[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 100 of about 4434
6. Thirthagiri E, Cheong LS, Yip CH, Teo SH: CHEK2*1100delC does not contribute to risk to breast cancer among Malay, Chinese and Indians in Malaysia. Fam Cancer; 2009;8(4):355-8
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.
  • [Title] CHEK2*1100delC does not contribute to risk to breast cancer among Malay, Chinese and Indians in Malaysia.
  • A truncating mutation (1100delC) in the cell cycle checkpoint kinase-2 gene, CHEK2, has been identified as a risk factor for familial and sporadic breast cancer in some Northern and Western European populations.
  • However, the prevalence of CHEK2*1100delC in breast cancer appears to be population dependent.
  • We analysed the prevalence of CHEK2*1100delC in 668 breast cancer cases, of which 542 were invasive breast cancers, from a hospital-based cohort of breast cancer patients from Kuala Lumpur, Malaysia.
  • The variant was not found in any patients in this cohort, suggesting that CHEK2*1100delC is rare in our population, and unlikely to contribute significantly to risk to breast cancer among the Malay, Chinese and Indian ethnic groups in Malaysia.
  • [MeSH-major] Breast Neoplasms / genetics. Protein-Serine-Threonine Kinases / genetics
  • [MeSH-minor] Adult. Aged. Checkpoint Kinase 2. Female. Genetic Predisposition to Disease. Humans. Malaysia. Middle Aged. Polymerase Chain Reaction. Risk Factors. Sequence Deletion. Young Adult

  • Genetic Alliance. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • 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] J Med Genet. 2006 Nov;43(11):863-6 [17085682.001]
  • [Cites] Hum Mutat. 2004 Jul;24(1):100-1 [15221794.001]
  • [Cites] Cancer Cell. 2007 Feb;11(2):103-5 [17292821.001]
  • [Cites] Zhonghua Yi Xue Yi Chuan Xue Za Zhi. 2006 Aug;23(4):443-5 [16883537.001]
  • [Cites] Eur J Hum Genet. 2007 Feb;15(2):237-41 [17106448.001]
  • [Cites] Am J Hum Genet. 2002 Aug;71(2):432-8 [12094328.001]
  • [Cites] Int J Cancer. 2007 Dec 15;121(12):2661-7 [17721994.001]
  • [Cites] Am J Hum Genet. 2003 Apr;72(4):1023-8 [12610780.001]
  • [Cites] J Med Genet. 2004 Oct;41(10):731-5 [15466005.001]
  • [Cites] Breast Cancer Res Treat. 2008 Dec;112(3):569-73 [18175216.001]
  • [Cites] Cancer Cell. 2003 May;3(5):421-9 [12781359.001]
  • [Cites] Int J Cancer. 2004 Sep 10;111(4):543-7 [15239132.001]
  • [Cites] Nat Genet. 2002 May;31(1):55-9 [11967536.001]
  • [Cites] Br J Cancer. 2003 Nov 17;89(10):1966-70 [14612911.001]
  • [Cites] Hum Mol Genet. 2005 Feb 15;14 (4):555-63 [15649950.001]
  • [Cites] Am J Hum Genet. 2003 May;72(5):1308-14 [12690581.001]
  • [Cites] Neoplasma. 2006;53(4):305-8 [16830057.001]
  • [Cites] JAMA. 2006 Mar 22;295(12):1379-88 [16551709.001]
  • [Cites] Am J Hum Genet. 2004 Dec;75(6):1131-5 [15492928.001]
  • [Cites] Asian Pac J Cancer Prev. 2003 Jul-Sep;4(3):203-8 [14507240.001]
  • [Cites] Science. 1999 Dec 24;286(5449):2528-31 [10617473.001]
  • [Cites] BMC Med Genet. 2003 Jan 15;4:1 [12529183.001]
  • [Cites] Oncogene. 2006 Sep 25;25(43):5912-9 [16998506.001]
  • [Cites] J Clin Oncol. 2007 Jan 1;25(1):64-9 [17132695.001]
  • [Cites] Int J Cancer. 2005 Aug 20;116(2):263-6 [15810020.001]
  • [Cites] Breast Cancer Res Treat. 2007 Mar;102(1):119-22 [16897426.001]
  • [Cites] J Clin Oncol. 2008 May 10;26(14):2419; author reply 2419-20 [18467741.001]
  • [Cites] Am J Hum Genet. 2003 Feb;72(2):270-80 [12533788.001]
  • [Cites] Breast Cancer Res. 2004;6(6):R629-35 [15535844.001]
  • [Cites] Int J Cancer. 2004 Jan 1;108(1):54-6 [14618615.001]
  • [Cites] Cancer Res. 2008 Apr 1;68(7):2154-7 [18381420.001]
  • [Cites] Eur J Cancer. 2005 Dec;41(18):2896-903 [16239104.001]
  • [Cites] Breast Cancer Res Treat. 2004 Jan;83(1):91-3 [14997059.001]
  • [Cites] Am J Hum Genet. 2004 Jun;74(6):1175-82 [15122511.001]
  • [Cites] J Med Genet. 2006 Jul;43(7):e34 [16816021.001]
  • [Cites] Lancet. 2005 Oct 29-Nov 4;366(9496):1554-7 [16257342.001]
  • (PMID = 19399639.001).
  • [ISSN] 1573-7292
  • [Journal-full-title] Familial cancer
  • [ISO-abbreviation] Fam. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] EC 2.7.1.11 / Checkpoint Kinase 2; EC 2.7.11.1 / CHEK2 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
  •  go-up   go-down


7. Fejerman L, John EM, Huntsman S, Beckman K, Choudhry S, Perez-Stable E, Burchard EG, Ziv E: Genetic ancestry and risk of breast cancer among U.S. Latinas. Cancer Res; 2008 Dec 1;68(23):9723-8
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.
  • [Title] Genetic ancestry and risk of breast cancer among U.S. Latinas.
  • U.S. Latinas have a lower incidence of breast cancer compared with non-Latina White women.
  • We used genetic markers to estimate the ancestry of Latina breast cancer cases and controls and assessed the association with genetic ancestry, adjusting for reproductive and other risk factors.
  • We typed a set of 106 ancestry informative markers in 440 Latina women with breast cancer and 597 Latina controls from the San Francisco Bay area and estimated genetic ancestry using a maximum likelihood method.
  • Higher European ancestry was associated with increased breast cancer risk.

