Готові списки джерел за темами / Cancer pathogenesis

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Добірка наукової літератури з теми "Cancer pathogenesis"

Автор: Grafiati

Опубліковано: 10 січня 2023

Оновлено: 28 січня 2023

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Статті в журналах з теми "Cancer pathogenesis"

Montironi, Rodolfo, and Per-Uno Malmström. "Bladder cancer: pathogenesis." Scandinavian Journal of Urology and Nephrology 42, sup218 (January 2008): 93–94. http://dx.doi.org/10.1080/03008880802291899.

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Berger, Hilmar, Miguel S. Marques, Rike Zietlow, Thomas F. Meyer, Jose C. Machado, and Ceu Figueiredo. "Gastric cancer pathogenesis." Helicobacter 21 (August 16, 2016): 34–38. http://dx.doi.org/10.1111/hel.12338.

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Bukhtoyarov, Oleg V., and Denis M. Samarin. "Pathogenesis of Cancer: Cancer Reparative Trap." Journal of Cancer Therapy 06, no. 05 (2015): 399–412. http://dx.doi.org/10.4236/jct.2015.65043.

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Franco, Omar E., Aubie K. Shaw, Douglas W. Strand, and Simon W. Hayward. "Cancer associated fibroblasts in cancer pathogenesis." Seminars in Cell & Developmental Biology 21, no. 1 (February 2010): 33–39. http://dx.doi.org/10.1016/j.semcdb.2009.10.010.

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Szabó, Diána, Adrienn Zsippai, Melinda Bendes, Zsófia Tömböl, Péter M. Szabó, Károly Rácz, and Péter Igaz. "Pathogenesis of adrenocortical cancer." Orvosi Hetilap 151, no. 29 (July 1, 2010): 1163–70. http://dx.doi.org/10.1556/oh.2010.28931.

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A mellékvesekéreg-carcinoma ritka, rossz prognózisú daganat. Döntően sporadikus előfordulású, de ismertek nagyon ritka öröklődő formái is, amelyek a patogenezis megértésében nagy segítséget nyújtanak. A mellékvesekéreg-daganatokra hajlamosító öröklődő szindrómák közé tartozik a Li–Fraumeni-szindróma, a Beckwith–Wiedemann-szindróma, a familiáris adenomatosus polyposis, illetve a döntően benignus daganatokkal társuló multiplex endokrin neoplasia 1-es típusa (MEN1), Carney-komplex és McCune–Albright-szindróma. A mellékvesekéreg-daganatok patogenezisében szereplő főbb mechanizmusok közé tartozik az inzulinszerű növekedési faktor-2 fokozott expressziója, a Wnt/β-katenin és a cAMP-proteinkináz-A jelátviteli utak aktivációja, valamint a p53 és MEN1 gének mutációi. A mellékvesekéreg-carcinoma kezelésében a gyógyszeres lehetőségek meglehetősen korlátozottak. Az utóbbi évek molekuláris-bioinformatikai kutatásai számos eddig ismeretlen patogenetikai út szerepét vetették fel, amelyek új gyógyszeres támadáspontok lehetőségét is jelenthetik. E tanulmányban a szerzők az öröklődő daganatszindrómák patogenezisét, a sporadikus daganatokban észlelt eltéréseket és a legújabb molekuláris-bioinformatikai eredményeket ismertetik.

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Yoon, Cheol-Yong, and Seok-Soo Byun. "Pathogenesis of Prostate Cancer." Journal of the Korean Medical Association 53, no. 2 (2010): 98. http://dx.doi.org/10.5124/jkma.2010.53.2.98.

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N, Gupta, Mujapara AK, Boraste A, Khairnar Y, Vamsi KK, Jhadav A, Gupta M, et al. "Toxicogenomics and cancer pathogenesis." International Journal of Genetics 1, no. 2 (December 30, 2009): 47–60. http://dx.doi.org/10.9735/0975-2862.1.2.47-60.

