BRCA1/2-related ovarian cancers are of tubal origin: a hypothesis

Piek, Jurgen M.J.; Verheijen, René H.M.; Kenemans, P.; Massuger, Leon F.A.G.; Bulten, Hans; Diest, Paul J. van

doi:10.1016/s0090-8258(03)00365-2

Cited by 117 publications

(81 citation statements)

References 4 publications

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“…These changes histologically resemble high grade serous ovarian cancer. 12 In present study, patients with yolk sac tumour, Mucinous cystadeno carcinoma and immature teratoma fallopian tube did not show any significant pathology.…”

supporting

confidence: 41%

Clinicopathological profile of ovarian tumors in the age group 10-20 years

Priya

2017

Int J Reprod Contracept Obstet Gynecol

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Background: Adolescence is the period of transition from childhood to adulthood. 1% neoplasm occurs in this age group below 17 years, of this, 3% are ovarian neoplasms. Aim was to study retrospectively the clinicopathological profile and outcome of ovarian tumors in the age group 10-20 years in Government Medical College, Kottayam, Kerala, India from January 2008 for six years. Methods: Fifty Patients who have undergone laparotomy in this institution during the period were taken for study. Data regarding age, mode of presentation, diagnostic methods, treatment and histopathology were recorded. Followup was also taken into consideration. Patients with polycystic ovary, corpus luteal cyst, follicular cyst and endometriotic cyst are excluded. Results: Majority of the patients fall between the age group 15-20 years. Major clinical presentation was pain (40%), followed by abdominal mass. Laparotomy was done for all cases except three where laparoscopy was done. Imprint cytology taken for 3 cases. Histopathology showed malignant tumors in 6 cases and benign tumors in 44 cases. Epithelial tumors outnumbered germ cell tumors. Conclusions: This study shows the predominance of epithelial neoplasms in the age group 10-20 years. Proportion of malignancy is 12%.

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supporting

confidence: 41%

Clinicopathological profile of ovarian tumors in the age group 10-20 years

Priya

2017

Int J Reprod Contracept Obstet Gynecol

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“…Although recent evidence shows that some HGSC originate from Mullerian cells (26), OSE cells remain a probable origin of several subtypes of EOCs (reviewed in ref. 27).…”

Section: Discussionmentioning

confidence: 99%

Divergent Roles of PAX2 in the Etiology and Progression of Ovarian Cancer

Al-Hujaily

Tang

Yao

et al. 2015

Cancer Prevention Research

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PAX2 is an essential transcription factor for development. Aberrant PAX2 expression in adult tissues is associated with carcinogenesis and experimental evidence shows that PAX2 generally exhibits oncogenic properties. Although PAX2 is not expressed in normal ovaries, it is highly expressed in low malignant potential and low-grade epithelial ovarian tumors, suggesting that PAX2 induction in ovarian surface epithelium (OSE) may contribute to transformation. Herein, we provide evidence that expression of PAX2 in normal murine OSE cells (mOSE) enhances their proliferation and survival and, with loss of p53, induces tumorigenicity. PAX2 expression in murine ovarian cancer cells enhanced or inhibited tumorigenicity, depending on the model system. In RM cells (mOSE transformed by K-RAS and c-MYC), PAX2 expression inhibited p53 and induced pERK1/2 and COX2, resulting in enhanced angiogenesis and decreased apoptosis of tumors arising from these cells. However, in a murine model of high-grade serous ovarian cancer (STOSE), PAX2 expression improved animal survival by reducing proliferation and metastasis, which correlated with increased Htra1 and decreased COX2. Thus, PAX2 may not be a classical oncogene or tumor suppressor but instead can act in either role by differential regulation of COX2 and/or HTRA1.

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“…The epithelial cells covering the ovaries have historically been considered the site of origin of all ovarian cancers but recent evidence suggests that high-grade serous carcinoma (HGSC) originates from FT epithelium or the tuboperitoneal junction rather than the OSE (Piek et al 2003, Crum et al 2007, Kindelberger et al 2007, Seidman et al 2011, Tone et al 2012. HGSCs are thought to originate in serous tubal intraepithelial carcinoma (STIC) lesions in the FTs, where ovulationrelated oxidative injury can result in genetic alterations and malignant transformation of the secretory epithelium of the FT fimbriae.…”

Section: Serous Cancersmentioning

confidence: 99%

The role of reproductive hormones in epithelial ovarian carcinogenesis

Gharwan

Bunch

Annunziata

2015

Endocrine-Related Cancer

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Epithelial ovarian cancer comprises w85% of all ovarian cancer cases. Despite acceptance regarding the influence of reproductive hormones on ovarian cancer risk and considerable advances in the understanding of epithelial ovarian carcinogenesis on a molecular level, complete understanding of the biologic processes underlying malignant transformation of ovarian surface epithelium is lacking. Various hypotheses have been proposed over the past several decades to explain the etiology of the disease. The role of reproductive hormones in epithelial ovarian carcinogenesis remains a key topic of research. Primary questions in the field of ovarian cancer biology center on its developmental cell of origin, the positive and negative effects of each class of hormones on ovarian cancer initiation and progression, and the role of the immune system in the ovarian cancer microenvironment. The development of the female reproductive tract is dictated by the hormonal milieu during embryogenesis. Intensive research efforts have revealed that ovarian cancer is a heterogenous disease that may develop from multiple extra-ovarian tissues, including both Mü llerian (fallopian tubes, endometrium) and non-Mü llerian structures (gastrointestinal tissue), contributing to its heterogeneity and distinct histologic subtypes. The mechanism underlying ovarian localization, however, remains unclear. Here, we discuss the role of reproductive hormones in influencing the immune system and tipping the balance against or in favor of developing ovarian cancer. We comment on animal models that are critical for experimentally validating existing hypotheses in key areas of endocrine research and useful for preclinical drug development. Finally, we address emerging therapeutic trends directed against ovarian cancer.

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BRCA1/2-related ovarian cancers are of tubal origin: a hypothesis

Cited by 117 publications

References 4 publications

Clinicopathological profile of ovarian tumors in the age group 10-20 years

Clinicopathological profile of ovarian tumors in the age group 10-20 years

Divergent Roles of PAX2 in the Etiology and Progression of Ovarian Cancer

The role of reproductive hormones in epithelial ovarian carcinogenesis

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