[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 10 of about 227
1. Erovic BM, Shah MD, Bruch G, Johnston M, Kim J, O'Sullivan B, Perez-Ordonez B, Weinreb I, Atenafu EG, de Almeida JR, Gullane PJ, Brown D, Gilbert RW, Irish JC, Goldstein DP: Outcome analysis of 215 patients with parotid gland tumors: a retrospective cohort analysis. J Otolaryngol Head Neck Surg; 2015;44:43
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Outcome analysis of 215 patients with parotid gland tumors: a retrospective cohort analysis.
  • BACKGROUND: To identify prognostic factors in patients with parotid gland carcinomas who were treated at the Princess Margaret Hospital.
  • RESULTS: Two-hundred-fifteen patients with adenoid cystic carcinoma (n = 20), adenocarcinoma (n = 19), acinic cell carcinoma (n = 62), basal cell adenocarcinoma (n = 7), carcinoma-ex-pleomorphic adenoma (n = 18), mucoepidermoid carcinoma (n = 70) and salivary duct carcinoma (n = 19) have been included.
  • The 5- and 10-year overall and disease-free survivals were 80.62%/69.48% and 74.37%/62.42%, respectively.
  • Multivariable analysis showed that age greater than 60 years, advanced pN classification, histopathological grade and the presence of lymphovascular invasion significantly worsened overall and disease-free survival.
  • Univariable analysis revealed periparotid lymph node involvement was associated with decreased overall (p < 0.0001) and disease-free survival (p < 0.0001).
  • [MeSH-major] Parotid Gland / pathology. Parotid Neoplasms / diagnosis
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Disease-Free Survival. Female. Follow-Up Studies. Humans. Lymphatic Metastasis. Male. Middle Aged. Ontario / epidemiology. Prognosis. Retrospective Studies. Survival Rate / trends. Time Factors. Young Adult

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Breast Cancer Res Treat. 2005 Jan;89(1):47-54 [15666196.001]
  • [Cites] Head Neck Surg. 1986 Jan-Feb;8(3):177-84 [3744850.001]
  • [Cites] Cancer. 2003 Mar 15;97(6):1453-63 [12627510.001]
  • [Cites] Oral Oncol. 2002 Oct;38(7):706-13 [12167424.001]
  • [Cites] Cancer. 2000 Sep 15;89(6):1195-204 [11002213.001]
  • [Cites] Ann Surg Oncol. 2015 Nov;22(12):4014-9 [25743328.001]
  • [Cites] JAMA Otolaryngol Head Neck Surg. 2013 Jul;139(7):698-705 [23788168.001]
  • [Cites] Int J Oral Maxillofac Surg. 2012 Mar;41(3):354-60 [22230288.001]
  • [Cites] J Surg Oncol. 2008 May 1;97(6):533-7 [18286522.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2007 Jul 1;68(3):714-8 [17398019.001]
  • [Cites] ANZ J Surg. 2006 Jun;76(6):458-61 [16768768.001]
  • [Cites] Cancer. 2007 May 15;109(10):2043-51 [17410532.001]
  • [Cites] CA Cancer J Clin. 2012 Jan-Feb;62(1):10-29 [22237781.001]
  • [Cites] Head Neck. 2010 Oct;32(10):1402-11 [20029981.001]
  • [Cites] Head Neck. 2009 Sep;31(9):1188-95 [19408288.001]
  • [Cites] J Oral Maxillofac Surg. 2009 Jul;67(7):1432-41 [19531414.001]
  • [Cites] Hum Pathol. 2009 Jun;40(6):887-92 [19200580.001]
  • [Cites] Acta Oncol. 2009;48(4):549-55 [19140053.001]
  • [Cites] Head Neck. 2009 Jan;31(1):58-63 [18853449.001]
  • [Cites] Clin Cancer Res. 2008 Aug 15;14(16):5181-7 [18698036.001]
  • [Cites] Eur J Surg Oncol. 2008 Aug;34(8):932-7 [18358679.001]
  • [Cites] Head Neck. 2008 Jun;30(6):800-9 [18429007.001]
  • [ErratumIn] J Otolaryngol Head Neck Surg. 2015;44:55. Johnston, U [corrected to Johnston, Meredith] [26671475.001]
  • (PMID = 26515170.001).
  • [ISSN] 1916-0216
  • [Journal-full-title] Journal of otolaryngology - head & neck surgery = Le Journal d'oto-rhino-laryngologie et de chirurgie cervico-faciale
  • [ISO-abbreviation] J Otolaryngol Head Neck Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC4625880
  •  go-up   go-down


2. Matthaei H, Semaan A, Hruban RH: The genetic classification of pancreatic neoplasia. J Gastroenterol; 2015 May;50(5):520-32
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The recent decline in the cost of DNA sequencing has allowed tumor sequencing to be conducted on a large scale, which, in turn, has led to an unprecedented understanding of the genetic events that drive neoplasia.
  • [MeSH-major] Adenocarcinoma, Mucinous / genetics. Biomarkers, Tumor / genetics. Carcinoma, Acinar Cell / genetics. Carcinoma, Pancreatic Ductal / genetics. Mutation. Pancreatic Neoplasms / genetics. Sequence Analysis, DNA