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Miller, York E. "Pathogenesis of Lung Cancer." American Journal of Respiratory Cell and Molecular Biology 33, no. 3 (September 2005): 216–23. http://dx.doi.org/10.1165/rcmb.2005-0158oe.

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Arnold, C. N., and H. E. Blum. "Colorectal cancer: molecular pathogenesis." DMW - Deutsche Medizinische Wochenschrift 130, no. 14 (April 2005): 880–82. http://dx.doi.org/10.1055/s-2005-865102.

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Ponz de Leon, M., and A. Percesepe. "Pathogenesis of colorectal cancer." Digestive and Liver Disease 32, no. 9 (December 2000): 807–21. http://dx.doi.org/10.1016/s1590-8658(00)80361-8.

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Дисертації з теми "Cancer pathogenesis"

Ng, Jia Nian, and 黃嘉年. "RNF168 expression in breast cancer." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/206551.

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Background: Breast cancer is the commonest female cancer. DNA double-strand breaks (DSBs) associated proteins such as BRCA1 have been shown to be involved in tumourigenesis of breast tissue. One of the key regulators of DSBs, the RING Finger Protein 168 (RNF168), controls DNA damage responses (including the manipulation of homologous recombinant and non-homologous end-joining repair) which are responsible for correction of errors that occur during DSBs in order to maintain genomic stability. The nature of this protein suggests that RNF168 may play an important role in development of breast cancer. Material and methods: This study investigated the relationship of RNF168 expression in breast cancer by immunohistochemistry staining of 118 breast cancer samples in tissue microarray. The nuclear stain and cytoplasmic stain of the sections were assessed. Nuclear localization score was obtained and correlated with clinico-pathological features of the patients. Results: Immunohistological staining of RNF168 was successful in 99 cases of the tested breast cancer specimens. The expression of RNF168 was found to be significantly correlated with the occurrence of breast cancer metastasis (p=0.032). Strong expression of the protein was also found to be significantly associated with poorer breast cancer prognosis (p=0.033). In addition, correlation analysis also showed marginal correlation between nuclear localization of RNF168 with the age of patients at their first disease diagnosis (p=0.061). Conclusion: RNF168 might play a critical role in promoting breast cancer metastasis during the advanced stage of breast cancer, which results in poor disease prognosis. Detailed mechanism involved in metastasis promotion remained to be revealed in further study.
published_or_final_version
Pathology
Master
Master of Medical Sciences

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Elshafae, Said Mohammed Abbas. "Pathogenesis and Treatment of Canine Prostate Cancer." The Ohio State University, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=osu1492081831172341.

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Lau, Yuen-ting, and 劉婉婷. "Functional characterization of cancer-associated fibroblasts in the regulation of cancer stem cell-like properties in hepatocellular carcinoma." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2015. http://hdl.handle.net/10722/209516.

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Thairu, Ngayu Munga. "Mechanisms of colorectal cancer pathogenesis : role of hypoxia." Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/14361.

