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Results: 1 to 20 of 98

Similar articles for PubMed (Select 19878864)

1.

It's a free for all--insulin-positive cells join the group of potential progenitors for pancreatic ductal adenocarcinoma.

Morris JP 4th, Hebrok M.

Cancer Cell. 2009 Nov 6;16(5):359-61. doi: 10.1016/j.ccr.2009.10.006.

2.

B7-H4 expression in normal and diseased human islet β cells.

Cheung SS, Ou D, Metzger DL, Meloche M, Ao Z, Ng SS, Owen D, Warnock GL.

Pancreas. 2014 Jan;43(1):128-34. doi: 10.1097/MPA.0b013e31829695d2.

PMID:
24326367
3.

The conditional expression of KRAS G12D in mouse pancreas induces disorganization of endocrine islets prior the onset of ductal pre-cancerous lesions.

Gout J, Pommier RM, Vincent DF, Ripoche D, Goddard-Léon S, Colombe A, Treilleux I, Valcourt U, Tomasini R, Dufresne M, Bertolino P, Bartholin L.

Pancreatology. 2013 May-Jun;13(3):191-5. doi: 10.1016/j.pan.2013.02.001. Epub 2013 Feb 18.

PMID:
23719586
4.

Identification of Sox9-dependent acinar-to-ductal reprogramming as the principal mechanism for initiation of pancreatic ductal adenocarcinoma.

Kopp JL, von Figura G, Mayes E, Liu FF, Dubois CL, Morris JP 4th, Pan FC, Akiyama H, Wright CV, Jensen K, Hebrok M, Sander M.

Cancer Cell. 2012 Dec 11;22(6):737-50. doi: 10.1016/j.ccr.2012.10.025. Epub 2012 Nov 29.

5.

Context-dependent transformation of adult pancreatic cells by oncogenic K-Ras.

Gidekel Friedlander SY, Chu GC, Snyder EL, Girnius N, Dibelius G, Crowley D, Vasile E, DePinho RA, Jacks T.

Cancer Cell. 2009 Nov 6;16(5):379-89. doi: 10.1016/j.ccr.2009.09.027.

6.

Origin of pancreatic ductal adenocarcinoma from atypical flat lesions: a comparative study in transgenic mice and human tissues.

Aichler M, Seiler C, Tost M, Siveke J, Mazur PK, Da Silva-Buttkus P, Bartsch DK, Langer P, Chiblak S, Dürr A, Höfler H, Klöppel G, Müller-Decker K, Brielmeier M, Esposito I.

J Pathol. 2012 Apr;226(5):723-34. doi: 10.1002/path.3017. Epub 2012 Jan 17.

PMID:
21984419
7.

Ras activity levels control the development of pancreatic diseases.

Ji B, Tsou L, Wang H, Gaiser S, Chang DZ, Daniluk J, Bi Y, Grote T, Longnecker DS, Logsdon CD.

Gastroenterology. 2009 Sep;137(3):1072-82, 1082.e1-6. doi: 10.1053/j.gastro.2009.05.052. Epub 2009 Jun 6. Erratum in: Gastroenterology. 2011 May;140(5):1696.

8.

Early requirement of Rac1 in a mouse model of pancreatic cancer.

Heid I, Lubeseder-Martellato C, Sipos B, Mazur PK, Lesina M, Schmid RM, Siveke JT.

Gastroenterology. 2011 Aug;141(2):719-30, 730.e1-7. doi: 10.1053/j.gastro.2011.04.043. Epub 2011 Apr 28.

PMID:
21684285
9.

Ribonucleoprotein HNRNPA2B1 interacts with and regulates oncogenic KRAS in pancreatic ductal adenocarcinoma cells.

Barceló C, Etchin J, Mansour MR, Sanda T, Ginesta MM, Sanchez-Arévalo Lobo VJ, Real FX, Capellà G, Estanyol JM, Jaumot M, Look AT, Agell N.

Gastroenterology. 2014 Oct;147(4):882-892.e8. doi: 10.1053/j.gastro.2014.06.041. Epub 2014 Jul 3.

PMID:
24998203
10.

EGF receptor is required for KRAS-induced pancreatic tumorigenesis.