  • Genetic Alliance. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Hispanic American Health.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Genet Epidemiol. 2001 Jan;20(1):4-16 [11119293.001]
  • [Cites] PLoS Genet. 2007 Nov;3(11):e185 [18039031.001]
  • [Cites] Theor Popul Biol. 2001 Nov;60(3):227-37 [11855957.001]
  • [Cites] Cancer. 2002 Jun 1;94(11):2844-54 [12115371.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2002 Sep;11(9):795-800 [12223421.001]
  • [Cites] Lancet. 2003 Feb 15;361(9357):598-604 [12598158.001]
  • [Cites] Hum Biol. 2003 Feb;75(1):1-11 [12713142.001]
  • [Cites] Am J Hum Genet. 2003 Jun;72(6):1492-1504 [12817591.001]
  • [Cites] Ann Intern Med. 2004 Feb 3;140(3):184-8 [14757616.001]
  • [Cites] Ann Hum Genet. 2004 Mar;68(Pt 2):139-53 [15008793.001]
  • [Cites] Nat Genet. 2004 May;36(5):512-7 [15052271.001]
  • [Cites] Breast Cancer Res. 2004;6(4):R375-89 [15217505.001]
  • [Cites] Am J Phys Anthropol. 1986 Aug;70(4):489-503 [3766715.001]
  • [Cites] Ethn Dis. 1991 Summer;1(3):245-56 [1842537.001]
  • [Cites] Am J Hum Genet. 1999 Jul;65(1):220-8 [10364535.001]
  • [Cites] Hum Hered. 2004;58(1):30-9 [15604562.001]
  • [Cites] J Natl Cancer Inst. 2005 Mar 16;97(6):439-48 [15770008.001]
  • [Cites] Am J Hum Genet. 2005 Jun;76(6):967-86 [15834813.001]
  • [Cites] Genet Epidemiol. 2005 Jul;29(1):76-86 [15918156.001]
  • [Cites] Am J Public Health. 2005 Dec;95(12):2161-8 [16257940.001]
  • [Cites] Hum Genet. 2006 Jan;118(5):626-39 [16273390.001]
  • [Cites] Hum Genet. 2006 Jan;118(5):652-64 [16283388.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2005 Dec;14(12):2905-13 [16365008.001]
  • [Cites] Hum Genet. 2005 Dec;118(3-4):424-33 [16208514.001]
  • [Cites] J Clin Oncol. 2006 Mar 20;24(9):1342-9 [16549828.001]
  • [Cites] Hum Genet. 2006 Jun;119(5):547-57 [16596417.001]
  • [Cites] CA Cancer J Clin. 2006 May-Jun;56(3):168-83 [16737949.001]
  • [Cites] Hum Genet. 2006 Jul;119(6):624-33 [16738946.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2006 Oct;15(10):1878-85 [17035394.001]
  • [Cites] Am J Epidemiol. 2007 Dec 15;166(12):1409-19 [17934201.001]
  • [Cites] Am J Hum Genet. 2001 Feb;68(2):466-77 [11170894.001]
  • (PMID = 19047150.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / K01 CA160607; United States / NCI NIH HHS / CA / U01 CA069417; United States / NCI NIH HHS / CA / R01 CA63446; United States / NCI NIH HHS / CA / U01CA069417; United States / NCI NIH HHS / CA / K22 CA109351-01; United States / NCI NIH HHS / CA / RFA CA-95-011; United States / NCI NIH HHS / CA / R01 CA77305; United States / NCI NIH HHS / CA / CA109351-01; United States / NCI NIH HHS / CA / K22 CA10935; United States / NHLBI NIH HHS / HL / R01 HL078885; United States / NCI NIH HHS / CA / K22 CA109351; United States / NCI NIH HHS / CA / U01-CA86117; United States / NCI NIH HHS / CA / U01 CA086117; United States / NCI NIH HHS / CA / R01 CA063446; United States / NCI NIH HHS / CA / R01 CA120120
  • [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] United States
  • [Other-IDs] NLM/ NIHMS94365; NLM/ PMC2674787
  •  go-up   go-down


8. Cimino D, Fuso L, Sfiligoi C, Biglia N, Ponzone R, Maggiorotto F, Russo G, Cicatiello L, Weisz A, Taverna D, Sismondi P, De Bortoli M: Identification of new genes associated with breast cancer progression by gene expression analysis of predefined sets of neoplastic tissues. Int J Cancer; 2008 Sep 15;123(6):1327-38
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] Identification of new genes associated with breast cancer progression by gene expression analysis of predefined sets of neoplastic tissues.
  • Gene expression profiles were studied by microarray analysis in 2 sets of archival breast cancer tissues from patients with distinct clinical outcome.
  • Seventy-seven differentially expressed genes were identified when comparing 30 cases with relapse and 30 cases without relapse within 72 months from surgery.
  • These genes had a specific ontological distribution and some of them have been linked to breast cancer in previous studies: AIB1, the two keratin genes KRT5 and KRT15, RAF1, WIF1 and MSH6.
  • Seven out of 77 differentially expressed genes were selected and analyzed by qRT-PCR in 127 cases of breast cancer.
  • The expression levels of 6 upregulated genes (CKMT1B, DDX21, PRKDC, PTPN1, SLPI, YWHAE) showed a significant association to both disease-free and overall survival.
  • CKMT1B expression was an independent prognostic marker in all 3 datasets, whereas other genes confirmed their association with disease-free survival in at least 1 dataset.
  • This work provides a novel set of genes that could be used as independent prognostic markers and potential drug targets for breast cancer.
  • [MeSH-major] Breast Neoplasms / genetics. Breast Neoplasms / mortality. Gene Expression. Gene Expression Profiling. Neoplasm Recurrence, Local / genetics
  • [MeSH-minor] Disease Progression. Disease-Free Survival. Female. Humans. Kaplan-Meier Estimate. Middle Aged. Oligonucleotide Array Sequence Analysis. Prognosis. Reverse Transcriptase Polymerase Chain Reaction