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Colorectal cancer (CRC) is the third most common cancer worldwide Hypoxia plays a pivotal role in cancer, regulating cellular processes such as angiogenesis via the Hypoxia Inducible Factor (HIF) pathway. HIF-1α and HIF-2α, isoforms of the α-subunit, were previously thought to be functionally redundant, but mounting evidence supports their divergent roles in many cancers. In CRC their relative roles remain unclear. This study aimed to elucidate their relative contribution to hypoxic regulation of CRC using the Caco-2 cell-line. Ex vivo cultures of primary cells isolated from CRC tissue were used to validate the Caco-2 data. Caco-2 cells were stimulated with hypoxia (1% O2) or the hypoxia-mimetic dimethyloxaloylglycine (DMOG), with normoxia (21% O2) controls. Expression of known hypoxia-induced genes was quantified by polymerase chain reaction (PCR) and a PCR-based array was used to further characterise angiogenic genes. Protein expression was determined using Western Blotting and ELISA. The effect of selective HIF-isoform knockdown on gene expression was evaluated. Tumour-derived cultures (TDCs) were established using tissue obtained from surgically resected CRC specimens. mRNA expression of epithelial cell markers (Ep-CAM, VE-Cadherin) was quantified by Q-PCR, and protein expression of the CRC tumour marker carcinoembryonic antigen (CEA) measured by ELISA. TDCs were exposed to hypoxia, and gene expression relative to normoxia was quantified by Q-PCR and PCR-based array. In Caco-2 cells, hypoxia upregulated both HIF isoform proteins, inducing genes involved in angiogenesis (VEGF, ANGPTL-4, EFNA-3, TGF-β1), metabolism (CA-IX, GLUT-1) and apoptosis (BNIP-3), with mRNA changes reflected at protein level. Three novel hypoxia-induced angiogenesis genes (ANGPTL-4, EFNA-3, TGF-β1) were identified. Hypoxia-induced ANGPTL-4, BNIP-3 and TGF-β1 expression was reduced by siHIF-1α only, while EFNA-3 and VEGF expression was reduced by both siHIF-1α and siHIF-2α. TDCs expressed epithelial CRC cell markers, and showed similar hypoxia-induced angiogenesis gene expression to Caco-2 cells, although there was significant inter-donor variability.

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Taraseviciute, Agne. "Tenascin-C in the pathogenesis of breast cancer /." Connect to full text via ProQuest. Limited to UCD Anschutz Medical Campus, 2008.

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Thesis (Ph.D. in Cell Biology, Stem Cells, and Development) -- University of Colorado Denver, 2008.
Typescript. Includes bibliographical references (leaves 102-114). Free to UCD Anschutz Medical Campus. Online version available via ProQuest Digital Dissertations;

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Cartón, García Fernando. "Myosin VB in intestinal pathogenesis." Doctoral thesis, Universitat Autònoma de Barcelona, 2017. http://hdl.handle.net/10803/458251.

