764.

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Abstract Thyroid cancer is the most common endocrine malignancy and one of the fastest growing cancers in the United States. Follicular thyroid carcinoma (FTC) represents the second most common form of thyroid cancer diagnosed in the US and is most often tied to mutations in the RAS protein family of the MAP kinase pathway. In addition to driver mutations, FTC is characterized by a unique tumor microenvironment (TME) composed of cellular and non-cellular components that impact tumorigenesis and disease progression. Preliminary data from our lab has shown that CD45+ immune cells account for approximately 68% of all cells found in whole tumors collected from mouse models of RAS-driven disease. Macrophages account for the largest portion of known immune cell populations. Further experiments have demonstrated that tumor cell lines isolated from our RAS-driven models secrete cytokines known to impact the recruitment and activation state of cells of the myeloid lineage, particularly macrophages. However, it’s unclear what type of functional characteristics are induced by these secreted factors and how the resulting macrophage phenotype affects disease progression. Here, we sought to determine how bidirectional communication between macrophages and thyroid cancer cell lines could contribute to the development of a protumorigenic microenvironment. First, we began by defining how RAS-driven thyroid cancer cell lines affected the functional phenotype of previously unstimulated macrophages. Through gene expression analysis encompassing several markers of macrophage activation states, we determined that tumor cell-secreted factors induced the expression of multiple genes associated with tumor associated macrophages (TAM). In particular, we observed consistent upregulation of IL-10 and TNF-alpha, factors that have been associated with worsening disease. These results were further validated through quantification of protein secretion. In addition, we determined the role of activated macrophages in the progression of thyroid cancer, and specifically the effect of macrophage-secreted factors on tumor cell proliferation. Through direct and indirect assays of proliferation, we determined that factors secreted by classically-activated M1 macrophages inhibited cell proliferation. Surprisingly, secretions from alternatively-activated M2 macrophages reduced in vitro cell growth in some cell lines. Further analysis demonstrated that reduced cell proliferation was not associated with cell death, but rather was a result of delayed progression through the cell cycle. These results help to further define the macrophage phenotype within our model of FTC and will identify potential therapeutic targets to reduce the activity of protumorigenic cell populations.

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Pancione, Massimo, Guido Giordano, Andrea Remo, Antonio Febbraro, Lina Sabatino, Erminia Manfrin, Michele Ceccarelli, and Vittorio Colantuoni. "Immune Escape Mechanisms in Colorectal Cancer Pathogenesis and Liver Metastasis." Journal of Immunology Research 2014 (2014): 1–11. http://dx.doi.org/10.1155/2014/686879.

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Over the past decade, growing evidence indicates that the tumor microenvironment (TME) contributes with genomic/epigenomic aberrations of malignant cells to enhance cancer cells survival, invasion, and dissemination. Many factors, produced orde novosynthesized by immune, stromal, or malignant cells, acting in a paracrine and autocrine fashion, remodel TME and the adaptive immune response culminating in metastasis. Taking into account the recent accomplishments in the field of immune oncology and using metastatic colorectal cancer (mCRC) as a model, we propose that the evasion of the immune surveillance and metastatic spread can be achieved through a number of mechanisms that include (a) intrinsic plasticity and adaptability of immune and malignant cells to paracrine and autocrine stimuli or genotoxic stresses; (b) alteration of positional schemes of myeloid-lineage cells, produced by factors controlling the balance between tumour-suppressing and tumour-promoting activities; (c) acquisition by cancer cells of aberrant immune-phenotypic traits (NT5E/CD73, CD68, and CD163) that enhance the interactions among TME components through the production of immune-suppressive mediators. These properties may represent the driving force of metastatic progression and thus clinically exploitable for cancer prevention and therapy. In this review we summarize results and suggest new hypotheses that favour the growing impact of tumor-infiltrating immune cells on tumour progression, metastasis, and therapy resistance.

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Ferrone, Cristina, and Glenn Dranoff. "Dual Roles for Immunity in Gastrointestinal Cancers." Journal of Clinical Oncology 28, no. 26 (September 10, 2010): 4045–51. http://dx.doi.org/10.1200/jco.2010.27.9992.

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Histopathologic examination reveals that most human tumors are associated with diverse immune cell infiltrates, but the roles of host reactions in disease pathogenesis and prognosis remain to be fully clarified. Recent investigations in genetically engineered murine tumor models have uncovered dual functions for immune responses during cancer development and progression. Alterations in tumor cell gene expression profiles and coding sequences may trigger the activation of cytotoxic lymphocytes, which act to restrain tumor growth. In contrast, persistent inflammatory reactions, which may be driven by infection, environmental toxins, or impaired immune regulation, create a microenvironment that fosters tumor cell growth, survival, invasion, and dissemination. The dynamic interplay of these competing responses appears to be a critical event in cancer pathogenesis, with tumor promotion and immune evasion proving dominant in clinically evident disease. Nonetheless, longitudinal studies of patient cohorts have demonstrated that particular histopathologic and genetic signatures of cytotoxic lymphocyte reactions provide important prognostic information. Here, we discuss the dual roles of immunity in cancer development, focusing on gastrointestinal malignancies, given the depth of recent insights into the mechanisms underlying these tumors.

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Travkina, Julia V., Tatiana N. Zhevak, and Peter F. Litvitsky. "Chordoma: Etiology, Pathogenesis, Diagnosis, Treatment." Current pediatrics 17, no. 4 (October 5, 2018): 266–71. http://dx.doi.org/10.15690/vsp.v17i4.1917.

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The lecture analyzes modern knowledge about etiology, key mechanisms of pathogenesis, clinical manifestations, types, diagnostic methods and treatment strategy of chordoma (tumor from notochordal cells). To assess the retention of the lecture material, a case problem and multiple-choice test questions are given.

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Journal articles on the topic 'Tumor pathogenesis'

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