  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Pancreas. 2006 Apr;32(3):276-80 [16628083.001]
  • [Cites] Mod Pathol. 2003 Nov;16(11):1086-94 [14614047.001]
  • [Cites] Clin Cancer Res. 2014 Aug 15;20(16):4381-9 [24938521.001]
  • [Cites] Am J Clin Pathol. 2003 Sep;120(3):398-404 [14502804.001]
  • [Cites] J Pathol. 2014 Mar;232(4):428-35 [24293293.001]
  • [Cites] Sci Transl Med. 2014 Feb 19;6(224):224ra24 [24553385.001]
  • [Cites] Semin Ophthalmol. 2013 Sep-Nov;28(5-6):377-86 [24138046.001]
  • [Cites] J Clin Oncol. 2008 Jun 20;26(18):3063-72 [18565894.001]
  • [Cites] Mol Cancer. 2003 Jan 07;2:9 [12556240.001]
  • [Cites] Am J Surg Pathol. 2002 Apr;26(4):466-71 [11914624.001]
  • [Cites] AJR Am J Roentgenol. 2008 Sep;191(3):802-7 [18716113.001]
  • [Cites] Clin Cancer Res. 2012 Sep 1;18(17):4713-24 [22723372.001]
  • [Cites] Virchows Arch. 2005 Mar;446(3):239-45 [15688169.001]
  • [Cites] Ann Surg. 1999 Oct;230(4):501-9; discussion 509-11 [10522720.001]
  • [Cites] Am J Clin Pathol. 2014 Feb;141(2):168-80 [24436263.001]
  • [Cites] Science. 2011 Mar 4;331(6021):1199-203 [21252315.001]
  • [Cites] Am J Surg Pathol. 2011 Jul;35(7):981-8 [21677537.001]
  • [Cites] Ann Oncol. 2008 Oct;19(10):1727-33 [18515795.001]
  • [Cites] Ann Oncol. 2013 Mar;24(3):734-41 [23139258.001]
  • [Cites] Hum Pathol. 2008 Feb;39(2):251-8 [17959228.001]
  • [Cites] Ann Surg. 2004 May;239(5):651-7; discussion 657-9 [15082969.001]
  • [Cites] Nat Rev Cancer. 2004 Jan;4(1):45-60 [14681689.001]
  • [Cites] Am J Gastroenterol. 2010 Sep;105(9):2079-84 [20354507.001]
  • [Cites] Am J Pathol. 2002 Mar;160(3):953-62 [11891193.001]
  • [Cites] Am J Surg Pathol. 2005 Apr;29(4):512-9 [15767807.001]
  • [Cites] J Gastroenterol Hepatol. 2008 Dec;23(12):1847-51 [18752561.001]
  • [Cites] Science. 2013 Mar 29;339(6127):1546-58 [23539594.001]
  • [Cites] Am J Pathol. 2001 Jan;158(1):317-21 [11141506.001]
  • [Cites] Am J Pathol. 2000 Nov;157(5):1615-21 [11073821.001]
  • [Cites] Genes Chromosomes Cancer. 2001 Oct;32(2):177-81 [11550286.001]
  • [Cites] Int J Pancreatol. 1995 Dec;18(3):197-206 [8708390.001]
  • (PMID = 25605630.001).
  • [ISSN] 1435-5922
  • [Journal-full-title] Journal of gastroenterology
  • [ISO-abbreviation] J. Gastroenterol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA62924
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  •  go-up   go-down


3. Mansfield A, Tafur A, Smithedajkul P, Corsini M, Quevedo F, Miller R: Mayo Clinic experience with very rare exocrine pancreatic neoplasms. Pancreas; 2010 Oct;39(7):972-5
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Available evidence suggests that VREP have different risk factors and prognoses from those of adenocarcinoma of the pancreas.
  • METHODS: We reviewed patients from 1975 to 2005 who had VREP and compared them to patients with adenocarcinomas that were matched for TNM, grade, and decade of treatment.
  • The most commonly identified neoplasms were acinar cell carcinoma (n = 15), small cell carcinoma (n = 12), and squamous cell carcinoma (n = 8).
  • There was no difference in the survival of patients with stage 4 disease between cases, 8 months (range, 2.3-21.8 months), and controls, 6.7 months (range, 2.3-10.8 months) (P = 0.17).
  • The overall survival of all patients with VREP was better than matched controls, but no statistical difference was seen between the groups with stage 4 disease.
  • [MeSH-minor] Adult. Aged. Carcinoma, Acinar Cell / mortality. Carcinoma, Small Cell / mortality. Carcinoma, Squamous Cell / mortality. Female. Humans. Male. Middle Aged. Neoplasm Staging

  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • MedlinePlus Health Information. consumer health - Rare Diseases.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20622706.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


Advertisement
4. Bavle RM, Makarla S, Nadaf A, Narasimhamurthy S: Solid blue dot tumour: minor salivary gland acinic cell carcinoma. BMJ Case Rep; 2014;2014
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Solid blue dot tumour: minor salivary gland acinic cell carcinoma.
  • Acinic cell adenocarcinoma (ACC) is a low-grade malignant salivary neoplasm that constitutes approximately 17% of all primary salivary gland malignancies.
  • Here we report the case of a woman in her 60s with an ACC in association with the labial minor salivary gland, presenting in the post-treatment period of squamous cell carcinoma of the tongue.
  • [MeSH-major] Carcinoma, Acinar Cell / etiology. Neoplasms, Radiation-Induced / etiology. Neoplasms, Second Primary / etiology. Salivary Gland Neoplasms / etiology. Salivary Glands, Minor
  • [MeSH-minor] Carcinoma, Squamous Cell / radiotherapy. Female. Humans. Middle Aged. Tongue Neoplasms / radiotherapy

  • Genetic Alliance. consumer health - Acinic Cell Carcinoma.
  • MedlinePlus Health Information. consumer health - Salivary Gland Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] 2014 BMJ Publishing Group Ltd.
  • (PMID = 24928927.001).
  • [ISSN] 1757-790X
  • [Journal-full-title] BMJ case reports
  • [ISO-abbreviation] BMJ Case Rep
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC4069807
  •  go-up   go-down