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Miosina VB es una proteína que actúa como un motor molecular usando la energía del ATP para moverse a lo largo de filamentos de actina. Participa en el trafico intracelular de endosomas de reciclaje en la parte subapical de células polarizadas y no polarizadas. Su expresión es muy abundante en el intestino donde participa en el establecimiento y mantenimiento de la polaridad de los enterocitos. Mutaciones en MYO5B causan la enfermedad de inclusión de microvellosidades, in raro trastorno congénito que afecta a las células epiteliales del intestino cursando con diarrea acuosa persistente que suele ser fatal. Esta enfermedad se caracteriza por la presencia de alteraciones morfológicas en los enterocitos, atrofia de las vellosidades y deslocalización de proteínas del polo apical y basolateral del enterocito. Su patología molecular no se conoce, principalmente por la falta de modelos animales. En el presente estudio, describimos un versátil modelo murino con inactivación constitutiva de Myo5b e inactivación condicional en las células epiteliales intestinales inducida por tamoxifeno. En ambos casos, los animales muestras un cuadro clínico muy semejantes al de los pacientes con enfermedad de inclusión de microvellosidades, presentado diarrea y deshidratación que causan la muerte del animal. A nivel histológico, el intestino muestra las mismas alteraciones en los enterocitos que las presentes en pacientes humanos, incluyendo atrofia de vellosidades y deslocalización de marcadores proteicos. Además, la inactivación de Myo5b también provocó hiperproliferación de las criptas intestinales. Por lo tanto, el modelo animal presentado constituye una herramienta muy útil para investigar las causas moleculares de la enfermedad y ensayar de manera preclínica fármacos u otras opciones terapéuticas. Por otro lado, la pérdida de polaridad y diferenciación es también una de las señas de identidad de los carcinomas metastásicos avanzados y correlaciona con un mal pronóstico de los pacientes. En concreto, para el cáncer colorrectal, investigaciones previas llevadas a cabo en nuestro laboratorio ya han demostrado que la pérdida de miosina IA promueve la progresión la enfermedad y tiene actividad supresora de tumores. Dicha proteína es abundante en el borde en cepillo de los enterocitos, y participa en el mantenimiento de la estructura polarizada. Otros estudios han señalado la relación entre la inactivación de MYO5B con un incremento en la motilidad e invasión de células de cáncer gástrico, aunque todavía no se conoce nada de su relación con en el cáncer colorrectal. Para resolver esta cuestión, hemos diseñado modelos in vitro inducibles por doxiciclina para sobre expresar y reducir la expresión de dicha proteína en líneas celulares de cáncer de colon. Además, se ha empleado la tecnología CRISPR/Cas9 para inactivar la expresión de MYO5B en la línea de cáncer de colon Caco2-BBE. Los resultados muestran cambios en la polarización y diferenciación de dichas líneas celulares, de acuerdo con observaciones previas. También se ha observado una posible relación entre MYO5B y la capacidad de movilidad e invasión de las líneas de cáncer de colon. Sin embargo, la hiperproliferación observada en el intestino de los ratones no se reproduce en las líneas de cáncer de colon empleadas tras reducir o sobre expresar MYO5B, o en modelos xenograft subcutáneos in vivo de dichas líneas. Por otro lado, usando un microarray de tejidos con 155 muestras de tumores primarios de pacientes con cáncer colorrectal en estadio Dukes C se ha comprobado que una reducción en la expresión de MYO5B se asocia con una disminución en el tiempo de recaída y en la supervivencia total de los pacientes de cáncer de colon. Además, tumores con un grado de diferenciación bajo también expresan niveles de MYO5B significativamente reducidos. Finalmente, todos estos resultados indican que MYO5B juega un papel importante en la diferenciación del intestino normal y de las líneas de cáncer de colon. De la misma manera, MYO5B también podría desempeñar un papel en la progresión del cáncer colorrectal promoviendo movilidad e invasión de las células tumorales.
Myosin VB is a molecular motor protein that uses the energy of ATP to move along actin filaments. It participates in the recycling endosomes trafficking in the subapical cytoplasmic region of non-polarized and polarized cells. It is highly expressed in the small and large intestine, where its role in the establishment of polarized function in enterocytes is also well known. Inactivating mutations of MYO5B have been associated with microvillus inclusion disease (MVID), a rare congenital disorder of the intestinal epithelial cells that presents with persistent life-threatening watery diarrhea. It is characterized by morphological enterocyte abnormalities such as microvillus atrophy and mislocalization of apical and basolateral protein transporters. The molecular pathology of the disease is not well known mainly due to the lack of animal models. In the present study, we report a versatile murine model with targeted inactivation of Myo5b. This model allowed us to generate and characterized a constitutive Myo5b knockout mice and a tamoxifen-inducible intestinal-epithelium-specific Myo5b knockout. In both cases, the mice closely resemble the phenotype of MVID patients, developing watery diarrhea and dehydration causing the death of the animal. Histological study of the intestine showed all the characteristic enterocyte defects observed in MVID patients, including microvillus atrophy and mislocalization of protein markers. Moreover, the inactivation of MYO5B also originated hyperproliferation of the intestinal crypts. Therefore, our mice constitute a useful model to further investigate the underlying molecular mechanism of this disease and to preclinically assess the efficacy of novel therapeutic approaches. In addition, hyperproliferation as well as loss of cell polarity, differentiation, and tissue architecture are hallmarks of advanced metastatic carcinomas and strongly correlate with poor patient prognosis. Specifically, for colorectal cancer, the third most common type of cancer worldwide, we have previously demonstrated that the loss of brush border MYO1A, also involved in cell polarity, promotes cancer progression and has tumor suppressor activity. Other studies have indicated a relationship between MYO5B inactivation and gastric cancer, promoting invasion and motility, but little is known regarding its role in colorectal cancer. To address this question, we have developed novel doxycycline-inducible in vitro models of MYO5B overexpression and downregulation. Moreover, we have generated MYO5B knockout Caco2-BBE cells using CRISPR/Cas9 technology. Our results showed changes in the polarization and differentiation of colon cancer cells, in agreement with previous observations in the normal intestine. Moreover, we have observed a relationship between MYO5B and the motility and invasion capacity of colon cancer cells, indicating a possible role of MYO5B in colon cancer progression. However, the effect of MYO5B loss in cell proliferation observed in our Myo5b knockout mice could not be confirmed in our models in vitro and in vivo, employing cell line-derived xenografts. In addition, using a tissue microarray containing triplicate samples from 155 primary Dukes C colorectal tumors, reduced MYO5B expression was found to be associated with shorter disease-free and overall survival of the patients. Moreover, poorly differentiated tumors showed significantly reduced expression of MYO5B. Collectively, our results indicate that MYO5B plays an important role in the differentiation of the normal intestinal epithelium and colon cancer cells, as well as a possible role in cancer progression promoting cell motility and invasion.

