Difference between revisions of "KRAS mutation"

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*[[Invasive ductal carcinoma of the pancreas]].
*[[Invasive ductal carcinoma of the pancreas]].
*[[Colorectal carcinoma]].<ref name=pmid19792050>{{Cite journal  | last1 = Monzon | first1 = FA. | last2 = Ogino | first2 = S. | last3 = Hammond | first3 = ME. | last4 = Halling | first4 = KC. | last5 = Bloom | first5 = KJ. | last6 = Nikiforova | first6 = MN. | title = The role of KRAS mutation testing in the management of patients with metastatic colorectal cancer. | journal = Arch Pathol Lab Med | volume = 133 | issue = 10 | pages = 1600-6 | month = Oct | year = 2009 | doi = 10.1043/1543-2165-133.10.1600 | PMID = 19792050 }}</ref>
*[[Colorectal carcinoma]].<ref name=pmid19792050>{{Cite journal  | last1 = Monzon | first1 = FA. | last2 = Ogino | first2 = S. | last3 = Hammond | first3 = ME. | last4 = Halling | first4 = KC. | last5 = Bloom | first5 = KJ. | last6 = Nikiforova | first6 = MN. | title = The role of KRAS mutation testing in the management of patients with metastatic colorectal cancer. | journal = Arch Pathol Lab Med | volume = 133 | issue = 10 | pages = 1600-6 | month = Oct | year = 2009 | doi = 10.1043/1543-2165-133.10.1600 | PMID = 19792050 }}</ref>
Not seen in the context of:
*ALK rearrangements in [[non-small cell lung cancer]].<ref name=pmid23729361>{{Cite journal  | last1 = Gainor | first1 = JF. | last2 = Varghese | first2 = AM. | last3 = Ou | first3 = SH. | last4 = Kabraji | first4 = S. | last5 = Awad | first5 = MM. | last6 = Katayama | first6 = R. | last7 = Pawlak | first7 = A. | last8 = Mino-Kenudson | first8 = M. | last9 = Yeap | first9 = BY. | title = ALK rearrangements are mutually exclusive with mutations in EGFR or KRAS: an analysis of 1,683 patients with non-small cell lung cancer. | journal = Clin Cancer Res | volume = 19 | issue = 15 | pages = 4273-81 | month = Aug | year = 2013 | doi = 10.1158/1078-0432.CCR-13-0318 | PMID = 23729361 }}</ref>


===Implication===
===Implication===

Revision as of 15:27, 6 September 2014

KRAS mutation is a re-occuring theme in molecular pathology. KRAS is an oncogene.[1]

General

Seen in:

Not seen in the context of:

Implication

In the context of colorectal carcinoma:[4][5]

  • Patient must have wild type KRAS to get drugs; KRAS mutation predicts resistance to cetuximab (Erbitux) and panitumumab (Vectibix).

Microscopic

Features:

See also

References

  1. Online 'Mendelian Inheritance in Man' (OMIM) 190070
  2. Monzon, FA.; Ogino, S.; Hammond, ME.; Halling, KC.; Bloom, KJ.; Nikiforova, MN. (Oct 2009). "The role of KRAS mutation testing in the management of patients with metastatic colorectal cancer.". Arch Pathol Lab Med 133 (10): 1600-6. doi:10.1043/1543-2165-133.10.1600. PMID 19792050.
  3. Gainor, JF.; Varghese, AM.; Ou, SH.; Kabraji, S.; Awad, MM.; Katayama, R.; Pawlak, A.; Mino-Kenudson, M. et al. (Aug 2013). "ALK rearrangements are mutually exclusive with mutations in EGFR or KRAS: an analysis of 1,683 patients with non-small cell lung cancer.". Clin Cancer Res 19 (15): 4273-81. doi:10.1158/1078-0432.CCR-13-0318. PMID 23729361.
  4. Dunn EF, Iida M, Myers RA, et al. (October 2010). "Dasatinib sensitizes KRAS mutant colorectal tumors to cetuximab". Oncogene. doi:10.1038/onc.2010.430. PMID 20956938.
  5. Di Nicolantonio F, Martini M, Molinari F, et al. (December 2008). "Wild-type BRAF is required for response to panitumumab or cetuximab in metastatic colorectal cancer". J. Clin. Oncol. 26 (35): 5705–12. doi:10.1200/JCO.2008.18.0786. PMID 19001320.