5. Reichert M, Rustgi AK: Pancreatic ductal cells in development, regeneration, and neoplasia. J Clin Invest; 2011 Dec;121(12):4572-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The pancreas is a complex organ comprised of three critical cell lineages: islet (endocrine), acinar, and ductal.
  • In particular, emphasis will be placed upon the regulation of ductal cells by specific transcriptional factors during development as well as the underpinnings of acinar-ductal metaplasia as an important adaptive response during injury and regeneration.
  • We also address the potential contributions of ductal cells to neoplastic transformation, specifically in pancreatic ductal adenocarcinoma.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Cell Biol. 2001 Nov 12;155(4):519-30 [11696558.001]
  • [Cites] Development. 2001 Dec;128(24):5109-17 [11748146.001]
  • [Cites] Dev Biol. 2001 Oct 1;238(1):185-201 [11784003.001]
  • [Cites] Dev Biol. 2001 Oct 1;238(1):202-12 [11784004.001]
  • [Cites] Development. 2002 May;129(10):2447-57 [11973276.001]
  • [Cites] Pancreatology. 2001;1(6):587-96 [12120241.001]
  • [Cites] Curr Opin Genet Dev. 2002 Oct;12(5):540-7 [12200159.001]
  • [Cites] Nat Genet. 2002 Sep;32(1):128-34 [12185368.001]
  • [Cites] Gastroenterology. 2003 Apr;124(4):1020-36 [12671899.001]
  • [Cites] Cancer Cell. 2003 Jun;3(6):565-76 [12842085.001]
  • [Cites] Dev Biol. 2003 Aug 15;260(2):426-37 [12921743.001]
  • [Cites] Annu Rev Cell Dev Biol. 2003;19:71-89 [14570564.001]
  • [Cites] Hum Mol Genet. 2003 Dec 15;12(24):3307-14 [14570708.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Dec 9;100(25):14920-5 [14657333.001]
  • [Cites] Genes Dev. 2003 Dec 15;17(24):3112-26 [14681207.001]
  • [Cites] Cancer Cell. 2003 Dec;4(6):437-50 [14706336.001]
  • [Cites] Mol Cell Biol. 2004 Apr;24(7):2673-81 [15024058.001]
  • [Cites] Dev Biol. 2004 May 1;269(1):252-63 [15081371.001]
  • [Cites] Nature. 2004 May 6;429(6987):41-6 [15129273.001]
  • [Cites] Dev Biol. 2004 Jun 15;270(2):443-54 [15183725.001]
  • [Cites] Dev Biol. 2004 Jun 15;270(2):474-86 [15183727.001]
  • [Cites] Gastroenterology. 2004 Jul;127(1):250-60 [15236190.001]
  • [Cites] Dev Biol. 1972 Dec;29(4):436-67 [4570759.001]
  • [Cites] Development. 2005 Aug;132(16):3767-76 [16020518.001]
  • [Cites] Cancer Cell. 2005 Sep;8(3):185-95 [16169464.001]
  • [Cites] Cancer Res. 2006 Jan 1;66(1):95-106 [16397221.001]
  • [Cites] Genes Dev. 2006 Jan 15;20(2):253-66 [16418487.001]
  • [Cites] Diabetes. 2006 Feb;55(2):269-72 [16361411.001]
  • [Cites] Gastroenterology. 2006 Feb;130(2):532-41 [16472605.001]
  • [Cites] Genes Dev. 2006 Jun 1;20(11):1435-40 [16751181.001]
  • [Cites] Genes Dev. 2006 Nov 15;20(22):3130-46 [17114584.001]
  • [Cites] J Biol Chem. 2006 Dec 15;281(50):38385-95 [17056599.001]
  • [Cites] Cancer Res. 2007 Feb 1;67(3):1030-7 [17283135.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Feb 6;104(6):1865-70 [17267606.001]
  • [Cites] Cancer Cell. 2007 Mar;11(3):229-43 [17349581.001]
  • [Cites] Dev Cell. 2007 May;12(5):817-26 [17488631.001]
  • [Cites] Development. 1996 Mar;122(3):983-95 [8631275.001]
  • [Cites] Diabetologia. 1995 Dec;38(12):1405-11 [8786013.001]
  • [Cites] Curr Biol. 1997 Oct 1;7(10):801-4 [9368764.001]
  • [Cites] Development. 1998 Mar;125(6):1017-24 [9463348.001]
  • [Cites] Genes Dev. 1998 Jun 1;12(11):1705-13 [9620856.001]
  • [Cites] J Cell Biol. 1998 Nov 2;143(3):827-36 [9813100.001]
  • [Cites] Genes Dev. 1998 Dec 1;12(23):3752-63 [9851981.001]
  • [Cites] Nature. 1999 Aug 26;400(6747):877-81 [10476967.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Feb 1;102(5):1490-5 [15668393.001]
  • [Cites] Pancreas. 2005 Mar;30(2):148-57 [15714137.001]
  • [Cites] Cancer Cell. 2011 Apr 12;19(4):456-69 [21481788.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Jun 19;104(25):10500-5 [17563382.001]
  • [Cites] Am J Pathol. 2007 Jul;171(1):263-73 [17591971.001]
  • [Cites] Dev Cell. 2007 Jul;13(1):103-14 [17609113.001]
  • [Cites] Gastroenterology. 2007 Jul;133(1):72-9; quiz 309-10 [17631133.001]
  • [Cites] Gastroenterology. 2007 Jul;133(1):345-50 [17631154.001]
  • [Cites] J Clin Invest. 2007 Sep;117(9):2553-61 [17786244.001]
  • [Cites] Cancer Res. 2007 Oct 1;67(19):9518-27 [17909062.001]
  • [Cites] Genes Dev. 2007 Oct 15;21(20):2629-43 [17938243.001]
  • [Cites] Gastroenterology. 2007 Dec;133(6):1999-2009 [18054571.001]
  • [Cites] Cell. 2008 Jan 25;132(2):197-207 [18243096.001]
  • [Cites] Dev Biol. 2008 Feb 15;314(2):406-17 [18155690.001]
  • [Cites] Cell Stem Cell. 2007 Sep 13;1(3):313-23 [18371365.001]
  • [Cites] Dev Biol. 2008 Apr 1;316(1):74-86 [18294628.001]
  • [Cites] Int J Dev Biol. 2008;52(7):823-35 [18956314.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Dec 2;105(48):18913-8 [19028870.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Dec 2;105(48):18907-12 [19028876.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Dec 16;105(50):19915-9 [19052237.001]
  • [Cites] Dev Biol. 2009 Feb 1;326(1):4-35 [19013144.001]
  • [Cites] PLoS Biol. 2007 Jul;5(7):e163 [17535113.001]
  • [Cites] Science. 2009 Jun 26;324(5935):1707-10 [19556507.001]
  • [Cites] Cancer Cell. 2009 Nov 6;16(5):379-89 [19878870.001]
  • [Cites] Mech Dev. 2009 Dec;126(11-12):958-73 [19766716.001]
  • [Cites] Cell. 2009 Nov 13;139(4):791-801 [19914171.001]
  • [Cites] Mol Biol Cell. 2009 Nov;20(22):4838-44 [19793922.001]
  • [Cites] Dev Cell. 2009 Dec;17(6):849-60 [20059954.001]
  • [Cites] Proc Natl Acad Sci U S A. 2010 Jan 5;107(1):75-80 [20018761.001]
  • [Cites] Dev Cell. 2010 Mar 16;18(3):342-56 [20230744.001]
  • [Cites] Diabetes. 2010 May;59(5):1211-21 [20185815.001]
  • [Cites] Gastroenterology. 2010 Sep;139(3):708-13, 713.e1-2 [20650278.001]
  • [Cites] PLoS One. 2010;5(8):e12311 [20808819.001]
  • [Cites] Prog Mol Biol Transl Sci. 2010;97:1-40 [21074728.001]
  • [Cites] Development. 2010 Dec;137(24):4295-305 [21098570.001]
  • [Cites] Nat Genet. 2011 Jan;43(1):34-41 [21113154.001]
  • [Cites] Development. 2011 Feb;138(4):653-65 [21266405.001]
  • [Cites] Dev Dyn. 2011 Mar;240(3):530-65 [21337462.001]
  • [Cites] Cancer Cell. 2011 Apr 12;19(4):441-55 [21481787.001]
  • [Cites] Nature. 1985 Feb 14-20;313(6003):600-2 [3844051.001]
  • [Cites] Eur J Cell Biol. 1990 Feb;51(1):64-75 [2184038.001]
  • [Cites] Cell. 1990 Jun 15;61(6):1121-35 [1693546.001]
  • [Cites] Nature. 1994 Oct 13;371(6498):606-9 [7935793.001]
  • [Cites] In Vitro Cell Dev Biol Anim. 1994 Sep;30A(9):622-35 [7529626.001]
  • [Cites] Gastroenterology. 2011 Aug;141(2):731-41, 741.e1-4 [21703267.001]
  • [Cites] Gastroenterology. 2007 Feb;132(2):745-62 [17258745.001]
  • [Cites] Gastroenterology. 1999 Dec;117(6):1416-26 [10579983.001]
  • [Cites] Semin Diagn Pathol. 2000 Feb;17(1):31-42 [10721805.001]
  • [Cites] Genesis. 2000 Feb;26(2):143-4 [10686611.001]
  • [Cites] Mol Cell Biol. 2000 Jun;20(12):4445-54 [10825208.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Jul 5;97(14):7999-8004 [10884429.001]
  • [Cites] Diabetologia. 2000 Jul;43(7):907-14 [10952464.001]
  • [Cites] Development. 2000 Nov;127(22):4905-13 [11044404.001]
  • [Cites] Nature. 2000 Dec 14;408(6814):864-8 [11130726.001]
  • [Cites] Am J Surg Pathol. 2001 May;25(5):579-86 [11342768.001]
  • [Cites] Diabetes. 2001 Jul;50(7):1571-9 [11423478.001]
  • (PMID = 22133881.001).
  • [ISSN] 1558-8238
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / P30 DK050306; United States / NIDDK NIH HHS / DK / P30-DK019525; United States / NIDDK NIH HHS / DK / P30-DK050306; United States / NIDDK NIH HHS / DK / R01 DK060694; United States / NIDDK NIH HHS / DK / P30 DK019525
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Transcription Factors
  • [Other-IDs] NLM/ PMC3225990
  •  go-up   go-down


