KRAS mutation - Revision history

Michael: /* Colorectal cancer */

2019-02-08T15:30:33Z

Colorectal cancer

← Older revision		Revision as of 15:30, 8 February 2019
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	* The vast majority of activating mutations are found in codon 12/13, 61 and 146.<ref>{{Cite journal \| last1 = Imamura \| first1 = Y. \| last2 = Lochhead \| first2 = P. \| last3 = Yamauchi \| first3 = M. \| last4 = Kuchiba \| first4 = A. \| last5 = Qian \| first5 = ZR. \| last6 = Liao \| first6 = X. \| last7 = Nishihara \| first7 = R. \| last8 = Jung \| first8 = S. \| last9 = Wu \| first9 = K. \| title = Analyses of clinicopathological, molecular, and prognostic associations of KRAS codon 61 and codon 146 mutations in colorectal cancer: cohort study and literature review. \| journal = Mol Cancer \| volume = 13 \| issue = \| pages = 135 \| month = May \| year = 2014 \| doi = 10.1186/1476-4598-13-135 \| PMID = 24885062 }}</ref>		* The vast majority of activating mutations are found in codon 12/13, 61 and 146.<ref>{{Cite journal \| last1 = Imamura \| first1 = Y. \| last2 = Lochhead \| first2 = P. \| last3 = Yamauchi \| first3 = M. \| last4 = Kuchiba \| first4 = A. \| last5 = Qian \| first5 = ZR. \| last6 = Liao \| first6 = X. \| last7 = Nishihara \| first7 = R. \| last8 = Jung \| first8 = S. \| last9 = Wu \| first9 = K. \| title = Analyses of clinicopathological, molecular, and prognostic associations of KRAS codon 61 and codon 146 mutations in colorectal cancer: cohort study and literature review. \| journal = Mol Cancer \| volume = 13 \| issue = \| pages = 135 \| month = May \| year = 2014 \| doi = 10.1186/1476-4598-13-135 \| PMID = 24885062 }}</ref>
	* KRAS mutations are usually stable between primary and metastatic tumors. <ref>{{Cite journal \| last1 = Petaccia de Macedo \| first1 = M. \| last2 = Melo \| first2 = FM. \| last3 = Ribeiro \| first3 = HSC. \| last4 = Marques \| first4 = MC. \| last5 = Kagohara \| first5 = LT. \| last6 = Begnami \| first6 = MD. \| last7 = Neto \| first7 = JC. \| last8 = Ribeiro \| first8 = JS. \| last9 = Soares \| first9 = FA. \| title = KRAS mutation status is highly homogeneous between areas of the primary tumor and the corresponding metastasis of colorectal adenocarcinomas: one less problem in patient care. \| journal = Am J Cancer Res \| volume = 7 \| issue = 9 \| pages = 1978-1989 \| month = \| year = 2017 \| doi = \| PMID = 28979819 }}</ref>		* KRAS mutations are usually stable between primary and metastatic tumors. <ref>{{Cite journal \| last1 = Petaccia de Macedo \| first1 = M. \| last2 = Melo \| first2 = FM. \| last3 = Ribeiro \| first3 = HSC. \| last4 = Marques \| first4 = MC. \| last5 = Kagohara \| first5 = LT. \| last6 = Begnami \| first6 = MD. \| last7 = Neto \| first7 = JC. \| last8 = Ribeiro \| first8 = JS. \| last9 = Soares \| first9 = FA. \| title = KRAS mutation status is highly homogeneous between areas of the primary tumor and the corresponding metastasis of colorectal adenocarcinomas: one less problem in patient care. \| journal = Am J Cancer Res \| volume = 7 \| issue = 9 \| pages = 1978-1989 \| month = \| year = 2017 \| doi = \| PMID = 28979819 }}</ref>
			* KRAS mutation predict poor response to FOLFOX treatment.<ref name=pmid25870609>{{Cite journal \| last1 = Zocche \| first1 = DM. \| last2 = Ramirez \| first2 = C. \| last3 = Fontao \| first3 = FM. \| last4 = Costa \| first4 = LD. \| last5 = Redal \| first5 = MA. \| title = Global impact of KRAS mutation patterns in FOLFOX treated metastatic colorectal cancer. \| journal = Front Genet \| volume = 6 \| issue = \| pages = 116 \| month = \| year = 2015 \| doi = 10.3389/fgene.2015.00116 \| PMID = 25870609 }}</ref>

	====Lung cancer====		====Lung cancer====
	In the context of lung cancer:<ref>{{Cite journal \| last1 = Riely \| first1 = GJ. \| last2 = Kris \| first2 = MG. \| last3 = Rosenbaum \| first3 = D. \| last4 = Marks \| first4 = J. \| last5 = Li \| first5 = A. \| last6 = Chitale \| first6 = DA. \| last7 = Nafa \| first7 = K. \| last8 = Riedel \| first8 = ER. \| last9 = Hsu \| first9 = M. \| title = Frequency and distinctive spectrum of KRAS mutations in never smokers with lung adenocarcinoma. \| journal = Clin Cancer Res \| volume = 14 \| issue = 18 \| pages = 5731-4 \| month = Sep \| year = 2008 \| doi = 10.1158/1078-0432.CCR-08-0646 \| PMID = 18794081 }}</ref>		In the context of lung cancer:<ref>{{Cite journal \| last1 = Riely \| first1 = GJ. \| last2 = Kris \| first2 = MG. \| last3 = Rosenbaum \| first3 = D. \| last4 = Marks \| first4 = J. \| last5 = Li \| first5 = A. \| last6 = Chitale \| first6 = DA. \| last7 = Nafa \| first7 = K. \| last8 = Riedel \| first8 = ER. \| last9 = Hsu \| first9 = M. \| title = Frequency and distinctive spectrum of KRAS mutations in never smokers with lung adenocarcinoma. \| journal = Clin Cancer Res \| volume = 14 \| issue = 18 \| pages = 5731-4 \| month = Sep \| year = 2008 \| doi = 10.1158/1078-0432.CCR-08-0646 \| PMID = 18794081 }}</ref>

