Ovarian tumorigenesis: a proposed model based on morphological and molecular genetic analysis.

By Ie-Ming Shih, R. Kurman. American Journal of Pathology, 2004

1,291 citations recorded by the source corpus.

Subfields: Cancer Research, Oncology, Reproductive Medicine

View Paper: https://www.semanticscholar.org/paper/8edc8031835608c39358be54d40302a706b83f5e

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cancer Research

1. Ie-Ming Shih
2. R. Kurman

In Oncology

1. Ie-Ming Shih
2. R. Kurman
3. J. Prat

In Reproductive Medicine

1. R. Kurman
2. Ie-Ming Shih
3. J. Prat
4. E. Lengyel

Citations in the corpus

• The Origin and Pathogenesis of Epithelial Ovarian Cancer- a Proposed Unifying Theory (2010, background): “On the basis of a series of morphologic and molecular genetic studies, we have proposed a dualistic model that categorizes various types of ovarian cancer into two groups designated type I and type II.43 Type I tumors are clinically indolent and usually present at a low stage.”
• The Dualistic Model of Ovarian Carcinogenesis: Revisited, Revised, and Expanded. (2016, background): “More than a decade ago we proposed a dualistic model of epithelial ovarian carcinogenesis (type I and type II tumors) in an attempt to unravel the complex molecular genetic pathways involved in pathogenesis of primary ovarian carcinomas and to correlate these pathways with the histopathologic classi”
• Molecular Pathogenesis and Extraovarian Origin of Epithelial Ovarian Cancer. Shifting the Paradigm (2011, neutral): “After this morphologic study linking APST to MPSC and LGSC, a series of molecular genetic studies was performed, which culminated in the proposal of a dualistic model to explain the pathogenesis of EOC [21].”
• The Tubal Fimbria Is a Preferred Site for Early Adenocarcinoma in Women With Familial Ovarian Cancer Syndrome (2006, background): “Coincidentally, the pathogenesis of endometrioid and mucinous tumors typically entails a multistep process, involving precursor lesions and mutations in k-ras.(13) In contrast, serous carcinomas typically arise in the absence of a precursor and accumulate mutated p53.”
• A candidate precursor to serous carcinoma that originates in the distal fallopian tube (2007, background): “The second involves mutations in the p53 tumour suppressor gene, a rapid progression to malignancy, and characterizes serous carcinomas [3,4].”
• The MAPK pathway across different malignancies: A new perspective (2014, background): “include low-grade serous and endometrioid, clear cell, mucinous, and borderline tumors (BOTs); low-grade serous tumors have mutations in KRAS (27%-36%), BRAF (33%-50%), and PIK3CA; whereas nearly all mucinous tumors may have KRAS mutations.(41,42,97) One study reported that 57% of BOTs or low-grade ”
• MicroRNA Expression Profiles in Serous Ovarian Carcinoma (2008, background): “Frequent overexpression or amplification of ERBB2 was reported inf20% of serous ovarian cancers (2, 32).”