Ardito CM, Grüner BM, Takeuchi KK, Lubeseder-Martellato C, Teichmann N, Mazur PK, Delgiorno KE, Carpenter ES, Halbrook CJ, Hall JC, Pal D, Briel T, Herner A, Trajkovic-Arsic M, Sipos B, Liou GY, Storz P, Murray NR, Threadgill DW, Sibilia M, Washington MK, Wilson CL, Schmid RM, Raines EW, Crawford HC, Siveke JT.

Cancer Cell. 2012 Sep 11;22(3):304-17. doi: 10.1016/j.ccr.2012.07.024.

11.

Downstream of mutant KRAS, the transcription regulator YAP is essential for neoplastic progression to pancreatic ductal adenocarcinoma.

Zhang W, Nandakumar N, Shi Y, Manzano M, Smith A, Graham G, Gupta S, Vietsch EE, Laughlin SZ, Wadhwa M, Chetram M, Joshi M, Wang F, Kallakury B, Toretsky J, Wellstein A, Yi C.

Sci Signal. 2014 May 6;7(324):ra42. doi: 10.1126/scisignal.2005049.

12.

Mist1-KrasG12D knock-in mice develop mixed differentiation metastatic exocrine pancreatic carcinoma and hepatocellular carcinoma.

Tuveson DA, Zhu L, Gopinathan A, Willis NA, Kachatrian L, Grochow R, Pin CL, Mitin NY, Taparowsky EJ, Gimotty PA, Hruban RH, Jacks T, Konieczny SF.

Cancer Res. 2006 Jan 1;66(1):242-7.

13.

Maintenance of acinar cell organization is critical to preventing Kras-induced acinar-ductal metaplasia.

Shi G, DiRenzo D, Qu C, Barney D, Miley D, Konieczny SF.

Oncogene. 2013 Apr 11;32(15):1950-8. doi: 10.1038/onc.2012.210. Epub 2012 Jun 4.

14.

A case of mistaken identity? Nonductal origins of pancreatic "ductal" cancers.

Murtaugh LC, Leach SD.

Cancer Cell. 2007 Mar;11(3):211-3.

15.

KRAS, Hedgehog, Wnt and the twisted developmental biology of pancreatic ductal adenocarcinoma.

Morris JP 4th, Wang SC, Hebrok M.

Nat Rev Cancer. 2010 Oct;10(10):683-95. doi: 10.1038/nrc2899. Epub 2010 Sep 3. Review.

16.

Notch and Kras in pancreatic cancer: at the crossroads of mutation, differentiation and signaling.

De La O JP, Murtaugh LC.

Cell Cycle. 2009 Jun 15;8(12):1860-4. Epub 2009 Jun 15.

17.

Notch1 functions as a tumor suppressor in a model of K-ras-induced pancreatic ductal adenocarcinoma.

Hanlon L, Avila JL, Demarest RM, Troutman S, Allen M, Ratti F, Rustgi AK, Stanger BZ, Radtke F, Adsay V, Long F, Capobianco AJ, Kissil JL.

Cancer Res. 2010 Jun 1;70(11):4280-6. doi: 10.1158/0008-5472.CAN-09-4645. Epub 2010 May 18.

18.

Disruption of p16 and activation of Kras in pancreas increase ductal adenocarcinoma formation and metastasis in vivo.

Qiu W, Sahin F, Iacobuzio-Donahue CA, Garcia-Carracedo D, Wang WM, Kuo CY, Chen D, Arking DE, Lowy AM, Hruban RH, Remotti HE, Su GH.

Oncotarget. 2011 Nov;2(11):862-73.

19.

The Nestin progenitor lineage is the compartment of origin for pancreatic intraepithelial neoplasia.

Carrière C, Seeley ES, Goetze T, Longnecker DS, Korc M.

Proc Natl Acad Sci U S A. 2007 Mar 13;104(11):4437-42. Epub 2007 Mar 5.

20.

Chronic pancreatitis is essential for induction of pancreatic ductal adenocarcinoma by K-Ras oncogenes in adult mice.

Guerra C, Schuhmacher AJ, Cañamero M, Grippo PJ, Verdaguer L, Pérez-Gallego L, Dubus P, Sandgren EP, Barbacid M.

Cancer Cell. 2007 Mar;11(3):291-302.

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