Michael: /* Implication */

2019-02-08T15:28:26Z

Implication

← Older revision		Revision as of 15:28, 8 February 2019
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	===Implication===		===Implication===
			====Colorectal cancer====
	In the context of colorectal carcinoma:<ref name=pmid20956938>{{cite journal \|author=Dunn EF, Iida M, Myers RA, ''et al.'' \|title=Dasatinib sensitizes KRAS mutant colorectal tumors to cetuximab \|journal=Oncogene \|volume= \|issue= \|pages= \|year=2010 \|month=October \|pmid=20956938 \|doi=10.1038/onc.2010.430 \|url=}}</ref><ref name=pmid19001320>{{cite journal \|author=Di Nicolantonio F, Martini M, Molinari F, ''et al.'' \|title=Wild-type BRAF is required for response to panitumumab or cetuximab in metastatic colorectal cancer \|journal=J. Clin. Oncol. \|volume=26 \|issue=35 \|pages=5705–12 \|year=2008 \|month=December \|pmid=19001320 \|doi=10.1200/JCO.2008.18.0786 \|url=}}</ref>		In the context of colorectal carcinoma:<ref name=pmid20956938>{{cite journal \|author=Dunn EF, Iida M, Myers RA, ''et al.'' \|title=Dasatinib sensitizes KRAS mutant colorectal tumors to cetuximab \|journal=Oncogene \|volume= \|issue= \|pages= \|year=2010 \|month=October \|pmid=20956938 \|doi=10.1038/onc.2010.430 \|url=}}</ref><ref name=pmid19001320>{{cite journal \|author=Di Nicolantonio F, Martini M, Molinari F, ''et al.'' \|title=Wild-type BRAF is required for response to panitumumab or cetuximab in metastatic colorectal cancer \|journal=J. Clin. Oncol. \|volume=26 \|issue=35 \|pages=5705–12 \|year=2008 \|month=December \|pmid=19001320 \|doi=10.1200/JCO.2008.18.0786 \|url=}}</ref>
	*Patient must have ''wild type'' KRAS to get drugs; KRAS mutation predicts resistance to [[cetuximab]] (Erbitux) and [[panitumumab]] (Vectibix).		*Patient must have ''wild type'' KRAS to get drugs; KRAS mutation predicts resistance to [[cetuximab]] (Erbitux) and [[panitumumab]] (Vectibix).
	* The vast majority of activating mutations are found in codon 12/13, 61 and 146.<ref>{{Cite journal \| last1 = Imamura \| first1 = Y. \| last2 = Lochhead \| first2 = P. \| last3 = Yamauchi \| first3 = M. \| last4 = Kuchiba \| first4 = A. \| last5 = Qian \| first5 = ZR. \| last6 = Liao \| first6 = X. \| last7 = Nishihara \| first7 = R. \| last8 = Jung \| first8 = S. \| last9 = Wu \| first9 = K. \| title = Analyses of clinicopathological, molecular, and prognostic associations of KRAS codon 61 and codon 146 mutations in colorectal cancer: cohort study and literature review. \| journal = Mol Cancer \| volume = 13 \| issue = \| pages = 135 \| month = May \| year = 2014 \| doi = 10.1186/1476-4598-13-135 \| PMID = 24885062 }}</ref>		* The vast majority of activating mutations are found in codon 12/13, 61 and 146.<ref>{{Cite journal \| last1 = Imamura \| first1 = Y. \| last2 = Lochhead \| first2 = P. \| last3 = Yamauchi \| first3 = M. \| last4 = Kuchiba \| first4 = A. \| last5 = Qian \| first5 = ZR. \| last6 = Liao \| first6 = X. \| last7 = Nishihara \| first7 = R. \| last8 = Jung \| first8 = S. \| last9 = Wu \| first9 = K. \| title = Analyses of clinicopathological, molecular, and prognostic associations of KRAS codon 61 and codon 146 mutations in colorectal cancer: cohort study and literature review. \| journal = Mol Cancer \| volume = 13 \| issue = \| pages = 135 \| month = May \| year = 2014 \| doi = 10.1186/1476-4598-13-135 \| PMID = 24885062 }}</ref>
	* KRAS mutations are usually stable between primary and metastatic tumors. <ref>{{Cite journal \| last1 = Petaccia de Macedo \| first1 = M. \| last2 = Melo \| first2 = FM. \| last3 = Ribeiro \| first3 = HSC. \| last4 = Marques \| first4 = MC. \| last5 = Kagohara \| first5 = LT. \| last6 = Begnami \| first6 = MD. \| last7 = Neto \| first7 = JC. \| last8 = Ribeiro \| first8 = JS. \| last9 = Soares \| first9 = FA. \| title = KRAS mutation status is highly homogeneous between areas of the primary tumor and the corresponding metastasis of colorectal adenocarcinomas: one less problem in patient care. \| journal = Am J Cancer Res \| volume = 7 \| issue = 9 \| pages = 1978-1989 \| month = \| year = 2017 \| doi = \| PMID = 28979819 }}</ref>		* KRAS mutations are usually stable between primary and metastatic tumors. <ref>{{Cite journal \| last1 = Petaccia de Macedo \| first1 = M. \| last2 = Melo \| first2 = FM. \| last3 = Ribeiro \| first3 = HSC. \| last4 = Marques \| first4 = MC. \| last5 = Kagohara \| first5 = LT. \| last6 = Begnami \| first6 = MD. \| last7 = Neto \| first7 = JC. \| last8 = Ribeiro \| first8 = JS. \| last9 = Soares \| first9 = FA. \| title = KRAS mutation status is highly homogeneous between areas of the primary tumor and the corresponding metastasis of colorectal adenocarcinomas: one less problem in patient care. \| journal = Am J Cancer Res \| volume = 7 \| issue = 9 \| pages = 1978-1989 \| month = \| year = 2017 \| doi = \| PMID = 28979819 }}</ref>
			====Lung cancer====
	In the context of lung cancer:<ref>{{Cite journal \| last1 = Riely \| first1 = GJ. \| last2 = Kris \| first2 = MG. \| last3 = Rosenbaum \| first3 = D. \| last4 = Marks \| first4 = J. \| last5 = Li \| first5 = A. \| last6 = Chitale \| first6 = DA. \| last7 = Nafa \| first7 = K. \| last8 = Riedel \| first8 = ER. \| last9 = Hsu \| first9 = M. \| title = Frequency and distinctive spectrum of KRAS mutations in never smokers with lung adenocarcinoma. \| journal = Clin Cancer Res \| volume = 14 \| issue = 18 \| pages = 5731-4 \| month = Sep \| year = 2008 \| doi = 10.1158/1078-0432.CCR-08-0646 \| PMID = 18794081 }}</ref>		In the context of lung cancer:<ref>{{Cite journal \| last1 = Riely \| first1 = GJ. \| last2 = Kris \| first2 = MG. \| last3 = Rosenbaum \| first3 = D. \| last4 = Marks \| first4 = J. \| last5 = Li \| first5 = A. \| last6 = Chitale \| first6 = DA. \| last7 = Nafa \| first7 = K. \| last8 = Riedel \| first8 = ER. \| last9 = Hsu \| first9 = M. \| title = Frequency and distinctive spectrum of KRAS mutations in never smokers with lung adenocarcinoma. \| journal = Clin Cancer Res \| volume = 14 \| issue = 18 \| pages = 5731-4 \| month = Sep \| year = 2008 \| doi = 10.1158/1078-0432.CCR-08-0646 \| PMID = 18794081 }}</ref>
	* Mutations are rare in never-smokers.		* Mutations are rare in never-smokers.