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Li, Bin, and 李斌. "ID1-induced activation of PI3K/AKT/NFkB pathway: mechanisms and significance in esophageal cancer." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B43783880.

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Chan, Yuk Kit. "The role of exosomes in nasopharyngeal carcinoma." HKBU Institutional Repository, 2013. http://repository.hkbu.edu.hk/etd_ra/1509.

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Ralston, Stuart H. "The pathogenesis and management of malignancy-associated hypercalcaemia." Thesis, University of Glasgow, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.304658.

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Banh, Taylor. "Exploration of Adipose in the Pathogenesis of Cancer Cachexia." The Ohio State University, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=osu1532520752821935.

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Книги з теми "Cancer pathogenesis"

Haigis, Kevin M. Molecular pathogenesis of colorectal cancer. New York: Springer, 2013.

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Dwivedi, Ashish, Anurag Tripathi, Ratan Singh Ray, and Abhishek Kumar Singh, eds. Skin Cancer: Pathogenesis and Diagnosis. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-16-0364-8.

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Haigis, Ph.D., Kevin M., ed. Molecular Pathogenesis of Colorectal Cancer. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-8412-7.

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Gregory, Christopher D., ed. Apoptosis in Cancer Pathogenesis and Anti-cancer Therapy. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-39406-0.

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Longoria, Miguel Angel, and Joris Ismael Alcalá. Adenocarcinoma: Pathogenesis, treatment, and prognosis. Hauppauge, N.Y: Nova Science Publisher's, 2011.

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Paula, Wells, and Halstead Regina, eds. Rectal cancer: Etiology, pathogenesis and treatment. Hauppauge, NY: Nova Science Publishers, 2009.

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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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Frank, David A., ed. Signaling Pathways in Cancer Pathogenesis and Therapy. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-1216-8.

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Bonavida, Benjamin, ed. Nitric Oxide and Cancer: Pathogenesis and Therapy. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-13611-0.

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Mercier, Isabelle, Jean-François Jasmin, and Michael P. Lisanti, eds. Caveolins in Cancer Pathogenesis, Prevention and Therapy. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-1001-0.

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Частини книг з теми "Cancer pathogenesis"

Drabkin, Harry A., and Jeffrey Turner. "Renal Cancer Pathogenesis." In Encyclopedia of Cancer, 1–6. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27841-9_6324-2.

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Purohit, Vinee, Kamiya Mehla, and Pankaj K. Singh. "Pancreatic Cancer Pathogenesis." In Encyclopedia of Cancer, 1–5. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27841-9_7188-4.

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Drabkin, Harry A., and Jeffrey Turner. "Renal Cancer Pathogenesis." In Encyclopedia of Cancer, 4000–4005. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-46875-3_6324.

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Purohit, Vinee, Kamiya Mehla, and Pankaj K. Singh. "Pancreatic Cancer Pathogenesis." In Encyclopedia of Cancer, 3413–17. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-662-46875-3_7188.

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Drabkin, Harry A., and Jeffrey Turner. "Renal Cancer Pathogenesis." In Encyclopedia of Cancer, 3238–41. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_6324.