6. Avivar-Valderas A, Bobrovnikova-Marjon E, Alan Diehl J, Bardeesy N, Debnath J, Aguirre-Ghiso JA: Regulation of autophagy during ECM detachment is linked to a selective inhibition of mTORC1 by PERK. Oncogene; 2013 Oct 10;32(41):4932-40
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • ECM detachment induces metabolic stress and programmed cell death via anoikis.
  • Moreover, enforced PERK or AMPK activation upregulates autophagy and causes luminal filling during acinar morphogenesis by perpetuating a population of surviving autophagic luminal cells that resist anoikis.
  • We propose that increased autophagy, secondary to persistent PERK and LKB1-AMPK signaling, can robustly protect cells from anoikis and promote luminal filling during early carcinoma progression.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Mol Biol Cell. 2008 Mar;19(3):797-806 [18094039.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Sep 11;104(37):14694-9 [17766436.001]
  • [Cites] Cancer Res. 2008 May 1;68(9):3260-8 [18451152.001]
  • [Cites] Cell Cycle. 2008 May 1;7(9):1146-50 [18418049.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Oct 21;105(42):16314-9 [18852460.001]
  • [Cites] Nature. 2009 Sep 3;461(7260):109-13 [19693011.001]
  • [Cites] J Cell Sci. 2009 Oct 15;122(Pt 20):3589-94 [19812304.001]
  • [Cites] Autophagy. 2010 Feb;6(2):239-47 [20104019.001]
  • [Cites] PLoS One. 2010;5(4):e10240 [20421921.001]
  • [Cites] J Natl Cancer Inst. 2010 May 5;102(9):627-37 [20427430.001]
  • [Cites] Mol Biol Cell. 2011 Jan 15;22(2):165-78 [21119005.001]
  • [Cites] Nat Cell Biol. 2011 Feb;13(2):132-41 [21258367.001]
  • [Cites] J Clin Invest. 2001 Oct;108(8):1167-74 [11602624.001]
  • [Cites] Sci Signal. 2011;4(161):ra10 [21343617.001]
  • [Cites] Mol Cell Biol. 2011 Sep;31(17):3616-29 [21709020.001]
  • [Cites] Cell Death Differ. 2012 Mar;19(3):501-10 [21941369.001]
  • [Cites] Proc Natl Acad Sci U S A. 2012 Feb 14;109(7):E388-97 [22308451.001]
  • [Cites] Nature. 2012 Feb 16;482(7385):410-3 [22318515.001]
  • [Cites] J Pharmacol Exp Ther. 2012 Sep;342(3):827-34 [22700432.001]
  • [Cites] Methods. 2003 Jul;30(3):256-68 [12798140.001]
  • [Cites] Genes Dev. 2003 Aug 1;17(15):1829-34 [12869586.001]
  • [Cites] Biochem J. 2003 Oct 1;375(Pt 1):75-86 [12841850.001]
  • [Cites] Curr Biol. 2003 Nov 11;13(22):2004-8 [14614828.001]
  • [Cites] EMBO J. 2004 Jan 14;23(1):169-79 [14713949.001]
  • [Cites] Trends Cell Biol. 2004 Jan;14(1):20-8 [14729177.001]
  • [Cites] J Biol. 2003;2(4):28 [14511394.001]
  • [Cites] Dev Cell. 2004 Aug;7(2):167-78 [15296714.001]
  • [Cites] Nature. 2004 Sep 2;431(7004):31-2 [15343317.001]
  • [Cites] Curr Opin Genet Dev. 1999 Feb;9(1):49-54 [10072357.001]
  • [Cites] Genes Dev. 1999 Jun 1;13(11):1422-37 [10364159.001]
  • [Cites] Mol Cell Biol. 2005 Jun;25(12):5282-91 [15923641.001]
  • [Cites] Cell Metab. 2005 Jul;2(1):9-19 [16054095.001]
  • [Cites] Cell Metab. 2005 Jul;2(1):21-33 [16054096.001]
  • [Cites] Cancer Res. 2006 Feb 1;66(3):1702-11 [16452230.001]
  • [Cites] Mol Cell. 2006 Feb 17;21(4):521-31 [16483933.001]
  • [Cites] Annu Rev Biochem. 2006;75:137-63 [16756488.001]
  • [Cites] Annu Rev Cell Dev Biol. 2006;22:287-309 [16824016.001]
  • [Cites] PLoS One. 2007;2(7):e615 [17637831.001]
  • [Cites] Mol Cell. 2008 Mar 14;29(5):541-51 [18342602.001]
  • (PMID = 23160380.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / 5R24CA095823-04; United States / NCI NIH HHS / CA / CA109182; United States / NIEHS NIH HHS / ES / R21 ES017146; United States / NCI NIH HHS / CA / R01 CA126792; United States / NCRR NIH HHS / RR / 1 S10RR0 9145-01; United States / NCI NIH HHS / CA / U54 CA163131; United States / NCI NIH HHS / CA / CA126792-S1; United States / NCI NIH HHS / CA / R01 CA109182; United States / NIEHS NIH HHS / ES / ES017146; United States / NCI NIH HHS / CA / P01 CA104838; United States / NCI NIH HHS / CA / CA163131; United States / NCI NIH HHS / CA / R24 CA095823
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Multiprotein Complexes; 0 / Tumor Suppressor Proteins; 0 / mechanistic target of rapamycin complex 1; 4JG2LF96VF / tuberous sclerosis complex 2 protein; EC 2.7.1.- / Stk11 protein, mouse; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.10.- / PERK kinase; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / eIF-2 Kinase
  • [Other-IDs] NLM/ NIHMS424625; NLM/ PMC3600386
  •  go-up   go-down