9. Bergman A, Karlsson P, Berggren J, Martinsson T, Björck K, Nilsson S, Wahlström J, Wallgren A, Nordling M: Genome-wide linkage scan for breast cancer susceptibility loci in Swedish hereditary non-BRCA1/2 families: suggestive linkage to 10q23.32-q25.3. Genes Chromosomes Cancer; 2007 Mar;46(3):302-9
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.
  • [Title] Genome-wide linkage scan for breast cancer susceptibility loci in Swedish hereditary non-BRCA1/2 families: suggestive linkage to 10q23.32-q25.3.
  • The two breast cancer genes BRCA1 and BRCA2 were identified more than 10 years ago and, depending on population, mutations in these genes are responsible for a varying percentage of familial breast cancer.
  • In more than half the families, the increased risk of breast cancer cannot be explained by mutations in these genes, and the goal of this study was to locate novel susceptibility genes.
  • One of the main difficulties in identifying the cause of hereditary non-BRCA1/BRCA2 breast cancer is genetic heterogeneity, possibly due to multiple, incompletely penetrant susceptibility genes, along with ethnic and geographic differences.
  • In this study, one large family and 13 small to medium-sized families with multiple cases of breast cancer were analyzed by genome-wide linkage analysis.
  • Our results indicate that one or more of the suggested regions may harbor genes that are involved in the development of breast cancer.
  • [MeSH-major] Breast Neoplasms / genetics. Chromosomes, Human, Pair 10 / genetics. European Continental Ancestry Group. Genes, BRCA1. Genes, BRCA2. Genetic Linkage


10. Saxena S, Chakraborty A, Kaushal M, Kotwal S, Bhatanager D, Mohil RS, Chintamani C, Aggarwal AK, Sharma VK, Sharma PC, Lenoir G, Goldgar DE, Szabo CI: Contribution of germline BRCA1 and BRCA2 sequence alterations to breast cancer in Northern India. BMC Med Genet; 2006;7:75
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] Contribution of germline BRCA1 and BRCA2 sequence alterations to breast cancer in Northern India.
  • BACKGROUND: A large number of distinct mutations in the BRCA1 and BRCA2 genes have been reported worldwide, but little is known regarding the role of these inherited susceptibility genes in breast cancer risk among Indian women.
  • We investigated the distribution and the nature of BRCA1 and BRCA2 germline mutations and polymorphisms in a cohort of 204 Indian breast cancer patients and 140 age-matched controls.
  • METHOD: Cases were selected with regard to early onset disease (< or =40 years) and family history of breast and ovarian cancer.
  • Two hundred four breast cancer cases along with 140 age-matched controls were analyzed for mutations.
  • Four previously reported polymorphisms (K1183R, S1613G, and M1652I in BRCA1, and 7470A>G in BRCA2) were detected in both controls and breast cancer patients.
  • Rare BRCA1/2 sequence alterations were observed in 15 out of 105 (14.2%) early-onset cases without family history and 11.7% (4/34) breast cancer cases with family history.
  • In addition, several variants of uncertain clinical significance were identified.
  • Among these are two missense variants, one alteration of a consensus splice donor sequence, and a variant that potentially disrupts translational initiation.
  • CONCLUSION: BRCA1 and BRCA2 mutations appear to account for a lower proportion of breast cancer patients at increased risk of harboring such mutations in Northern India (6/204, 2.9%) than has been reported in other populations.
  • However, given the limited extent of reported family history among these patients, the observed mutation frequency is not dissimilar from that reported in other cohorts of early onset breast cancer patients.
  • [MeSH-major] Breast Neoplasms / genetics. Genes, BRCA1. Genes, BRCA2. Germ-Line Mutation
  • [MeSH-minor] Adolescent. Adult. Aged. Breast Neoplasms, Male / epidemiology. Breast Neoplasms, Male / genetics. Case-Control Studies. Female. Frameshift Mutation. Humans. India / epidemiology. Male. Middle Aged. Mutation, Missense

