Tumorigenesis: RAF/RAS oncogenes and mismatch-repair status

By H. Rajagopalan, A. Bardelli, Christoph Lengauer, Kenneth W. Kinzler, Bert Vogelstein, Victor E. Velculescu. Nature, 2002

1,331 citations recorded by the source corpus.

Subfields: Cancer Research, Oncology, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/c64cb62f0d8a42256dac1de2d820046229d23f5a

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. L. Diaz
2. Ie-Ming Shih
3. R. Kurman
4. Bert Vogelstein
5. Victor E. Velculescu
6. Michael R. Stratton
7. Kenneth W. Kinzler
8. Christopher Sander

In Oncology

1. A. Mantovani
2. A. Sica
3. P. Allavena
4. C. Garlanda
5. F. Colotta
6. Bert Vogelstein
7. Mingzhao Xing
8. Y. Nikiforov

In Pathology and Forensic Medicine

1. L. Diaz
2. Bert Vogelstein
3. Kenneth W. Kinzler
4. J. Jass
5. C. Der
6. P. Roberts
7. A. Bardelli

Citations in the corpus

• Mutant PIK3CA promotes cell growth and invasion of human cancer cells. (2005, background): “The high frequency of mutations in these hotspots is reminiscent of mutations found in oncogenes such as KRAS and BRAF (Bos et al., 1987; Davies et al., 2002; Rajagopalan et al., 2002), and is consistent with the premise that alterations in PIK3CA are activating.”
• A comprehensive survey of genomic alterations in gastric cancer reveals systematic patterns of molecular exclusivity and co-occurrence among distinct therapeutic targets (2012, methodology): “19 e 21 Additional details, including methods associated with dimension reduction permutation (DRP), fl uorescence in-situ hybridisation (FISH) assays, and functional assays, are presented in the supplementary materials (available online only).”
• BAY 43-9006 Exhibits Broad Spectrum Oral Antitumor Activity and Targets the RAF/MEK/ERK Pathway and Receptor Tyrosine Kinases Involved in Tumor Progression and Angiogenesis (2004, background): “BRAF is reportedly mutated in 70% of malignant melanomas (10), in 33% of papillary thyroid carcinomas (11), and in lower frequencies in other cancers (12).”
• Mechanism of activation of the RAF-ERK signaling pathway by oncogenic mutations of B-RAF. (2004, background): “Here of malignant melanomas and occur with moderate towe show that of 22 B-RAF mutants analyzed, 18 have high frequency in colorectal (Rajagopalan et al., 2002),elevated kinase activity and signal to ERK in vivo.”
• Colorectal carcinoma: Pathologic aspects. (2012, background): “First, activating BRAF and KRAS mutations are almost always mutually exclusive (135,136), and thus mutation testing of the BRAF gene should be considered following a negative KRAS mutation analysis.”
• BRAF mutation in thyroid cancer. (2005, background): “…and other common genetic alterations in thyroid cancer Mutual exclusivity between BRAF mutation and ras mutation was seen in several types of human cancer, including, for example, colorectal cancer (Rajagopalan et al. 2002), melanoma (Omholt et al. 2003), and ovarian cancer (Singer et al. 2003).”
• BRAF mutations and RET/PTC rearrangements are alternative events in the etiopathogenesis of PTC (2003, background): “In all, 5–10% of the colon cancers were shown to have BRAF mutation, but in the setting of the mismatch repair deficient tumors, the frequency rose to 30% of the tumors (Rajagopalan et al., 2002).”
• Mismatch repair status and BRAF mutation status in metastatic colorectal cancer patients: a pooled analysis of the CAIRO, CAIRO2, COIN and FOCUS studies (2014, neutral): “The strong inter-relationship between BRAF and dMMR is well established in early-stage colorectal cancer (14, 34); however, the etiology of both alterations still needs to be”
• 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).”
• Cancer-related inflammation, the seventh hallmark of cancer: links to genetic instability. (2009, background): “Genetic instability in cancer reflects an increased rate of DNA alterations in tumor cells, which may arise either from increased rates of damage or defective mechanisms that maintain genetic integrity within cells [100,101].”
• BRAF and RAS mutations in human lung cancer and melanoma. (2002, background): “2)]. This (2) and a subsequent report ( 3 ) provide evidence that BRAF kinase mutations are present in 10% of colon cancers overall and in 31% of mismatch repair-deficient tumors (P 106; Ref.”