7. Baer R, Cintas C, Dufresne M, Cassant-Sourdy S, Schönhuber N, Planque L, Lulka H, Couderc B, Bousquet C, Garmy-Susini B, Vanhaesebroeck B, Pyronnet S, Saur D, Guillermet-Guibert J: Pancreatic cell plasticity and cancer initiation induced by oncogenic Kras is completely dependent on wild-type PI 3-kinase p110α. Genes Dev; 2014 Dec 1;28(23):2621-35
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pancreatic cell plasticity and cancer initiation induced by oncogenic Kras is completely dependent on wild-type PI 3-kinase p110α.
  • Increased PI 3-kinase (PI3K) signaling in pancreatic ductal adenocarcinoma (PDAC) correlates with poor prognosis, but the role of class I PI3K isoforms during its induction remains unclear.
  • Inactivation of this single isoform blocked the irreversible transition of exocrine acinar cells into pancreatic preneoplastic ductal lesions by oncogenic Kras and/or pancreatic injury.
  • Hitting the other ubiquitous isoform, p110β, did not prevent preneoplastic lesion initiation. p110α signaling through small GTPase Rho and actin cytoskeleton controls the reprogramming of acinar cells and regulates cell morphology in vivo and in vitro.
  • Finally, p110α was necessary for pancreatic ductal cancers to arise from Kras-induced preneoplastic lesions by increasing epithelial cell proliferation in the context of mutated p53.
  • These data are critical for a better understanding of the development of this lethal disease that is currently without efficient treatment.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / genetics. Carcinoma, Pancreatic Ductal / physiopathology. Class Ia Phosphatidylinositol 3-Kinase / genetics. Class Ia Phosphatidylinositol 3-Kinase / metabolism. Pancreatic Neoplasms / genetics. Pancreatic Neoplasms / physiopathology. Proto-Oncogene Proteins p21(ras) / metabolism
  • [MeSH-minor] Animals. Animals, Genetically Modified. Cell Proliferation. Epithelial Cells / cytology. Gene Silencing. Humans. Mice. Mutation. Signal Transduction