  • Genetic Alliance. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • 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
  • [Cites] J Natl Cancer Inst. 1999 Jun 2;91(11):943-9 [10359546.001]
  • [Cites] Science. 1999 May 21;284(5418):1354-6 [10334989.001]
  • [Cites] J Natl Cancer Inst. 1999 Aug 4;91(15):1310-6 [10433620.001]
  • [Cites] Hum Mutat. 2004 Dec;24(6):534 [15532023.001]
  • [Cites] Cancer Res. 2004 Nov 15;64(22):8143-7 [15548676.001]
  • [Cites] Breast Cancer Res Treat. 2004 Nov;88(2):177-86 [15564800.001]
  • [Cites] CA Cancer J Clin. 2005 Mar-Apr;55(2):74-108 [15761078.001]
  • [Cites] JAMA. 2006 Mar 22;295(12):1379-88 [16551709.001]
  • [Cites] Am J Hum Genet. 2000 Oct;67(4):841-50 [10978226.001]
  • [Cites] Nature. 2000 Nov 23;408(6811):429-32 [11100717.001]
  • [Cites] J Natl Cancer Inst. 2002 Sep 18;94(18):1358-65 [12237281.001]
  • [Cites] Hum Mutat. 2002 Dec;20(6):473-4 [12442273.001]
  • [Cites] Oncogene. 2000 Dec 11;19(53):6152-8 [11156529.001]
  • [Cites] Oncogene. 2000 Dec 11;19(53):6159-75 [11156530.001]
  • [Cites] Oncogene. 2000 Dec 11;19(53):6176-83 [11156531.001]
  • [Cites] Hum Mol Genet. 2001 Apr;10(7):705-13 [11257103.001]
  • [Cites] J Med Genet. 2001 Dec;38(12):824-33 [11748305.001]
  • [Cites] Int J Cancer. 2002 Apr 1;98(4):596-603 [11920621.001]
  • [Cites] Breast Cancer Res. 2002;4(4):R6 [12100744.001]
  • [Cites] Cancer Biol Ther. 2002 Jan-Feb;1(1):18-21 [12170759.001]
  • [Cites] Am J Hum Genet. 2002 Sep;71(3):595-606 [12181777.001]
  • [Cites] Singapore Med J. 2002 Apr;43(4):194-7 [12188064.001]
  • [Cites] Hum Mutat. 2003 Jan;21(1):98-9 [12497638.001]
  • [Cites] Cancer Res. 2003 Apr 1;63(7):1449-53 [12670888.001]
  • [Cites] Hum Mol Genet. 2003 May 1;12(9):1055-61 [12700174.001]
  • [Cites] Am J Hum Genet. 2003 May;72(5):1117-30 [12677558.001]
  • [Cites] Methods Mol Biol. 2003;223:403-12 [12777742.001]
  • [Cites] Hum Mutat. 2003 Aug;22(2):178-9 [12872265.001]
  • [Cites] Hum Mutat. 2004 Feb;23(2):205 [14722926.001]
  • [Cites] J Med Genet. 2004 Feb;41(2):e21 [14757871.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2004 Feb;13(2):181-9 [14973102.001]
  • [Cites] Am J Hum Genet. 2004 Oct;75(4):535-44 [15290653.001]
  • [Cites] Cancer. 1985 Sep 1;56(5):1206-8 [4016708.001]
  • [Cites] Science. 1990 Dec 21;250(4988):1684-9 [2270482.001]
  • [Cites] Prog Clin Biol Res. 1991;369:21-34 [1946519.001]
  • [Cites] Eur J Cancer Prev. 1992 Oct;1(6):395-9 [1463995.001]
  • [Cites] Lancet. 1994 Mar 19;343(8899):692-5 [7907678.001]
  • [Cites] Science. 1994 Sep 30;265(5181):2088-90 [8091231.001]
  • [Cites] Science. 1994 Oct 7;266(5182):66-71 [7545954.001]
  • [Cites] Nat Genet. 1995 Oct;11(2):198-200 [7550349.001]
  • [Cites] Nature. 1995 Dec 21-28;378(6559):789-92 [8524414.001]
  • [Cites] Am J Hum Genet. 1996 Feb;58(2):271-80 [8571953.001]
  • [Cites] Nat Genet. 1996 Mar;12(3):333-7 [8589730.001]
  • [Cites] Nat Genet. 1996 May;13(1):22-3 [8673099.001]
  • [Cites] Nature. 1996 Aug 22;382(6593):678-9 [8751436.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Nov 26;93(24):13595-9 [8942979.001]
  • [Cites] Genes Chromosomes Cancer. 1997 Feb;18(2):102-10 [9115959.001]
  • [Cites] Am J Hum Genet. 1997 Mar;60(3):486-95 [9042907.001]
  • [Cites] Am J Hum Genet. 1997 May;60(5):1013-20 [9150148.001]
  • [Cites] Am J Hum Genet. 1997 Sep;61(3):761-2 [9326340.001]
  • [Cites] Am J Hum Genet. 1998 Mar;62(3):676-89 [9497246.001]
  • [Cites] Hum Mol Genet. 1998 May;7(5):801-5 [9536083.001]
  • [Cites] Oncogene. 1998 Apr 2;16(13):1713-21 [9582019.001]
  • [Cites] Cancer Res. 1999 Jan 15;59(2):455-61 [9927062.001]
  • [Cites] Hum Mol Genet. 1999 Mar;8(3):413-23 [9971877.001]
  • [Cites] Science. 1999 Jul 30;285(5428):747-50 [10426999.001]
  • (PMID = 17018160.001).
  • [ISSN] 1471-2350
  • [Journal-full-title] BMC medical genetics
  • [ISO-abbreviation] BMC Med. Genet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1617095
  •  go-up   go-down


11. Muller FM, Dawe RS, Moseley H, Fleming CJ: Randomized comparison of Mohs micrographic surgery and surgical excision for small nodular basal cell carcinoma: tissue-sparing outcome. Dermatol Surg; 2009 Sep;35(9):1349-54
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.
  • [Title] Randomized comparison of Mohs micrographic surgery and surgical excision for small nodular basal cell carcinoma: tissue-sparing outcome.
  • BACKGROUND: Mohs micrographic surgery (MMS) is recognized globally as the criterion standard for high-risk basal cell carcinoma (BCC).
  • The main advantage of MMS over conventional surgery is the chance of complete tumor removal, but it is also thought, based on experience, to be tissue sparing.
  • OBJECTIVE: To determine whether MMS leaves smaller surgical defects than standard surgery.
  • METHODS AND MATERIALS: This was a randomized trial involving 30 patients with a clinical diagnosis of BCC.
  • In the standard surgery group the BCCs were excised with 4-mm margins.
  • In the MMS group, tumors were excised with 2-mm margins and subsequent stages of MMS until the tumor was completely removed.
  • [MeSH-major] Carcinoma, Basal Cell / surgery. Mohs Surgery / methods. Skin Neoplasms / surgery
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Follow-Up Studies. Humans. Male. Middle Aged. Neoplasm Staging. Single-Blind Method. Treatment Outcome


12. Kishikawa M, Koyama K, Iseki M, Kobuke T, Yonehara S, Soda M, Ron E, Tokunaga M, Preston DL, Mabuchi K, Tokuoka S: Histologic characteristics of skin cancer in Hiroshima and Nagasaki: background incidence and radiation effects. Int J Cancer; 2005 Nov 10;117(3):363-9
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] Histologic characteristics of skin cancer in Hiroshima and Nagasaki: background incidence and radiation effects.
  • Skin cancers, though rare in Japan, have reportedly been on the rise, but little else is known about epidemiologic features of different histologic types of skin cancer.
  • The Life Span Study cohort, which consists of 93,700 atomic-bomb survivors, many of whom were exposed to negligibly low radiation doses, and 26,600 people not exposed to radiation, enables a population-based study of spontaneous as well as radiation-related cancer risk.
  • Skin tumor incident cases diagnosed between 1958 and 1987 were ascertained by linkage to the Hiroshima and Nagasaki tumor registries augmented by searches of other data sources.
  • Study pathologists reviewed tumor specimens and pathology reports and classified tumors using the World Health Organization classification scheme.
  • They identified 274 primary incident skin cancers, of which 106 were basal cell carcinoma (BCC), 81 were squamous cell carcinoma (SCC), and 14 were malignant melanomas.
  • BCC and SCC background incidence rates were both about 3 per 100,000 per year.
  • BCCs were mainly on the head/neck (81%), whereas SCCs occurred most frequently on the arms/legs (45%) and head/neck (29%), consistent with the presumed role played by solar UV exposure in skin cancer.
  • The BCC rates increased significantly between 1958 and 1987, whereas the SCC rates remained unchanged.
  • The excess absolute risk of BCC per unit skin surface area related to atomic-bomb radiation exposure did not differ between UV-exposed and shielded parts of the body, suggesting the additivity of the radiation-related and background BCC risks.
  • [MeSH-major] Nuclear Warfare. Skin Neoplasms / epidemiology. Skin Neoplasms / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Cohort Studies. Female. Humans. Incidence. Japan / epidemiology. Male. Middle Aged. Neoplasms, Radiation-Induced. Radioactive Fallout