Michael: /* See also */

2019-01-23T18:18:16Z

Michael at 16:30, 1 March 2018

2018-03-01T16:30:28Z

← Older revision		Revision as of 16:30, 1 March 2018
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	*[[Colorectal carcinoma]] (40%).<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><ref>{{Cite journal \| last1 = Imamura \| first1 = Y. \| last2 = Lochhead \| first2 = P. \| last3 = Yamauchi \| first3 = M. \| last4 = Kuchiba \| first4 = A. \| last5 = Qian \| first5 = ZR. \| last6 = Liao \| first6 = X. \| last7 = Nishihara \| first7 = R. \| last8 = Jung \| first8 = S. \| last9 = Wu \| first9 = K. \| title = Analyses of clinicopathological, molecular, and prognostic associations of KRAS codon 61 and codon 146 mutations in colorectal cancer: cohort study and literature review. \| journal = Mol Cancer \| volume = 13 \| issue = \| pages = 135 \| month = May \| year = 2014 \| doi = 10.1186/1476-4598-13-135 \| PMID = 24885062 }}</ref>		*[[Colorectal carcinoma]] (40%).<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><ref>{{Cite journal \| last1 = Imamura \| first1 = Y. \| last2 = Lochhead \| first2 = P. \| last3 = Yamauchi \| first3 = M. \| last4 = Kuchiba \| first4 = A. \| last5 = Qian \| first5 = ZR. \| last6 = Liao \| first6 = X. \| last7 = Nishihara \| first7 = R. \| last8 = Jung \| first8 = S. \| last9 = Wu \| first9 = K. \| title = Analyses of clinicopathological, molecular, and prognostic associations of KRAS codon 61 and codon 146 mutations in colorectal cancer: cohort study and literature review. \| journal = Mol Cancer \| volume = 13 \| issue = \| pages = 135 \| month = May \| year = 2014 \| doi = 10.1186/1476-4598-13-135 \| PMID = 24885062 }}</ref>
	*lung adenocarcinomas (approx 30%)<ref>{{Cite journal \| last1 = Korpanty \| first1 = GJ. \| last2 = Graham \| first2 = DM. \| last3 = Vincent \| first3 = MD. \| last4 = Leighl \| first4 = NB. \| title = Biomarkers That Currently Affect Clinical Practice in Lung Cancer: EGFR, ALK, MET, ROS-1, and KRAS. \| journal = Front Oncol \| volume = 4 \| issue = \| pages = 204 \| month = \| year = 2014 \| doi = 10.3389/fonc.2014.00204 \| PMID = 25157335 }}</ref>		*lung adenocarcinomas (approx 30%)<ref>{{Cite journal \| last1 = Korpanty \| first1 = GJ. \| last2 = Graham \| first2 = DM. \| last3 = Vincent \| first3 = MD. \| last4 = Leighl \| first4 = NB. \| title = Biomarkers That Currently Affect Clinical Practice in Lung Cancer: EGFR, ALK, MET, ROS-1, and KRAS. \| journal = Front Oncol \| volume = 4 \| issue = \| pages = 204 \| month = \| year = 2014 \| doi = 10.3389/fonc.2014.00204 \| PMID = 25157335 }}</ref>
	*~~squamous~~ NSCLC (~5%)		*Squamous NSCLC (~5%).
			*[[Mucinous ovarian tumours]].<ref name=pmid9118042>{{Cite journal \| last1 = Cuatrecasas \| first1 = M. \| last2 = Villanueva \| first2 = A. \| last3 = Matias-Guiu \| first3 = X. \| last4 = Prat \| first4 = J. \| title = K-ras mutations in mucinous ovarian tumors: a clinicopathologic and molecular study of 95 cases. \| journal = Cancer \| volume = 79 \| issue = 8 \| pages = 1581-6 \| month = Apr \| year = 1997 \| doi = \| PMID = 9118042 }}</ref>

