Format
Sort by

Send to

Choose Destination

Links from PubMed

Items: 1 to 20 of 262

1.

Effect of KRAS oncogene substitutions on protein behavior: implications for signaling and clinical outcome.

Ihle NT, Byers LA, Kim ES, Saintigny P, Lee JJ, Blumenschein GR, Tsao A, Liu S, Larsen JE, Wang J, Diao L, Coombes KR, Chen L, Zhang S, Abdelmelek MF, Tang X, Papadimitrakopoulou V, Minna JD, Lippman SM, Hong WK, Herbst RS, Wistuba II, Heymach JV, Powis G.

J Natl Cancer Inst. 2012 Feb 8;104(3):228-39. doi: 10.1093/jnci/djr523.

2.

KRAS oncogene substitutions in Korean NSCLC patients: clinical implication and relationship with pAKT and RalGTPases expression.

Kim EY, Kim A, Kim SK, Kim HJ, Chang J, Ahn CM, Lee JS, Shim HS, Chang YS.

Lung Cancer. 2014 Aug;85(2):299-305. doi: 10.1016/j.lungcan.2014.04.012.

PMID:
24863005
3.

Oncogenic KRAS-induced epiregulin overexpression contributes to aggressive phenotype and is a promising therapeutic target in non-small-cell lung cancer.

Sunaga N, Kaira K, Imai H, Shimizu K, Nakano T, Shames DS, Girard L, Soh J, Sato M, Iwasaki Y, Ishizuka T, Gazdar AF, Minna JD, Mori M.

Oncogene. 2013 Aug 22;32(34):4034-42. doi: 10.1038/onc.2012.402.

4.

A randomized phase II study of the MEK1/MEK2 inhibitor trametinib (GSK1120212) compared with docetaxel in KRAS-mutant advanced non-small-cell lung cancer (NSCLC)†.

Blumenschein GR Jr, Smit EF, Planchard D, Kim DW, Cadranel J, De Pas T, Dunphy F, Udud K, Ahn MJ, Hanna NH, Kim JH, Mazieres J, Kim SW, Baas P, Rappold E, Redhu S, Puski A, Wu FS, Jänne PA.

Ann Oncol. 2015 May;26(5):894-901. doi: 10.1093/annonc/mdv072.

5.

LKB1 Loss induces characteristic patterns of gene expression in human tumors associated with NRF2 activation and attenuation of PI3K-AKT.

Kaufman JM, Amann JM, Park K, Arasada RR, Li H, Shyr Y, Carbone DP.

J Thorac Oncol. 2014 Jun;9(6):794-804. doi: 10.1097/JTO.0000000000000173.

6.

A gene expression signature of RAS pathway dependence predicts response to PI3K and RAS pathway inhibitors and expands the population of RAS pathway activated tumors.

Loboda A, Nebozhyn M, Klinghoffer R, Frazier J, Chastain M, Arthur W, Roberts B, Zhang T, Chenard M, Haines B, Andersen J, Nagashima K, Paweletz C, Lynch B, Feldman I, Dai H, Huang P, Watters J.

BMC Med Genomics. 2010 Jun 30;3:26. doi: 10.1186/1755-8794-3-26.

7.

Knockdown of oncogenic KRAS in non-small cell lung cancers suppresses tumor growth and sensitizes tumor cells to targeted therapy.

Sunaga N, Shames DS, Girard L, Peyton M, Larsen JE, Imai H, Soh J, Sato M, Yanagitani N, Kaira K, Xie Y, Gazdar AF, Mori M, Minna JD.

Mol Cancer Ther. 2011 Feb;10(2):336-46. doi: 10.1158/1535-7163.MCT-10-0750.

8.

Immunohistochemical Loss of LKB1 Is a Biomarker for More Aggressive Biology in KRAS-Mutant Lung Adenocarcinoma.

Calles A, Sholl LM, Rodig SJ, Pelton AK, Hornick JL, Butaney M, Lydon C, Dahlberg SE, Oxnard GR, Jackman DM, Jänne PA.

Clin Cancer Res. 2015 Jun 15;21(12):2851-60. doi: 10.1158/1078-0432.CCR-14-3112.

9.

Oncogenic KRAS-induced interleukin-8 overexpression promotes cell growth and migration and contributes to aggressive phenotypes of non-small cell lung cancer.

Sunaga N, Imai H, Shimizu K, Shames DS, Kakegawa S, Girard L, Sato M, Kaira K, Ishizuka T, Gazdar AF, Minna JD, Mori M.