  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • COS Scholar Universe. author profiles.
  • 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] (c) 2005 Wiley-Liss, Inc.
  • (PMID = 15900592.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CP / N01-CP-31012; United States / NCI NIH HHS / CP / N01-CP-71015
  • [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.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Radioactive Fallout
  •  go-up   go-down


13. Heal CF, Raasch BA, Buettner PG, Weedon D: Accuracy of clinical diagnosis of skin lesions. Br J Dermatol; 2008 Sep;159(3):661-8
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.
  • [Title] Accuracy of clinical diagnosis of skin lesions.
  • BACKGROUND: Skin cancer is an increasing problem in fair-skinned populations worldwide.
  • It is important that doctors are able to diagnose skin lesions accurately.
  • OBJECTIVES: To compare the clinical with the histological diagnosis of excised skin lesions from a set of epidemiological data.
  • We analysed diagnostic accuracy stratified by histological subtype and body site and examined the histological nature of misclassified diagnosis.
  • METHODS: All excised and histologically confirmed skin cancers in Townsville/Thuringowa, Australia from December 1996 to October 1999 were recorded.
  • RESULTS: Skin excisions in 8694 patients were examined.
  • PPVs for the clinical diagnoses were: basal cell carcinoma (BCC) 72.7%; squamous cell carcinoma (SCC) 49.4%; cutaneous melanoma (CM) 33.3%.
  • Sensitivities for the clinical diagnosis were: BCC 63.9%; SCC 41.1%; CM 33.8%.
  • For BCC, PPVs and sensitivities were higher for the trunk, the shoulders and the face and lower for the extremities.
  • CONCLUSIONS: Diagnostic accuracy was highest for BCC, the most prevalent lesion.
  • Most excisions were correctly diagnosed or resulted in the removal of malignant lesions.
  • With nonmelanocytic lesions, doctors tended to misclassify benign lesions as malignant, but were less likely to do the reverse.
  • Accuracy of diagnosis was dependent on body site.
  • [MeSH-major] Clinical Competence. Dermatology. Family Practice. Pathology, Clinical / standards. Skin Diseases / diagnosis
  • [MeSH-minor] Adult. Aged. Australia. Carcinoma, Basal Cell / diagnosis. Carcinoma, Basal Cell / pathology. Carcinoma, Squamous Cell / diagnosis. Carcinoma, Squamous Cell / pathology. False Negative Reactions. False Positive Reactions. Female. Humans. Male. Melanoma / diagnosis. Melanoma / pathology. Middle Aged. Nevus / diagnosis. Nevus / pathology. Nevus, Pigmented / diagnosis. Nevus, Pigmented / pathology. Predictive Value of Tests. Skin Neoplasms / diagnosis. Skin Neoplasms / pathology

  • MedlinePlus Health Information. consumer health - Skin Conditions.
  • COS Scholar Universe. author profiles.
  • 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
  • (PMID = 18616767.001).
  • [ISSN] 1365-2133
  • [Journal-full-title] The British journal of dermatology
  • [ISO-abbreviation] Br. J. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  •  go-up   go-down


1
Advertisement
4. Mc Menamin ME, Goh SG, Poblet E, Gostelow BE, Robson A, Calonje E: Sarcomatoid basal cell carcinoma--predilection for osteosarcomatous differentiation: a series of 11 cases. Am J Surg Pathol; 2006 Oct;30(10):1299-308
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.
  • [Title] Sarcomatoid basal cell carcinoma--predilection for osteosarcomatous differentiation: a series of 11 cases.
  • Primary cutaneous carcinomas rarely show heterologous malignant mesenchymal differentiation.
  • We report 11 cases of sarcomatoid basal cell carcinoma (BCC) with osteosarcomatous differentiation.
  • Seven patients were alive without evidence of disease (follow-up interval 5 to 24 mo) and 1 patient died of unrelated causes at 7 months without evidence of disease.
  • On histology, the tumors were dermal in location with 2 cases showing focal subcutaneous involvement.
  • Ten tumors were well-circumscribed and 1 tumor showed focally infiltrative edges.
  • Ten tumors revealed conventional BCC associated with varying proportions of osteosarcomatous and undifferentiated sarcomatous stroma.
  • Transition from neoplastic epithelial to mesenchymal cells was seen in 8 cases.
  • One case showed a purely osteoclastic giant cell rich malignant mesenchyme, interpreted as representing early stages of osteosarcomatous transformation.
  • Previously unreported in sarcomatoid BCC, the mesenchymal component of another two cases displayed predominant malignant giant cell tumor like areas and 1 further case disclosed areas reminiscent of telangiectatic osteosarcoma.
  • MNF116 and EMA were focally positive in osteosarcomatous tumor cells of 1 case.
  • Although the follow-up interval is short, our data suggest an excellent prognosis for polypoid and exophytic sarcomatoid BCC after complete surgical resection.
  • [MeSH-major] Carcinoma, Basal Cell / pathology. Carcinosarcoma / pathology. Cell Transformation, Neoplastic / pathology. Osteosarcoma / pathology. Skin Neoplasms / pathology
  • [MeSH-minor] Aged. Biomarkers, Tumor / analysis. Fatal Outcome. Female. Humans. Male. Middle Aged

  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • 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
  • (PMID = 17001162.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  •  go-up   go-down


