Mutations in BRAF and KRAS characterize the development of low-grade ovarian serous carcinoma.

By G. Singer, Robert J. Oldt, Y. Cohen, Brant G Wang, D. Sidransky, R. Kurman, Ie-Ming Shih. Journal of the National Cancer Institute, 2003

899 citations recorded by the source corpus.

Subfields: Cancer Research, Hepatology, Reproductive Medicine

View Paper: https://www.semanticscholar.org/paper/f44eca217b34122cdfc0396c39573dc0bc14e0e4

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
3. C. Der
4. P. Roberts

In Reproductive Medicine

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

Citations in the corpus

• BRAF mutation in thyroid cancer. (2005, background): “Among the three forms of Raf kinases, BRAF, with its gene located on chromosome 7, is the most potent activator of the MAK kinase pathway (Sithanandam et al. 1992, Mercer & Pritchard 2003).”
• Targeting the Raf-MEK-ERK mitogen-activated protein kinase cascade for the treatment of cancer (2007, background): “…in melanomas, colorectal carcinomas, papillary thyroid carcinomas, serous ovarian carcinomas and lung cancers suggests that Ras function is facilitated primarily by activation of Raf (Rajagopalan et al., 2002; Mercer and Pritchard, 2003; Singer et al., 2003; Vos et al., 2003; Sieben et al., 2004).”
• Mechanism of activation of the RAF-ERK signaling pathway by oncogenic mutations of B-RAF. (2004, background): “Surovarian (Singer et al., 2003), and papillary thyroid carci-prisingly, three mutants have reduced kinase activity nomas (Brose et al., 2002; Cohen et al., 2003), implicat-towards MEK in vitro but, by activating C-RAF in vivo, ing activating oncogenic mutations of B-RAF as critical signal to ERK…”
• Staging classification for cancer of the ovary, fallopian tube, and peritoneum (2014, background): “By contrast, LGSCs are much less common, usually contain a serous borderline component, and carry KRAS and BRAF mutations [9,10].”
• Molecular Pathogenesis and Extraovarian Origin of Epithelial Ovarian Cancer. Shifting the Paradigm (2011, positive): “For example, the MAPK signaling pathway is important for the cellular response to a variety of growth and differentiation factors and activating mutations in KRAS or one of its downstream effectors, BRAF, (mutations of KRAS and BRAF are mutually exclusive) results in constitutive activation of MAPK-”
• 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 ”
• Targeting the mitogen-activated protein kinase cascade to treat cancer (2004, neutral): “gov/cancertopics/pdq/treatment/ovarianepithelial/healthprofessional">ovarian”
• Ovarian carcinomas: five distinct diseases with different origins, genetic alterations, and clinicopathological features (2012, background): “LGSCs are associated, in most cases, with a serous borderline component, carry KRAS and BRAF mutations, and are unrelated to TP53 mutations and BRCA abnormalities [21, 22].”
• BRAF mutation is associated with DNA methylation in serrated polyps and cancers of the colorectum (2004, background): “40 Activated BRAF signals through RAS/RAF/MEK/ERK/ MAP-kinase to promote proliferation but it is also known to have an antiapoptotic role.”