	Not seen in the context of:		Not seen in the context of:

Jensflorian: /* Implication */

2017-10-10T15:15:29Z

Implication

← Older revision		Revision as of 15:15, 10 October 2017
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	In the context of lung cancer:<ref>{{Cite journal \| last1 = Riely \| first1 = GJ. \| last2 = Kris \| first2 = MG. \| last3 = Rosenbaum \| first3 = D. \| last4 = Marks \| first4 = J. \| last5 = Li \| first5 = A. \| last6 = Chitale \| first6 = DA. \| last7 = Nafa \| first7 = K. \| last8 = Riedel \| first8 = ER. \| last9 = Hsu \| first9 = M. \| title = Frequency and distinctive spectrum of KRAS mutations in never smokers with lung adenocarcinoma. \| journal = Clin Cancer Res \| volume = 14 \| issue = 18 \| pages = 5731-4 \| month = Sep \| year = 2008 \| doi = 10.1158/1078-0432.CCR-08-0646 \| PMID = 18794081 }}</ref>		In the context of lung cancer:<ref>{{Cite journal \| last1 = Riely \| first1 = GJ. \| last2 = Kris \| first2 = MG. \| last3 = Rosenbaum \| first3 = D. \| last4 = Marks \| first4 = J. \| last5 = Li \| first5 = A. \| last6 = Chitale \| first6 = DA. \| last7 = Nafa \| first7 = K. \| last8 = Riedel \| first8 = ER. \| last9 = Hsu \| first9 = M. \| title = Frequency and distinctive spectrum of KRAS mutations in never smokers with lung adenocarcinoma. \| journal = Clin Cancer Res \| volume = 14 \| issue = 18 \| pages = 5731-4 \| month = Sep \| year = 2008 \| doi = 10.1158/1078-0432.CCR-08-0646 \| PMID = 18794081 }}</ref>
	* Mutations are rare in never-smokers.		* Mutations are rare in never-smokers.
			* KRAS G12C is the most common G > T transversion mutation in smokers.<ref>{{Cite journal \| last1 = Dogan \| first1 = S. \| last2 = Shen \| first2 = R. \| last3 = Ang \| first3 = DC. \| last4 = Johnson \| first4 = ML. \| last5 = D'Angelo \| first5 = SP. \| last6 = Paik \| first6 = PK. \| last7 = Brzostowski \| first7 = EB. \| last8 = Riely \| first8 = GJ. \| last9 = Kris \| first9 = MG. \| title = Molecular epidemiology of EGFR and KRAS mutations in 3,026 lung adenocarcinomas: higher susceptibility of women to smoking-related KRAS-mutant cancers. \| journal = Clin Cancer Res \| volume = 18 \| issue = 22 \| pages = 6169-77 \| month = Nov \| year = 2012 \| doi = 10.1158/1078-0432.CCR-11-3265 \| PMID = 23014527 }}</ref>
	* Biomarker for MEK inhibitors selumetinib and trametinib.		* Biomarker for MEK inhibitors selumetinib and trametinib.