15. Archontaki M, Stavrianos SD, Korkolis DP, Arnogiannaki N, Vassiliadis V, Liapakis IE, Christ H, Rapidis AD, Kokkalis G: Giant Basal cell carcinoma: clinicopathological analysis of 51 cases and review of the literature. Anticancer Res; 2009 Jul;29(7):2655-63
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] Giant Basal cell carcinoma: clinicopathological analysis of 51 cases and review of the literature.
  • BACKGROUND: Giant basal cell carcinoma (GBCC) is an aggressive malignant neoplasm.
  • Because of the rarity of the tumor and its recognized high risk of recurrence, there are no guidelines for its treatment.
  • Data from 48 patients obtained from 30 individual articles were added to our 3 cases, producing a total number of 51 cases of GBCC.
  • A clinical database was established in order to define the behavior of this tumor, prognostic factors and optimal treatment.
  • It develops as long-standing dermal tumor with mean disease duration of 14.5 years and is most commonly located on the back, followed by the face and upper extremity.
  • Wide local excision of the tumor with or without postoperative radiochemotherapy represents the optimal treatment.
  • CONCLUSION: Optimal management of GBCC consists of wide local excision with histologically confirmed tumor-free margins, frequently followed by adjuvant therapy.
  • In cases of lymphatic spread, a regional lymphadenectomy is also necessary.
  • [MeSH-major] Carcinoma, Basal Cell / pathology. Skin Neoplasms / pathology
  • [MeSH-minor] Aged. Aged, 80 and over. Female. Humans. Male. Middle Aged. Neoplasm Metastasis

  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19596942.001).
  • [ISSN] 1791-7530
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Greece
  • [Number-of-references] 54
  •  go-up   go-down


16. Braun RP, Klumb F, Girard C, Bandon D, Salomon D, Skaria A, Adatto M, French LE, Saurat JH, Vallée JP: Three-dimensional reconstruction of basal cell carcinomas. Dermatol Surg; 2005 May;31(5):562-6; discussion 566-8
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.
  • [Title] Three-dimensional reconstruction of basal cell carcinomas.
  • BACKGROUND: Basal cell carcinoma (BCC) is the most common type of skin cancer.
  • One of the main problems with BCC is the risk of local recurrence of the tumor after treatment.
  • OBJECTIVE: To better understand the tumor morphology and growth pattern of BCC, we tried to develop a method that provides a precise three-dimensional model of the tumor.
  • METHODS: Because Mohs surgery provides the best overview of the tumor and the tumor margins (both lateral and in depth), the reconstruction was based on slides from Mohs surgery.
  • After digitization and processing of the slides, the tumor was then surrounded by a Mohs surgeon on a computer screen.
  • These selections (lines) were used for a three-dimensional reconstruction of the tumor using MedSurf3D software.
  • RESULTS: This method allows three-dimensional reconstruction of any given BCC.
  • The MedSurf3D software enables visualization of a three-dimensional model of the tissue, which is removed during the surgical procedure.
  • CONCLUSIONS: Three-dimensional reconstruction is a fascinating tool that might improve our understanding of the behavior, growth pattern, and tumor morphology of BCCs.
  • This technique might also be useful in other fields of cutaneous oncology, such as the calculation of the tumor volume of melanomas.
  • [MeSH-major] Carcinoma, Basal Cell / surgery. Mohs Surgery / methods. Skin Neoplasms / surgery

  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15962742.001).
  • [ISSN] 1076-0512
  • [Journal-full-title] Dermatologic surgery : official publication for American Society for Dermatologic Surgery [et al.]
  • [ISO-abbreviation] Dermatol Surg
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 24
  •  go-up   go-down


17. Santiago F, Serra D, Vieira R, Figueiredo A: Incidence and factors associated with recurrence after incomplete excision of basal cell carcinomas: a study of 90 cases. J Eur Acad Dermatol Venereol; 2010 Dec;24(12):1421-4
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.
  • [Title] Incidence and factors associated with recurrence after incomplete excision of basal cell carcinomas: a study of 90 cases.
  • BACKGROUND: Management of incompletely excised basal cell carcinomas (BCC) remains controversial.
  • OBJECTIVE: The aim of this study was to assess the rate and the factors associated with the recurrence of incompletely excised BCC.
  • METHODS: In this retrospective monocentric study, data from all surgically excised BCC during 4 years (2000 to 2003) were analysed.
  • RESULTS: A total of 947 BCC were excised.
  • Recurrence of incompletely excised BCC was significantly higher (P < 0.05) in younger patients, in aggressive histological types and in localizations like postauricular and nasogenian folds.
  • CONCLUSION: Observation might be an acceptable option in many situations, but for patients with aggressive types of BCC, or with tumours localized in risk areas of the face, immediate re-excision appears to be the treatment of choice.
  • [MeSH-major] Carcinoma, Basal Cell / pathology. Skin Neoplasms / pathology

  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] © 2010 The Authors. Journal compilation © 2010 European Academy of Dermatology and Venereology.
  • (PMID = 20384689.001).
  • [ISSN] 1468-3083
  • [Journal-full-title] Journal of the European Academy of Dermatology and Venereology : JEADV
  • [ISO-abbreviation] J Eur Acad Dermatol Venereol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  •  go-up   go-down


18. Tiftikcioğlu YO, Karaaslan O, Aksoy HM, Aksoy B, Koçer U: Basal cell carcinoma in Turkey. J Dermatol; 2006 Feb;33(2):91-5
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.
  • [Title] Basal cell carcinoma in Turkey.
  • Basal cell carcinoma (BCC) is the most common form of cancer in Caucasians.
  • This study was undertaken to define clinical features of BCC treated by surgical excision in Turkish patients.
  • One-hundred and ninety-eight patients with 216 BCC, all treated by surgical excision, were studied prospectively.
  • Age and sex distribution, personal and family history, skin type, site and size of the lesions, clinical type of the lesions, status of surgical margins and incidence of recurrence were analyzed.
  • There was also personal and/or family history of cancer in 24.8% of our cases.
  • Of all BCC treated, 83.8% had a noduloulcerative clinical appearance.
  • In conclusion, clinical characteristics of BCC in Turkish patients have both similarities and differences compared with other countries.
  • [MeSH-major] Carcinoma, Basal Cell / epidemiology. Neoplasm Recurrence, Local / epidemiology. Skin Neoplasms / epidemiology
  • [MeSH-minor] Adult. Age Distribution. Aged. Aged, 80 and over. Biopsy, Needle. Cohort Studies. Female. Humans. Immunohistochemistry. Incidence. Male. Middle Aged. Mohs Surgery / methods. Neoplasm Staging. Prognosis. Prospective Studies. Sex Distribution. Turkey / epidemiology