8. Wong FK, Zumsteg ZS, Langevin CJ, Ali N, Maclary S, Balzer BL, Ho AS: Mucinous Carcinoma with Neuroendocrine Differentiation of Salivary Gland Origin. Head Neck Pathol; 2017 Jun;11(2):249-255
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mucinous Carcinoma with Neuroendocrine Differentiation of Salivary Gland Origin.
  • Primary mucinous adenocarcinomas of the salivary gland are rare malignancies defined by aggregates of epithelial cells suspended in large pools of extracellular mucin.
  • We report a case of a giant mucinous adenocarcinoma of salivary gland origin, with low-grade cytoarchitectural features and neuroendocrine differentiation arising in the submental region.
  • Grossly, the tumor measured 12.5 × 13.4 × 8.2 cm and replaced the bone and soft tissues of the anterior oral cavity.
  • Microscopically, the neoplasm was composed of large extracellular pools of mucin, which contained papillary and acinar aggregates, and small nodules of ductal type epithelium with minimal nuclear enlargement, powdery chromatin and little pleomorphism.
  • The nodules comprised 20 % of the tumor and showed morphologic and immunohistochemical evidence of neuroendocrine differentiation.
  • This is the first case reported of mucin-rich carcinoma of salivary gland origin exhibiting neuroendocrine differentiation.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Gastroenterol Res Pract. 2012;2012:780453 [22675346.001]
  • [Cites] Histopathology. 2010 Sep;57(3):395-409 [20738418.001]
  • [Cites] Int J Dermatol. 2014 Oct;53(10):1228-34 [25219513.001]
  • [Cites] Am J Surg Pathol. 1997 Dec;21(12):1501-6 [9414195.001]
  • [Cites] Cancer. 1973 Jan;31(1):117-29 [4345606.001]
  • [Cites] Am J Surg Pathol. 2004 Aug;28(8):1040-4 [15252310.001]
  • [Cites] Am J Surg Pathol. 2005 Oct;29(10):1330-9 [16160476.001]
  • [Cites] Kaohsiung J Med Sci. 2008 May;24(5):227-32 [18508419.001]
  • [Cites] Mod Pathol. 2004 May;17(5):568-72 [15001999.001]
  • [Cites] Mod Pathol. 2008 Oct;21(10):1217-23 [18469795.001]
  • [Cites] J Periodontol. 2010 Apr;81(4):626-31 [20367105.001]
  • [Cites] Head Neck Pathol. 2013 Jul;7 Suppl 1:S59-67 [23821212.001]
  • [Cites] J Oral Pathol Med. 2004 Jan;33(1):59-63 [14675143.001]
  • [Cites] Otolaryngol Head Neck Surg. 2016 May;154(5):875-9 [26908552.001]
  • [Cites] Virchows Arch. 2009 Jan;454(1):55-60 [19037659.001]
  • (PMID = 27534564.001).
  • [ISSN] 1936-0568
  • [Journal-full-title] Head and neck pathology
  • [ISO-abbreviation] Head Neck Pathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Keywords] NOTNLM ; Head and neck cancer / Mucin-rich carcinoma / Mucinous adenocarcinoma / Neuroendocrine differentiation / Reconstructive surgery / Salivary cancer / Salivary duct carcinoma
  •  go-up   go-down


9. Ding L, Han L, Li Y, Zhao J, He P, Zhang W: Neurogenin 3-directed cre deletion of Tsc1 gene causes pancreatic acinar carcinoma. Neoplasia; 2014 Nov;16(11):909-17
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Neurogenin 3-directed cre deletion of Tsc1 gene causes pancreatic acinar carcinoma.
  • The present study shows that neurogenin 3 directed Cre deletion of Tsc1 gene induces the development of pancreatic acinar carcinoma.
  • All Neurog3-Tsc1-/- mice developed notable adenocarcinoma-like lesions in pancreas starting from the age of 100 days old.
  • The tumor lesions are composed of cells with morphological and molecular resemblance to acinar cells.
  • Our studies indicate that activation of mTOR signaling in the pancreatic progenitor cells may trigger the development of acinar carcinoma.
  • Thus, mTOR may serve as a potential target for treatment of pancreatic acinar carcinoma.
  • [MeSH-major] Basic Helix-Loop-Helix Transcription Factors / genetics. Carcinoma, Acinar Cell / genetics. Nerve Tissue Proteins / genetics. Pancreatic Neoplasms / genetics. Tumor Suppressor Proteins / genetics