Int J Cancer. 2012 Apr 15;130(8):1733-44. doi: 10.1002/ijc.26164.

10.

Contributions of KRAS and RAL in non-small-cell lung cancer growth and progression.

Guin S, Ru Y, Wynes MW, Mishra R, Lu X, Owens C, Barn AE, Vasu VT, Hirsch FR, Kern JA, Theodorescu D.

J Thorac Oncol. 2013 Dec;8(12):1492-501. doi: 10.1097/JTO.0000000000000007.

11.

KRAS mutant lung cancer cells are differentially responsive to MEK inhibitor due to AKT or STAT3 activation: implication for combinatorial approach.

Yoon YK, Kim HP, Han SW, Oh DY, Im SA, Bang YJ, Kim TY.

Mol Carcinog. 2010 Apr;49(4):353-62. doi: 10.1002/mc.20607.

PMID:
20358631
12.

Survival outcome according to KRAS mutation status in newly diagnosed patients with stage IV non-small cell lung cancer treated with platinum doublet chemotherapy.

Brady AK, McNeill JD, Judy B, Bauml J, Evans TL, Cohen RB, Langer C, Vachani A, Aggarwal C.

Oncotarget. 2015 Oct 6;6(30):30287-94. doi: 10.18632/oncotarget.4711.

13.

Targeting KRAS-mutant non-small cell lung cancer with the Hsp90 inhibitor ganetespib.

Acquaviva J, Smith DL, Sang J, Friedland JC, He S, Sequeira M, Zhang C, Wada Y, Proia DA.

Mol Cancer Ther. 2012 Dec;11(12):2633-43. doi: 10.1158/1535-7163.MCT-12-0615.

14.

microRNA classifiers are powerful diagnostic/prognostic tools in ALK-, EGFR-, and KRAS-driven lung cancers.

Gasparini P, Cascione L, Landi L, Carasi S, Lovat F, Tibaldi C, Alì G, D'Incecco A, Minuti G, Chella A, Fontanini G, Fassan M, Cappuzzo F, Croce CM.

Proc Natl Acad Sci U S A. 2015 Dec 1;112(48):14924-9. doi: 10.1073/pnas.1520329112.

15.

Sorafenib inhibits non-small cell lung cancer cell growth by targeting B-RAF in KRAS wild-type cells and C-RAF in KRAS mutant cells.

Takezawa K, Okamoto I, Yonesaka K, Hatashita E, Yamada Y, Fukuoka M, Nakagawa K.

Cancer Res. 2009 Aug 15;69(16):6515-21. doi: 10.1158/0008-5472.CAN-09-1076.

16.

Selumetinib in advanced non small cell lung cancer (NSCLC) harbouring KRAS mutation: endless clinical challenge to KRAS-mutant NSCLC.

Paolo M, Assunta S, Antonio R, Claudia SP, Anna BM, Clorinda S, Francesca C, Fortunato C, Cesare G.

Rev Recent Clin Trials. 2013 Jun;8(2):93-100. Review.

PMID:
24063423
17.

Epidermal growth factor receptor gene and protein and gefitinib sensitivity in non-small-cell lung cancer.

Cappuzzo F, Hirsch FR, Rossi E, Bartolini S, Ceresoli GL, Bemis L, Haney J, Witta S, Danenberg K, Domenichini I, Ludovini V, Magrini E, Gregorc V, Doglioni C, Sidoni A, Tonato M, Franklin WA, Crino L, Bunn PA Jr, Varella-Garcia M.

J Natl Cancer Inst. 2005 May 4;97(9):643-55.

PMID:
15870435
18.

Significance of KRAS/PAK1/Crk pathway in non-small cell lung cancer oncogenesis.

Mortazavi F, Lu J, Phan R, Lewis M, Trinidad K, Aljilani A, Pezeshkpour G, Tamanoi F.

BMC Cancer. 2015 May 9;15:381. doi: 10.1186/s12885-015-1360-4.

19.

LKB1/KRAS mutant lung cancers constitute a genetic subset of NSCLC with increased sensitivity to MAPK and mTOR signalling inhibition.

Mahoney CL, Choudhury B, Davies H, Edkins S, Greenman C, Haaften Gv, Mironenko T, Santarius T, Stevens C, Stratton MR, Futreal PA.

Br J Cancer. 2009 Jan 27;100(2):370-5. doi: 10.1038/sj.bjc.6604886.

Items per page

Supplemental Content

Support Center