  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16556274.001).
  • [ISSN] 0385-2407
  • [Journal-full-title] The Journal of dermatology
  • [ISO-abbreviation] J. Dermatol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Japan
  •  go-up   go-down


19. Stacey SN, Sulem P, Masson G, Gudjonsson SA, Thorleifsson G, Jakobsdottir M, Sigurdsson A, Gudbjartsson DF, Sigurgeirsson B, Benediktsdottir KR, Thorisdottir K, Ragnarsson R, Scherer D, Hemminki K, Rudnai P, Gurzau E, Koppova K, Botella-Estrada R, Soriano V, Juberias P, Saez B, Gilaberte Y, Fuentelsaz V, Corredera C, Grasa M, Höiom V, Lindblom A, Bonenkamp JJ, van Rossum MM, Aben KK, de Vries E, Santinami M, Di Mauro MG, Maurichi A, Wendt J, Hochleitner P, Pehamberger H, Gudmundsson J, Magnusdottir DN, Gretarsdottir S, Holm H, Steinthorsdottir V, Frigge ML, Blondal T, Saemundsdottir J, Bjarnason H, Kristjansson K, Bjornsdottir G, Okamoto I, Rivoltini L, Rodolfo M, Kiemeney LA, Hansson J, Nagore E, Mayordomo JI, Kumar R, Karagas MR, Nelson HH, Gulcher JR, Rafnar T, Thorsteinsdottir U, Olafsson JH, Kong A, Stefansson K: New common variants affecting susceptibility to basal cell carcinoma. Nat Genet; 2009 Aug;41(8):909-14
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] New common variants affecting susceptibility to basal cell carcinoma.
  • In a follow-up to our previously reported genome-wide association study of cutaneous basal cell carcinoma (BCC), we describe here several new susceptibility variants.
  • SNP rs11170164, encoding a G138E substitution in the keratin 5 (KRT5) gene, affects risk of BCC (OR = 1.35, P = 2.1 x 10(-9)).
  • A variant at 9p21 near CDKN2A and CDKN2B also confers susceptibility to BCC (rs2151280[C]; OR = 1.19, P = 6.9 x 10(-9)), as does rs157935[T] at 7q32 near the imprinted gene KLF14 (OR = 1.23, P = 5.7 x 10(-10)).
  • A melanoma- and pigmentation-associated variant in the SLC45A2 gene, L374F, is associated with risk of both BCC and squamous cell carcinoma.
  • Finally, we report conclusive evidence that rs401681[C] in the TERT-CLPTM1L locus confers susceptibility to BCC but protects against melanoma.

  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • SciCrunch. OMIM: Data: Gene Annotation .
  • SciCrunch. Clinical Genomic Database: Data: Gene Annotation .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Proc Natl Acad Sci U S A. 1993 Aug 1;90(15):7414-8 [7688477.001]
  • [Cites] Nat Genet. 2009 Feb;41(2):221-7 [19151717.001]
  • [Cites] Hum Mutat. 2005 Mar;25(3):278-84 [15714523.001]
  • [Cites] Eur J Dermatol. 2006 Mar-Apr;16(2):132-5 [16581562.001]
  • [Cites] Cell. 2006 Oct 20;127(2):265-75 [17055429.001]
  • [Cites] Cancer Res. 2007 Apr 15;67(8):3963-9 [17440112.001]
  • [Cites] PLoS Genet. 2007 May 4;3(5):e65 [17480121.001]
  • [Cites] Nat Genet. 2007 Jun;39(6):770-5 [17460697.001]
  • [Cites] Science. 2007 Jun 1;316(5829):1331-6 [17463246.001]
  • [Cites] Science. 2007 Jun 1;316(5829):1341-5 [17463248.001]
  • [Cites] Science. 2007 Jun 1;316(5829):1336-41 [17463249.001]
  • [Cites] Exp Cell Res. 2007 Jun 10;313(10):1995-2009 [17531221.001]
  • [Cites] Int J Mol Med. 2007 Jul;20(1):75-8 [17549391.001]
  • [Cites] Science. 2007 Jun 8;316(5830):1491-3 [17478679.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2007 Jul;16(7):1499-502 [17627017.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Oct 2;104(40):15805-10 [17890317.001]
  • [Cites] Nat Genet. 2007 Dec;39(12):1443-52 [17952075.001]
  • [Cites] Histochem Cell Biol. 2008 Jun;129(6):705-33 [18461349.001]
  • [Cites] Nat Genet. 2008 Jul;40(7):886-91 [18488027.001]
  • [Cites] Nat Genet. 2008 Jul;40(7):835-7 [18488028.001]
  • [Cites] Br J Dermatol. 2008 Aug;159(2):286-91 [18547303.001]
  • [Cites] Hum Mutat. 2008 Sep;29(9):1161-7 [18563784.001]
  • [Cites] Hum Mutat. 2008 Sep;29(9):1154-60 [18683857.001]
  • [Cites] Nat Rev Cancer. 2008 Oct;8(10):743-54 [18813320.001]
  • [Cites] Nat Genet. 2008 Nov;40(11):1313-8 [18849993.001]
  • [Cites] J Invest Dermatol. 2009 Feb;129(2):415-21 [18668136.001]
  • [Cites] Nat Genet. 2008 Sep;40(9):1068-75 [19165921.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Jul 7;95(14):8141-6 [9653154.001]
  • (PMID = 19578363.001).
  • [ISSN] 1546-1718
  • [Journal-full-title] Nature genetics
  • [ISO-abbreviation] Nat. Genet.
  • [Language] ENG
  • [Databank-accession-numbers] GENBANK/ DQ485453; RefSeq/ NM/ 000424/ NP/ 000415/ NP/ 001012527
  • [Grant] United States / NCI NIH HHS / CA / R01 CA057494; United States / NCI NIH HHS / CA / R01CA082354; United States / NCI NIH HHS / CA / R01 CA057494-16; United States / PHS HHS / / T32E007155; United States / NCI NIH HHS / CA / R01CA57494; United States / NIEHS NIH HHS / ES / T32 ES007155; United States / NCI NIH HHS / CA / R01 CA082354
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CLPTM1L protein, human; 0 / Keratin-5; 0 / Membrane Proteins; 0 / Neoplasm Proteins
  • [Other-IDs] NLM/ NIHMS216815; NLM/ PMC2973331
  •  go-up   go-down