  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • Hazardous Substances Data Bank. SIROLIMUS .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] CA Cancer J Clin. 2004 Jan-Feb;54(1):8-29 [14974761.001]
  • [Cites] Cancer Res. 2003 May 1;63(9):2016-9 [12727811.001]
  • [Cites] Genes Dev. 2004 Aug 15;18(16):1926-45 [15314020.001]
  • [Cites] Clin Cancer Res. 2004 Oct 15;10(20):6993-7000 [15501979.001]
  • [Cites] N Engl J Med. 1992 Feb 13;326(7):455-65 [1732772.001]
  • [Cites] Am J Pathol. 1994 Sep;145(3):696-701 [8080049.001]
  • [Cites] Nature. 1999 Aug 26;400(6747):877-81 [10476967.001]
  • [Cites] Cancer Invest. 2004;22(4):588-603 [15565817.001]
  • [Cites] CA Cancer J Clin. 2005 Mar-Apr;55(2):74-108 [15761078.001]
  • [Cites] Surgery. 2005 Sep;138(3):450-5 [16213898.001]
  • [Cites] Int J Cancer. 2006 May 1;118(9):2337-43 [16331623.001]
  • [Cites] Breast Cancer Res. 2006;8(4):R46 [16859513.001]
  • [Cites] Clin Cancer Res. 2007 Apr 1;13(7):2281-9 [17404113.001]
  • [Cites] Hepatogastroenterology. 2007 Oct-Nov;54(79):2129-33 [18251175.001]
  • [Cites] Diabetes. 2008 Apr;57(4):817-27 [18192543.001]
  • [Cites] Science. 2008 Sep 26;321(5897):1801-6 [18772397.001]
  • [Cites] Endocrinology. 2009 Aug;150(8):3637-44 [19406939.001]
  • [Cites] Dev Biol. 2010 Mar 1;339(1):26-37 [20025861.001]
  • [Cites] J Clin Oncol. 2011 Feb 20;29(6):e150-3 [21189378.001]
  • [Cites] Science. 2011 Mar 4;331(6021):1199-203 [21252315.001]
  • [Cites] Mod Pathol. 2011 Sep;24(9):1229-36 [21572398.001]
  • [Cites] Neuroendocrinology. 2011;94(3):177-90 [21893937.001]
  • [Cites] Dev Biol. 2012 Jan 15;361(2):277-85 [22056785.001]
  • [Cites] Oncologist. 2011;16(12):1714-20 [22042785.001]
  • [Cites] Sci Signal. 2012 Mar 27;5(217):ra24 [22457330.001]
  • [Cites] Gastroenterology. 2012 May;142(5):1079-92 [22406637.001]
  • [Cites] Tumour Biol. 2012 Jun;33(3):757-65 [22170433.001]
  • [Cites] Cancer Discov. 2011 Jul;1(2):158-69 [21984975.001]
  • [Cites] Hepatology. 2012 Dec;56(6):2255-67 [22898879.001]
  • [Cites] Methods Mol Biol. 2013;980:249-66 [23359158.001]
  • [Cites] Cancer Res. 2013 Mar 15;73(6):1811-20 [23361300.001]
  • [Cites] Sci Rep. 2013;3:3230 [24231729.001]
  • [Cites] J Pathol. 2014 Mar;232(4):428-35 [24293293.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Feb 15;97(4):1607-11 [10677506.001]
  • [Cites] Diabetes. 2000 Feb;49(2):163-76 [10868931.001]
  • [Cites] Am J Pathol. 2002 Mar;160(3):953-62 [11891193.001]
  • [Cites] Development. 2002 May;129(10):2447-57 [11973276.001]
  • [Cites] Pancreatology. 2001;1(4):363-8 [12120215.001]
  • [Cites] Dev Biol. 2004 Jun 15;270(2):443-54 [15183725.001]
  • (PMID = 25425965.001).
  • [ISSN] 1476-5586
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Nerve Tissue Proteins; 0 / Neurog3 protein, mouse; 0 / Tumor Suppressor Proteins; 0 / tuberous sclerosis complex 1 protein; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, mouse; W36ZG6FT64 / Sirolimus
  • [Other-IDs] NLM/ PMC4240920
  • [Keywords] NOTNLM ; 4EBP-1, 4E binding protein 1 / ACC, acinar cell carcinoma / Neurog3, neurogenin 3 / PDA, pancreatic ductal adenocarcinoma / S6, ribosomal protein S6 / TSC, tuberous sclerosis complex / mTOR, mammlian target of rapamycin
  •  go-up   go-down


10. Davies CC, Harvey E, McMahon RF, Finegan KG, Connor F, Davis RJ, Tuveson DA, Tournier C: Impaired JNK signaling cooperates with KrasG12D expression to accelerate pancreatic ductal adenocarcinoma. Cancer Res; 2014 Jun 15;74(12):3344-56
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Impaired JNK signaling cooperates with KrasG12D expression to accelerate pancreatic ductal adenocarcinoma.
  • The c-Jun N-terminal protein kinase (JNK) and its two direct activators, namely the mitogen-activated protein kinase (MAPK) kinase 4 (MKK4) and MKK7, constitute a signaling node frequently mutated in human pancreatic ductal adenocarcinoma (PDAC).
  • More specifically, impaired JNK signaling in a subpopulation of Pdx1-expressing cells dramatically accelerated the appearance of Kras(G12D)-induced acinar-to-ductal metaplasia and pancreatic intraepithelial neoplasias, which rapidly progressed to invasive PDAC within 10 weeks of age.
  • Furthermore, inactivation of mkk4/mkk7 compromised acinar regeneration following acute inflammatory stress by locking damaged exocrine cells in a permanently de-differentiated state.
  • Therefore, we propose that JNK signaling exerts its tumor suppressive function in the pancreas by antagonizing the metaplastic conversion of acinar cells toward a ductal fate capable of responding to oncogenic stimulation.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / metabolism. MAP Kinase Kinase 4 / genetics. MAP Kinase Kinase 7 / genetics. Pancreatic Neoplasms / metabolism. Proto-Oncogene Proteins p21(ras) / genetics
  • [MeSH-minor] Acinar Cells / enzymology. Animals. Carcinogenesis / metabolism. Cell Dedifferentiation. MAP Kinase Signaling System. Mice. Mice, Transgenic. Mutation, Missense. Pancreas / enzymology. Pancreas / pathology. Pancreas / physiopathology. Regeneration