Jensflorian: CRC update

2017-10-10T14:57:22Z

CRC update

← Older revision		Revision as of 14:57, 10 October 2017
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	Seen in:		Seen in:
	*[[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]] (40%).<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><ref>{{Cite journal \| last1 = Imamura \| first1 = Y. \| last2 = Lochhead \| first2 = P. \| last3 = Yamauchi \| first3 = M. \| last4 = Kuchiba \| first4 = A. \| last5 = Qian \| first5 = ZR. \| last6 = Liao \| first6 = X. \| last7 = Nishihara \| first7 = R. \| last8 = Jung \| first8 = S. \| last9 = Wu \| first9 = K. \| title = Analyses of clinicopathological, molecular, and prognostic associations of KRAS codon 61 and codon 146 mutations in colorectal cancer: cohort study and literature review. \| journal = Mol Cancer \| volume = 13 \| issue = \| pages = 135 \| month = May \| year = 2014 \| doi = 10.1186/1476-4598-13-135 \| PMID = 24885062 }}</ref>
	*lung adenocarcinomas (approx 30%)<ref>{{Cite journal \| last1 = Korpanty \| first1 = GJ. \| last2 = Graham \| first2 = DM. \| last3 = Vincent \| first3 = MD. \| last4 = Leighl \| first4 = NB. \| title = Biomarkers That Currently Affect Clinical Practice in Lung Cancer: EGFR, ALK, MET, ROS-1, and KRAS. \| journal = Front Oncol \| volume = 4 \| issue = \| pages = 204 \| month = \| year = 2014 \| doi = 10.3389/fonc.2014.00204 \| PMID = 25157335 }}</ref>		*lung adenocarcinomas (approx 30%)<ref>{{Cite journal \| last1 = Korpanty \| first1 = GJ. \| last2 = Graham \| first2 = DM. \| last3 = Vincent \| first3 = MD. \| last4 = Leighl \| first4 = NB. \| title = Biomarkers That Currently Affect Clinical Practice in Lung Cancer: EGFR, ALK, MET, ROS-1, and KRAS. \| journal = Front Oncol \| volume = 4 \| issue = \| pages = 204 \| month = \| year = 2014 \| doi = 10.3389/fonc.2014.00204 \| PMID = 25157335 }}</ref>
	*squamous NSCLC (~5%)		*squamous NSCLC (~5%)
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	In the context of colorectal carcinoma:<ref name=pmid20956938>{{cite journal \|author=Dunn EF, Iida M, Myers RA, ''et al.'' \|title=Dasatinib sensitizes KRAS mutant colorectal tumors to cetuximab \|journal=Oncogene \|volume= \|issue= \|pages= \|year=2010 \|month=October \|pmid=20956938 \|doi=10.1038/onc.2010.430 \|url=}}</ref><ref name=pmid19001320>{{cite journal \|author=Di Nicolantonio F, Martini M, Molinari F, ''et al.'' \|title=Wild-type BRAF is required for response to panitumumab or cetuximab in metastatic colorectal cancer \|journal=J. Clin. Oncol. \|volume=26 \|issue=35 \|pages=5705–12 \|year=2008 \|month=December \|pmid=19001320 \|doi=10.1200/JCO.2008.18.0786 \|url=}}</ref>		In the context of colorectal carcinoma:<ref name=pmid20956938>{{cite journal \|author=Dunn EF, Iida M, Myers RA, ''et al.'' \|title=Dasatinib sensitizes KRAS mutant colorectal tumors to cetuximab \|journal=Oncogene \|volume= \|issue= \|pages= \|year=2010 \|month=October \|pmid=20956938 \|doi=10.1038/onc.2010.430 \|url=}}</ref><ref name=pmid19001320>{{cite journal \|author=Di Nicolantonio F, Martini M, Molinari F, ''et al.'' \|title=Wild-type BRAF is required for response to panitumumab or cetuximab in metastatic colorectal cancer \|journal=J. Clin. Oncol. \|volume=26 \|issue=35 \|pages=5705–12 \|year=2008 \|month=December \|pmid=19001320 \|doi=10.1200/JCO.2008.18.0786 \|url=}}</ref>
	*Patient must have ''wild type'' KRAS to get drugs; KRAS mutation predicts resistance to [[cetuximab]] (Erbitux) and [[panitumumab]] (Vectibix).		*Patient must have ''wild type'' KRAS to get drugs; KRAS mutation predicts resistance to [[cetuximab]] (Erbitux) and [[panitumumab]] (Vectibix).
			* The vast majority of activating mutations are found in codon 12/13, 61 and 146.<ref>{{Cite journal \| last1 = Imamura \| first1 = Y. \| last2 = Lochhead \| first2 = P. \| last3 = Yamauchi \| first3 = M. \| last4 = Kuchiba \| first4 = A. \| last5 = Qian \| first5 = ZR. \| last6 = Liao \| first6 = X. \| last7 = Nishihara \| first7 = R. \| last8 = Jung \| first8 = S. \| last9 = Wu \| first9 = K. \| title = Analyses of clinicopathological, molecular, and prognostic associations of KRAS codon 61 and codon 146 mutations in colorectal cancer: cohort study and literature review. \| journal = Mol Cancer \| volume = 13 \| issue = \| pages = 135 \| month = May \| year = 2014 \| doi = 10.1186/1476-4598-13-135 \| PMID = 24885062 }}</ref>
	* KRAS mutations are usually stable between primary and metastatic tumors. <ref>{{Cite journal \| last1 = Petaccia de Macedo \| first1 = M. \| last2 = Melo \| first2 = FM. \| last3 = Ribeiro \| first3 = HSC. \| last4 = Marques \| first4 = MC. \| last5 = Kagohara \| first5 = LT. \| last6 = Begnami \| first6 = MD. \| last7 = Neto \| first7 = JC. \| last8 = Ribeiro \| first8 = JS. \| last9 = Soares \| first9 = FA. \| title = KRAS mutation status is highly homogeneous between areas of the primary tumor and the corresponding metastasis of colorectal adenocarcinomas: one less problem in patient care. \| journal = Am J Cancer Res \| volume = 7 \| issue = 9 \| pages = 1978-1989 \| month = \| year = 2017 \| doi = \| PMID = 28979819 }}</ref>		* KRAS mutations are usually stable between primary and metastatic tumors. <ref>{{Cite journal \| last1 = Petaccia de Macedo \| first1 = M. \| last2 = Melo \| first2 = FM. \| last3 = Ribeiro \| first3 = HSC. \| last4 = Marques \| first4 = MC. \| last5 = Kagohara \| first5 = LT. \| last6 = Begnami \| first6 = MD. \| last7 = Neto \| first7 = JC. \| last8 = Ribeiro \| first8 = JS. \| last9 = Soares \| first9 = FA. \| title = KRAS mutation status is highly homogeneous between areas of the primary tumor and the corresponding metastasis of colorectal adenocarcinomas: one less problem in patient care. \| journal = Am J Cancer Res \| volume = 7 \| issue = 9 \| pages = 1978-1989 \| month = \| year = 2017 \| doi = \| PMID = 28979819 }}</ref>
	In the context of lung cancer:<ref>{{Cite journal \| last1 = Riely \| first1 = GJ. \| last2 = Kris \| first2 = MG. \| last3 = Rosenbaum \| first3 = D. \| last4 = Marks \| first4 = J. \| last5 = Li \| first5 = A. \| last6 = Chitale \| first6 = DA. \| last7 = Nafa \| first7 = K. \| last8 = Riedel \| first8 = ER. \| last9 = Hsu \| first9 = M. \| title = Frequency and distinctive spectrum of KRAS mutations in never smokers with lung adenocarcinoma. \| journal = Clin Cancer Res \| volume = 14 \| issue = 18 \| pages = 5731-4 \| month = Sep \| year = 2008 \| doi = 10.1158/1078-0432.CCR-08-0646 \| PMID = 18794081 }}</ref>		In the context of lung cancer:<ref>{{Cite journal \| last1 = Riely \| first1 = GJ. \| last2 = Kris \| first2 = MG. \| last3 = Rosenbaum \| first3 = D. \| last4 = Marks \| first4 = J. \| last5 = Li \| first5 = A. \| last6 = Chitale \| first6 = DA. \| last7 = Nafa \| first7 = K. \| last8 = Riedel \| first8 = ER. \| last9 = Hsu \| first9 = M. \| title = Frequency and distinctive spectrum of KRAS mutations in never smokers with lung adenocarcinoma. \| journal = Clin Cancer Res \| volume = 14 \| issue = 18 \| pages = 5731-4 \| month = Sep \| year = 2008 \| doi = 10.1158/1078-0432.CCR-08-0646 \| PMID = 18794081 }}</ref>