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Ponz de Leon, Maurizio. "Pathogenesis of Colorectal Cancer." In Colorectal Cancer, 23–48. Berlin, Heidelberg: Springer Berlin Heidelberg, 2002. http://dx.doi.org/10.1007/978-3-642-56008-8_2.

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Lo, Jennifer A., and David E. Fisher. "Melanoma Pathogenesis." In Cancer Drug Discovery and Development, 25–45. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-2143-0_2.

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Schlottmann, Francisco, and Marco G. Patti. "Esophageal Adenocarcinoma: Pathogenesis and Epidemiology." In Esophageal Cancer, 21–28. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-91830-3_3.

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Figge, James J., Nikolai A. Kartel, Dima Yarmolinsky, and Gennady Ermak. "Molecular Pathogenesis of Thyroid Cancer." In Thyroid Cancer, 15–32. Totowa, NJ: Humana Press, 2006. http://dx.doi.org/10.1007/978-1-59259-995-0_3.

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Figge, James. "Molecular Pathogenesis of Thyroid Cancer." In Thyroid Cancer, 57–75. Totowa, NJ: Humana Press, 2000. http://dx.doi.org/10.1007/978-1-59259-199-2_6.

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Тези доповідей конференцій з теми "Cancer pathogenesis"

ZIEGLER, JOHN L. "INFECTIOUS AGENTS AND CANCER: PATHOGENESIS." In International Seminar on Nuclear War and Planetary Emergencies 38th Session. WORLD SCIENTIFIC, 2008. http://dx.doi.org/10.1142/9789812834645_0039.

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Liu, Yang, Hongqiang Ma, and Jianquan Xu. "Visualizing cancer pathogenesis at the nanoscale." In Microscopy Histopathology and Analytics. Washington, D.C.: OSA, 2020. http://dx.doi.org/10.1364/microscopy.2020.mw1a.1.

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Chu, Tianjiao. "The pathogenesis and treatment of primary liver cancer." In 2017 4th International Conference on Machinery, Materials and Computer (MACMC 2017). Paris, France: Atlantis Press, 2018. http://dx.doi.org/10.2991/macmc-17.2018.86.

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Hapca, Sandra, Daniel P. Brice, Susan Berry, Graeme I. Murray, and Mairi H. McLean. "PTU-040 HMGB1 in the pathogenesis of colorectal cancer." In British Society of Gastroenterology, Annual General Meeting, 4–7 June 2018, Abstracts. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2018. http://dx.doi.org/10.1136/gutjnl-2018-bsgabstracts.381.

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Bar-Sagi, Dafna. "Abstract IA21: Ras oncogene in cancer pathogenesis and therapy." In Abstracts: Fourth AACR International Conference on Frontiers in Basic Cancer Research; October 23-26, 2015; Philadelphia, PA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.fbcr15-ia21.

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Dickson, Elizabeth Louise, Lihua Li, Samuel Leung, Christine Chow, Rachel Isaksson Vogel, David Huntsman, C. Blake Gilks, and Subbaya Subramanian. "Abstract A17: FBxW7 duality in ovarian cancer: Novel insight into ovarian cancer pathogenesis." In Abstracts: AACR Special Conference on Advances in Ovarian Cancer Research: From Concept to Clinic; September 18-21, 2013; Miami, FL. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1078-0432.ovca13-a17.

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Sen, Shrinka, Samsiddhi Bhattacharjee, Indranil Mukhopadhyay, Paramita Mandal, Sweta Sharma, Rahul Roy Chowdhury, and Sharmila Sengupta. "Abstract 1056: Impact of host methylome on cervical cancer pathogenesis." 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.am2015-1056.

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Asaturova, A., M. Sannikova, and N. Kondrikov. "EP782 Transition zones and progenitor cells in ovarian cancer pathogenesis." In ESGO Annual Meeting Abstracts. BMJ Publishing Group Ltd, 2019. http://dx.doi.org/10.1136/ijgc-2019-esgo.833.