  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] ©2014 American Association for Cancer Research.
  • [Cites] Oncogene. 2014 Jun 5;33(23):2956-67 [23851493.001]
  • [Cites] PLoS One. 2010;5(5):e10443 [20454618.001]
  • [Cites] Mol Cell Biol. 2007 Nov;27(22):7935-46 [17875933.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Oct 2;104(40):15759-64 [17893331.001]
  • [Cites] Science. 2008 Sep 26;321(5897):1801-6 [18772397.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Dec 2;105(48):18913-8 [19028870.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Dec 2;105(48):18907-12 [19028876.001]
  • [Cites] Cancer Cell. 2009 Nov 6;16(5):379-89 [19878870.001]
  • [Cites] Nat Rev Cancer. 2010 Jan;10(1):51-7 [20029423.001]
  • [Cites] J Clin Invest. 2010 Feb;120(2):508-20 [20071774.001]
  • [Cites] PLoS One. 2010;5(8):e12469 [20814571.001]
  • [Cites] Nature. 2011 Feb 10;470(7333):214-20 [21307934.001]
  • [Cites] Nat Genet. 2011 Mar;43(3):212-9 [21317887.001]
  • [Cites] Genes Dev. 2011 Mar 15;25(6):634-45 [21406557.001]
  • [Cites] Cancer Cell. 2011 Apr 12;19(4):441-55 [21481787.001]
  • [Cites] Cancer Cell. 2011 Apr 12;19(4):456-69 [21481788.001]
  • [Cites] Cancer Cell. 2011 Jun 14;19(6):728-39 [21665147.001]
  • [Cites] Mol Cell Biol. 2011 Nov;31(21):4270-85 [21896780.001]
  • [Cites] J Neurosci. 2011 Nov 23;31(47):16969-76 [22114267.001]
  • [Cites] Cancer Res. 2012 Jan 15;72(2):472-81 [22127926.001]
  • [Cites] Semin Cancer Biol. 2012 Feb;22(1):33-40 [22210179.001]
  • [Cites] Genes Dev. 2001 Jun 1;15(11):1419-26 [11390361.001]
  • [Cites] Genes Dev. 2001 Dec 15;15(24):3243-8 [11751630.001]
  • [Cites] Development. 2002 May;129(10):2447-57 [11973276.001]
  • [Cites] Cancer Res. 2003 May 1;63(9):2005-9 [12727809.001]
  • [Cites] Cancer Cell. 2003 Jun;3(6):565-76 [12842085.001]
  • [Cites] Genes Dev. 2003 Dec 15;17(24):3112-26 [14681207.001]
  • [Cites] Cancer Cell. 2003 Dec;4(6):437-50 [14706336.001]
  • [Cites] Nat Cell Biol. 2004 Mar;6(3):215-26 [15039780.001]
  • [Cites] Mol Cell. 2004 Jul 23;15(2):269-78 [15260977.001]
  • [Cites] Cell. 1988 May 20;53(4):549-54 [2453289.001]
  • [Cites] Nature. 1991 Dec 12;354(6353):494-6 [1749429.001]
  • [Cites] N Engl J Med. 1993 May 20;328(20):1433-7 [8479461.001]
  • [Cites] Genes Dev. 1993 Nov;7(11):2135-48 [8224842.001]
  • [Cites] Cell. 1994 Mar 25;76(6):1025-37 [8137421.001]
  • [Cites] Cell. 1997 Mar 7;88(5):593-602 [9054499.001]
  • [Cites] Cancer Res. 1997 Oct 1;57(19):4177-82 [9331070.001]
  • [Cites] Cancer Res. 1998 Jun 1;58(11):2339-42 [9622070.001]
  • [Cites] Nature. 1999 Aug 26;400(6747):877-81 [10476967.001]
  • [Cites] Clin Cancer Res. 2004 Dec 15;10(24):8516-20 [15623633.001]
  • [Cites] Gastroenterology. 2005 Mar;128(3):728-41 [15765408.001]
  • [Cites] Cancer Cell. 2007 Mar;11(3):291-302 [17349585.001]
  • [Cites] Am J Pathol. 2007 Jul;171(1):263-73 [17591971.001]
  • [Cites] Biochim Biophys Acta. 2007 Aug;1773(8):1349-57 [17157936.001]
  • [Cites] Proc Natl Acad Sci U S A. 2012 Apr 17;109(16):5934-41 [22421440.001]
  • [Cites] Nature. 2012 Jun 14;486(7402):266-70 [22699621.001]
  • [Cites] Nature. 2012 Jun 21;486(7403):346-52 [22522925.001]
  • [Cites] Proc Natl Acad Sci U S A. 2012 Jul 24;109(30):12046-51 [22753496.001]
  • [Cites] Gut. 2012 Dec;61(12):1723-32 [22271799.001]
  • [Cites] Nature. 2012 Nov 15;491(7424):399-405 [23103869.001]
  • [Cites] Cancer Cell. 2012 Dec 11;22(6):737-50 [23201164.001]
  • [Cites] Gastroenterology. 2007 Dec;133(6):1999-2009 [18054571.001]
  • (PMID = 24713432.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United Kingdom / Wellcome Trust / / 090207/Z/09/Z; United Kingdom / Worldwide Cancer Research / / 10-0134; United Kingdom / Cancer Research UK / / ; United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.12.2 / MAP Kinase Kinase 4; EC 2.7.12.2 / MAP Kinase Kinase 7; EC 2.7.12.2 / Map2k7 protein, mouse; EC 3.6.5.2 / Kras2 protein, mouse; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras)
  • [Other-IDs] NLM/ EMS58094; NLM/ PMC4058314
  •  go-up   go-down






Advertisement