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Items: 7

1.

Particular aspects in the cytogenetics and molecular biology of salivary gland tumours - current review of reports.

Ochal-Choińska AJ, Osuch-Wójcikiewicz E.

Contemp Oncol (Pozn). 2016;20(4):281-6. doi: 10.5114/wo.2016.61847. Epub 2016 Sep 5. Review.

2.

Differential in vivo tumorigenicity of diverse KRAS mutations in vertebrate pancreas: A comprehensive survey.

Park JT, Johnson N, Liu S, Levesque M, Wang YJ, Ho H, Huso D, Maitra A, Parsons MJ, Prescott JD, Leach SD.

Oncogene. 2015 May 21;34(21):2801-6. doi: 10.1038/onc.2014.223. Epub 2014 Jul 28.

3.

HRAS mutations in epithelial-myoepithelial carcinoma.

Chiosea SI, Miller M, Seethala RR.

Head Neck Pathol. 2014 Jun;8(2):146-50. doi: 10.1007/s12105-013-0506-4. Epub 2013 Nov 26.

4.

Functional specificity of ras isoforms: so similar but so different.

Castellano E, Santos E.

Genes Cancer. 2011 Mar;2(3):216-31. doi: 10.1177/1947601911408081.

5.

Overexpression of sphingosine kinase 1 is associated with salivary gland carcinoma progression and might be a novel predictive marker for adjuvant therapy.

Liu G, Zheng H, Zhang Z, Wu Z, Xiong H, Li J, Song L.

BMC Cancer. 2010 Sep 16;10:495. doi: 10.1186/1471-2407-10-495.

6.

Activation of the EGFR/ERK pathway in high-grade mucoepidermoid carcinomas of the salivary glands.

Lujan B, Hakim S, Moyano S, Nadal A, Caballero M, Diaz A, Valera A, Carrera M, Cardesa A, Alos L.

Br J Cancer. 2010 Aug 10;103(4):510-6. doi: 10.1038/sj.bjc.6605788. Epub 2010 Jul 27.

7.

Activated Kras, but not Hras or Nras, may initiate tumors of endodermal origin via stem cell expansion.

Quinlan MP, Quatela SE, Philips MR, Settleman J.

Mol Cell Biol. 2008 Apr;28(8):2659-74. doi: 10.1128/MCB.01661-07. Epub 2008 Feb 11.

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