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Ji, Xiangming Ji, Jun Qian, Jamshedur Rahman, Brad Harris, Megan Hoeksema, Heidi Chen, Rosana Eisenberg, and Jamey Young. "Abstract A10: SLC7A11 contributes to the pathogenesis of lung cancer." In Abstracts: AACR Special Conference: Metabolism and Cancer; June 7-10, 2015; Bellevue, WA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1557-3125.metca15-a10.

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Mazumdar, Darshana. "Association of organochlorine pesticides and risk of epithelial ovarian cancer: A case control study." In 16th Annual International Conference RGCON. Thieme Medical and Scientific Publishers Private Ltd., 2016. http://dx.doi.org/10.1055/s-0039-1685303.

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Анотація:

Background: Organochlorine pesticides (OCPs) belongs to the class of hydrocarbons characterized by its cyclic structure. Due to their persistent nature OCP gets accumulated in the food chain and cause possible adverse health effects specifically various hormone mediated disorders. Ovarian cancer is also one of the hormone dependant cancer and begins with the transformation of cells that comprises the ovaries including surface epithelial, germ cells, etc. It has been suggested that endocrine disruption, exposure to xenobiotic and subsequent oxidative stress may antedate ovarian cancer and contribute to its pathogenesis. However, no report regarding any association of OCP level with etiology of epithelial ovarian cancer is so far available among North Indian population. Methods: A total of 120 subjects were included in this case control study, consisting of 60 histological proven cases of epithelial ovarian cancer and 60 controls subjects. Quantification of OCP levels was done by Perkin Elmer Gas Chromatograph (GC) equipped with 63Ni selective Electron Capture Detector. Results: Levels of b-HCH, endosulfan I, p’p’-DDT, p’p’-DDE and heptachlor were found significantly high in cases of epithelial ovarian cancer as compared to control. A significant association was also observed between higher levels of b-HCH and heptachlor and EOC with odds ratio of 2.76 and 2.97 respectively. Conclusion: Results indicate the plausible role of OCPs with the pathogenesis of epithelial ovarian cancer among North Indian population. Moreover, it is one of the first report suggesting significant level of heptachlor among north Indian women population with epithelial ovarian cancer.

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Звіти організацій з теми "Cancer pathogenesis"

Adami, Hans-Olov. The Infectious Pathogenesis of Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, March 2009. http://dx.doi.org/10.21236/ada503532.

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Sood, Anil K. Early Events in Ovarian Cancer Pathogenesis. Fort Belvoir, VA: Defense Technical Information Center, January 2012. http://dx.doi.org/10.21236/ada608121.

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Adami, Hans-Olov. The Infectious Pathogenesis of Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, March 2010. http://dx.doi.org/10.21236/ada526530.

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Sood, Anil K. Early Events in Ovarian Cancer Pathogenesis. Fort Belvoir, VA: Defense Technical Information Center, November 2010. http://dx.doi.org/10.21236/ada542176.

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Adami, Hans-Olov, and Lorelei Mucci. The Infectious Pathogenesis Of Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, April 2011. http://dx.doi.org/10.21236/ada549351.

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Adami, Hans-Olov, and Lorelei A. Mucci. The Infectious Pathogenesis of Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, March 2008. http://dx.doi.org/10.21236/ada482578.

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Bae-Jump, Victoria, and Betty Diamond. Obesity Exposure Across the Lifespan on Ovarian Cancer Pathogenesis. Fort Belvoir, VA: Defense Technical Information Center, June 2014. http://dx.doi.org/10.21236/ada614105.

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Bagasra, Omar. Role of Zinc in the Pathogenesis of Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, May 2003. http://dx.doi.org/10.21236/ada417674.

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Kalinichenko, Tanya. Role of Foxm1 in the Pathogenesis of Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2011. http://dx.doi.org/10.21236/ada554568.

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Bae-Jump, Victoria. Obesity Exposure Across the Lifespan on Ovarian Cancer Pathogenesis. Fort Belvoir, VA: Defense Technical Information Center, August 2015. http://dx.doi.org/10.21236/ada624507.

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