Jensflorian: /* Implication */ heterogeneity

2017-10-10T13:08:59Z

Implication: heterogeneity

← Older revision		Revision as of 13:08, 10 October 2017
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	In the context of colorectal carcinoma:<ref name=pmid20956938>{{cite journal \|author=Dunn EF, Iida M, Myers RA, ''et al.'' \|title=Dasatinib sensitizes KRAS mutant colorectal tumors to cetuximab \|journal=Oncogene \|volume= \|issue= \|pages= \|year=2010 \|month=October \|pmid=20956938 \|doi=10.1038/onc.2010.430 \|url=}}</ref><ref name=pmid19001320>{{cite journal \|author=Di Nicolantonio F, Martini M, Molinari F, ''et al.'' \|title=Wild-type BRAF is required for response to panitumumab or cetuximab in metastatic colorectal cancer \|journal=J. Clin. Oncol. \|volume=26 \|issue=35 \|pages=5705–12 \|year=2008 \|month=December \|pmid=19001320 \|doi=10.1200/JCO.2008.18.0786 \|url=}}</ref>		In the context of colorectal carcinoma:<ref name=pmid20956938>{{cite journal \|author=Dunn EF, Iida M, Myers RA, ''et al.'' \|title=Dasatinib sensitizes KRAS mutant colorectal tumors to cetuximab \|journal=Oncogene \|volume= \|issue= \|pages= \|year=2010 \|month=October \|pmid=20956938 \|doi=10.1038/onc.2010.430 \|url=}}</ref><ref name=pmid19001320>{{cite journal \|author=Di Nicolantonio F, Martini M, Molinari F, ''et al.'' \|title=Wild-type BRAF is required for response to panitumumab or cetuximab in metastatic colorectal cancer \|journal=J. Clin. Oncol. \|volume=26 \|issue=35 \|pages=5705–12 \|year=2008 \|month=December \|pmid=19001320 \|doi=10.1200/JCO.2008.18.0786 \|url=}}</ref>
	*Patient must have ''wild type'' KRAS to get drugs; KRAS mutation predicts resistance to [[cetuximab]] (Erbitux) and [[panitumumab]] (Vectibix).		*Patient must have ''wild type'' KRAS to get drugs; KRAS mutation predicts resistance to [[cetuximab]] (Erbitux) and [[panitumumab]] (Vectibix).
			* KRAS mutations are usually stable between primary and metastatic tumors. <ref>{{Cite journal \| last1 = Petaccia de Macedo \| first1 = M. \| last2 = Melo \| first2 = FM. \| last3 = Ribeiro \| first3 = HSC. \| last4 = Marques \| first4 = MC. \| last5 = Kagohara \| first5 = LT. \| last6 = Begnami \| first6 = MD. \| last7 = Neto \| first7 = JC. \| last8 = Ribeiro \| first8 = JS. \| last9 = Soares \| first9 = FA. \| title = KRAS mutation status is highly homogeneous between areas of the primary tumor and the corresponding metastasis of colorectal adenocarcinomas: one less problem in patient care. \| journal = Am J Cancer Res \| volume = 7 \| issue = 9 \| pages = 1978-1989 \| month = \| year = 2017 \| doi = \| PMID = 28979819 }}</ref>
	In the context of lung cancer:<ref>{{Cite journal \| last1 = Riely \| first1 = GJ. \| last2 = Kris \| first2 = MG. \| last3 = Rosenbaum \| first3 = D. \| last4 = Marks \| first4 = J. \| last5 = Li \| first5 = A. \| last6 = Chitale \| first6 = DA. \| last7 = Nafa \| first7 = K. \| last8 = Riedel \| first8 = ER. \| last9 = Hsu \| first9 = M. \| title = Frequency and distinctive spectrum of KRAS mutations in never smokers with lung adenocarcinoma. \| journal = Clin Cancer Res \| volume = 14 \| issue = 18 \| pages = 5731-4 \| month = Sep \| year = 2008 \| doi = 10.1158/1078-0432.CCR-08-0646 \| PMID = 18794081 }}</ref>		In the context of lung cancer:<ref>{{Cite journal \| last1 = Riely \| first1 = GJ. \| last2 = Kris \| first2 = MG. \| last3 = Rosenbaum \| first3 = D. \| last4 = Marks \| first4 = J. \| last5 = Li \| first5 = A. \| last6 = Chitale \| first6 = DA. \| last7 = Nafa \| first7 = K. \| last8 = Riedel \| first8 = ER. \| last9 = Hsu \| first9 = M. \| title = Frequency and distinctive spectrum of KRAS mutations in never smokers with lung adenocarcinoma. \| journal = Clin Cancer Res \| volume = 14 \| issue = 18 \| pages = 5731-4 \| month = Sep \| year = 2008 \| doi = 10.1158/1078-0432.CCR-08-0646 \| PMID = 18794081 }}</ref>
	* Mutations are rare in never-smokers.		* Mutations are rare in never-smokers.

Jensflorian: /* General */ update on lung cancer

2017-08-31T10:14:03Z

General: update on lung cancer

← Older revision		Revision as of 10:14, 31 August 2017
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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>
			*lung adenocarcinomas (approx 30%)<ref>{{Cite journal \| last1 = Korpanty \| first1 = GJ. \| last2 = Graham \| first2 = DM. \| last3 = Vincent \| first3 = MD. \| last4 = Leighl \| first4 = NB. \| title = Biomarkers That Currently Affect Clinical Practice in Lung Cancer: EGFR, ALK, MET, ROS-1, and KRAS. \| journal = Front Oncol \| volume = 4 \| issue = \| pages = 204 \| month = \| year = 2014 \| doi = 10.3389/fonc.2014.00204 \| PMID = 25157335 }}</ref>
			*squamous NSCLC (~5%)

	Not seen in the context of:		Not seen in the context of:
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	In the context of colorectal carcinoma:<ref name=pmid20956938>{{cite journal \|author=Dunn EF, Iida M, Myers RA, ''et al.'' \|title=Dasatinib sensitizes KRAS mutant colorectal tumors to cetuximab \|journal=Oncogene \|volume= \|issue= \|pages= \|year=2010 \|month=October \|pmid=20956938 \|doi=10.1038/onc.2010.430 \|url=}}</ref><ref name=pmid19001320>{{cite journal \|author=Di Nicolantonio F, Martini M, Molinari F, ''et al.'' \|title=Wild-type BRAF is required for response to panitumumab or cetuximab in metastatic colorectal cancer \|journal=J. Clin. Oncol. \|volume=26 \|issue=35 \|pages=5705–12 \|year=2008 \|month=December \|pmid=19001320 \|doi=10.1200/JCO.2008.18.0786 \|url=}}</ref>		In the context of colorectal carcinoma:<ref name=pmid20956938>{{cite journal \|author=Dunn EF, Iida M, Myers RA, ''et al.'' \|title=Dasatinib sensitizes KRAS mutant colorectal tumors to cetuximab \|journal=Oncogene \|volume= \|issue= \|pages= \|year=2010 \|month=October \|pmid=20956938 \|doi=10.1038/onc.2010.430 \|url=}}</ref><ref name=pmid19001320>{{cite journal \|author=Di Nicolantonio F, Martini M, Molinari F, ''et al.'' \|title=Wild-type BRAF is required for response to panitumumab or cetuximab in metastatic colorectal cancer \|journal=J. Clin. Oncol. \|volume=26 \|issue=35 \|pages=5705–12 \|year=2008 \|month=December \|pmid=19001320 \|doi=10.1200/JCO.2008.18.0786 \|url=}}</ref>
	*Patient must have ''wild type'' KRAS to get drugs; KRAS mutation predicts resistance to [[cetuximab]] (Erbitux) and [[panitumumab]] (Vectibix).		*Patient must have ''wild type'' KRAS to get drugs; KRAS mutation predicts resistance to [[cetuximab]] (Erbitux) and [[panitumumab]] (Vectibix).
			In the context of lung cancer:<ref>{{Cite journal \| last1 = Riely \| first1 = GJ. \| last2 = Kris \| first2 = MG. \| last3 = Rosenbaum \| first3 = D. \| last4 = Marks \| first4 = J. \| last5 = Li \| first5 = A. \| last6 = Chitale \| first6 = DA. \| last7 = Nafa \| first7 = K. \| last8 = Riedel \| first8 = ER. \| last9 = Hsu \| first9 = M. \| title = Frequency and distinctive spectrum of KRAS mutations in never smokers with lung adenocarcinoma. \| journal = Clin Cancer Res \| volume = 14 \| issue = 18 \| pages = 5731-4 \| month = Sep \| year = 2008 \| doi = 10.1158/1078-0432.CCR-08-0646 \| PMID = 18794081 }}</ref>
			* Mutations are rare in never-smokers.
			* Biomarker for MEK inhibitors selumetinib and trametinib.

	==Gross==		==Gross==

Abraham: /* General */

2017-08-28T23:31:25Z

General

← Older revision		Revision as of 23:31, 28 August 2017
Line 3:		Line 3:
	==General==		==General==
	Kirsten RAS (KRAS) is a member of the Ras gene familiy, which encodes small G proteins with intrinsic GTPase activity.		Kirsten RAS (KRAS) is a member of the Ras gene familiy, which encodes small G proteins with intrinsic GTPase activity.

	Seen in:		Seen in:
	*[[Invasive ductal carcinoma of the pancreas]].		*[[Invasive ductal carcinoma of the pancreas]].

Abraham: /* General */

2017-08-28T22:48:09Z

General

← Older revision		Revision as of 22:48, 28 August 2017
Line 2:		Line 2:

	==General==		==General==
			Kirsten RAS (KRAS) is a member of the Ras gene familiy, which encodes small G proteins with intrinsic GTPase activity.
	Seen in:		Seen in:
	*[[Invasive ductal carcinoma of the pancreas]].		*[[Invasive ductal carcinoma of the pancreas]].

← Older revision		Revision as of 15:30, 8 February 2019
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	* The vast majority of activating mutations are found in codon 12/13, 61 and 146.<ref>{{Cite journal \| last1 = Imamura \| first1 = Y. \| last2 = Lochhead \| first2 = P. \| last3 = Yamauchi \| first3 = M. \| last4 = Kuchiba \| first4 = A. \| last5 = Qian \| first5 = ZR. \| last6 = Liao \| first6 = X. \| last7 = Nishihara \| first7 = R. \| last8 = Jung \| first8 = S. \| last9 = Wu \| first9 = K. \| title = Analyses of clinicopathological, molecular, and prognostic associations of KRAS codon 61 and codon 146 mutations in colorectal cancer: cohort study and literature review. \| journal = Mol Cancer \| volume = 13 \| issue = \| pages = 135 \| month = May \| year = 2014 \| doi = 10.1186/1476-4598-13-135 \| PMID = 24885062 }}</ref>		* The vast majority of activating mutations are found in codon 12/13, 61 and 146.<ref>{{Cite journal \| last1 = Imamura \| first1 = Y. \| last2 = Lochhead \| first2 = P. \| last3 = Yamauchi \| first3 = M. \| last4 = Kuchiba \| first4 = A. \| last5 = Qian \| first5 = ZR. \| last6 = Liao \| first6 = X. \| last7 = Nishihara \| first7 = R. \| last8 = Jung \| first8 = S. \| last9 = Wu \| first9 = K. \| title = Analyses of clinicopathological, molecular, and prognostic associations of KRAS codon 61 and codon 146 mutations in colorectal cancer: cohort study and literature review. \| journal = Mol Cancer \| volume = 13 \| issue = \| pages = 135 \| month = May \| year = 2014 \| doi = 10.1186/1476-4598-13-135 \| PMID = 24885062 }}</ref>
	* KRAS mutations are usually stable between primary and metastatic tumors. <ref>{{Cite journal \| last1 = Petaccia de Macedo \| first1 = M. \| last2 = Melo \| first2 = FM. \| last3 = Ribeiro \| first3 = HSC. \| last4 = Marques \| first4 = MC. \| last5 = Kagohara \| first5 = LT. \| last6 = Begnami \| first6 = MD. \| last7 = Neto \| first7 = JC. \| last8 = Ribeiro \| first8 = JS. \| last9 = Soares \| first9 = FA. \| title = KRAS mutation status is highly homogeneous between areas of the primary tumor and the corresponding metastasis of colorectal adenocarcinomas: one less problem in patient care. \| journal = Am J Cancer Res \| volume = 7 \| issue = 9 \| pages = 1978-1989 \| month = \| year = 2017 \| doi = \| PMID = 28979819 }}</ref>		* KRAS mutations are usually stable between primary and metastatic tumors. <ref>{{Cite journal \| last1 = Petaccia de Macedo \| first1 = M. \| last2 = Melo \| first2 = FM. \| last3 = Ribeiro \| first3 = HSC. \| last4 = Marques \| first4 = MC. \| last5 = Kagohara \| first5 = LT. \| last6 = Begnami \| first6 = MD. \| last7 = Neto \| first7 = JC. \| last8 = Ribeiro \| first8 = JS. \| last9 = Soares \| first9 = FA. \| title = KRAS mutation status is highly homogeneous between areas of the primary tumor and the corresponding metastasis of colorectal adenocarcinomas: one less problem in patient care. \| journal = Am J Cancer Res \| volume = 7 \| issue = 9 \| pages = 1978-1989 \| month = \| year = 2017 \| doi = \| PMID = 28979819 }}</ref>
			* KRAS mutation predict poor response to FOLFOX treatment.<ref name=pmid25870609>{{Cite journal \| last1 = Zocche \| first1 = DM. \| last2 = Ramirez \| first2 = C. \| last3 = Fontao \| first3 = FM. \| last4 = Costa \| first4 = LD. \| last5 = Redal \| first5 = MA. \| title = Global impact of KRAS mutation patterns in FOLFOX treated metastatic colorectal cancer. \| journal = Front Genet \| volume = 6 \| issue = \| pages = 116 \| month = \| year = 2015 \| doi = 10.3389/fgene.2015.00116 \| PMID = 25870609 }}</ref>

	====Lung cancer====		====Lung cancer====
	In the context of lung cancer:<ref>{{Cite journal \| last1 = Riely \| first1 = GJ. \| last2 = Kris \| first2 = MG. \| last3 = Rosenbaum \| first3 = D. \| last4 = Marks \| first4 = J. \| last5 = Li \| first5 = A. \| last6 = Chitale \| first6 = DA. \| last7 = Nafa \| first7 = K. \| last8 = Riedel \| first8 = ER. \| last9 = Hsu \| first9 = M. \| title = Frequency and distinctive spectrum of KRAS mutations in never smokers with lung adenocarcinoma. \| journal = Clin Cancer Res \| volume = 14 \| issue = 18 \| pages = 5731-4 \| month = Sep \| year = 2008 \| doi = 10.1158/1078-0432.CCR-08-0646 \| PMID = 18794081 }}</ref>		In the context of lung cancer:<ref>{{Cite journal \| last1 = Riely \| first1 = GJ. \| last2 = Kris \| first2 = MG. \| last3 = Rosenbaum \| first3 = D. \| last4 = Marks \| first4 = J. \| last5 = Li \| first5 = A. \| last6 = Chitale \| first6 = DA. \| last7 = Nafa \| first7 = K. \| last8 = Riedel \| first8 = ER. \| last9 = Hsu \| first9 = M. \| title = Frequency and distinctive spectrum of KRAS mutations in never smokers with lung adenocarcinoma. \| journal = Clin Cancer Res \| volume = 14 \| issue = 18 \| pages = 5731-4 \| month = Sep \| year = 2008 \| doi = 10.1158/1078-0432.CCR-08-0646 \| PMID = 18794081 }}</ref>

← Older revision		Revision as of 18:18, 23 January 2019
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	*[[Molecular pathology]].		*[[Molecular pathology]].
	*[[Oncogene]].		*[[Oncogene]].
			*[[BRAF mutation]].

	==References==		==References==