20. Dunning K, Gopaldas RR, Rohatgi C: The role of amputation in treating large Basal cell carcinomas of the extremity. Plast Reconstr Surg; 2007 May;119(6):1974-6
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.
  • [Title] The role of amputation in treating large Basal cell carcinomas of the extremity.
  • [MeSH-major] Amputation / methods. Arm / surgery. Carcinoma, Basal Cell / surgery. Lymph Nodes / pathology. Neoplasm Invasiveness / pathology. Skin Neoplasms / surgery
  • [MeSH-minor] Aged, 80 and over. Axilla. Biopsy, Needle. Humans. Immunohistochemistry. Neoplasm Staging. Prognosis. Quality of Life. Risk Assessment. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17440409.001).
  • [ISSN] 1529-4242
  • [Journal-full-title] Plastic and reconstructive surgery
  • [ISO-abbreviation] Plast. Reconstr. Surg.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] United States
  •  go-up   go-down


21. Birt B, Cowling I, Coyne S, Michael G: The effect of the eye's surface topography on the total irradiance of ultraviolet radiation on the inner canthus. J Photochem Photobiol B; 2007 Apr 2;87(1):27-36
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.
  • Basal cell carcinoma is the most commonly occurring skin cancer in sub tropical climates.
  • The link between ultraviolet radiation (UVR) and basal cell carcinomas (BCC) is strong.
  • Numerous studies have investigated the spatial distribution of BCCs over the head and neck region and the relative UVR dose, with little or no correlation found between the UVR dose and occurrence rates.
  • Yet, the occurrence rate here of BCC's when compared to other regions that are more directly exposed to the environment is significantly higher.
  • [MeSH-minor] Carcinoma, Basal Cell / epidemiology. Face / radiation effects. Humans. Models, Biological. Models, Theoretical. Skin Neoplasms / epidemiology. Software. Tropical Climate

  • MedlinePlus Health Information. consumer health - Eye Care.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17280839.001).
  • [ISSN] 1011-1344
  • [Journal-full-title] Journal of photochemistry and photobiology. B, Biology
  • [ISO-abbreviation] J. Photochem. Photobiol. B, Biol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  •  go-up   go-down


22. Jordan DR, Belliveau MJ, Brownstein S, McEachren T, Kyrollos M: Medial canthal tophus. Ophthal Plast Reconstr Surg; 2008 Sep-Oct;24(5):403-4
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 raised, nodular lesion was skin colored, had a raised pearly border and a central depression with superficial crusting.
  • Basal cell carcinoma was suspected and an excisional biopsy was performed.
  • Gouty tophi are extremely rare in the periocular area but should be considered in the differential diagnosis of basal cell carcinoma as they may have a similar clinical appearance.

  • MedlinePlus Health Information. consumer health - Eyelid Disorders.
  • MedlinePlus Health Information. consumer health - Gout.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18806664.001).
  • [ISSN] 1537-2677
  • [Journal-full-title] Ophthalmic plastic and reconstructive surgery
  • [ISO-abbreviation] Ophthal Plast Reconstr Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 268B43MJ25 / Uric Acid
  •  go-up   go-down


23. Leibovitch I, McNab A, Sullivan T, Davis G, Selva D: Orbital invasion by periocular basal cell carcinoma. Ophthalmology; 2005 Apr;112(4):717-23
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.
  • [Title] Orbital invasion by periocular basal cell carcinoma.
  • OBJECTIVES: To present a large series of patients with orbital invasion by periocular basal cell carcinoma (BCC).
  • DESIGN: Retrospective, noncomparative, interventional case series.
  • PATIENTS: All cases diagnosed with orbital invasion by periocular BCC between January 1985 and July 2004 in 3 Orbital Units in Australia.
  • MAIN OUTCOME MEASURES: Patients' demographics, clinical presentation, histologic subtypes, treatment modalities, recurrence rate, and tumor-related death.
  • During a mean follow-up period of 3.6 years, 3 cases of recurrence (4.7%) were diagnosed.
  • Only 1 patient (1.6%) died from tumor-related causes.
  • CONCLUSIONS: Orbital invasion by periocular BCC is an uncommon event that may be associated with significant ocular morbidity and, rarely, death.
  • [MeSH-major] Carcinoma, Basal Cell / secondary. Eyelid Neoplasms / pathology. Neoplasm Recurrence, Local. Orbital Neoplasms / secondary
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Combined Modality Therapy. Female. Humans. Male. Middle Aged. Neoplasm Invasiveness. Orbit Evisceration. Peripheral Nervous System Neoplasms / radiotherapy. Peripheral Nervous System Neoplasms / secondary. Peripheral Nervous System Neoplasms / surgery. Radiotherapy. Retrospective Studies. Tomography, X-Ray Computed

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15808267.001).
  • [ISSN] 1549-4713
  • [Journal-full-title] Ophthalmology
  • [ISO-abbreviation] Ophthalmology
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] United States
  •  go-up   go-down


24. Terrill PJ, Fairbanks S, Bailey M: Is there just one lesion? The need for whole body skin examination in patients presenting with non-melanocytic skin cancer. ANZ J Surg; 2009 Oct;79(10):707-12
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.
  • [Title] Is there just one lesion? The need for whole body skin examination in patients presenting with non-melanocytic skin cancer.
  • BACKGROUND: In patients presenting with non-melanoma skin cancer (NMSC) the frequency of concurrently presenting tumours is poorly documented.
  • Whole body skin examination is recommended but in a recent survey of Australian General Practitioners and skin cancer clinics doctors it was infrequently performed.
  • The aim of this study was to examine the incidence of concurrent skin cancer at initial presentation and therefore to examine the need for whole body skin examination for NMSC presentations.
  • METHOD: One hundred consecutive patients with a referral diagnosis indicative of NMSC were examined.
  • Data was analysed as to the referring doctor's diagnosis, whole body skin examination findings and histology of excised lesions.
  • RESULTS: One hundred patients, 41 males and 59 females, with a mean age of 70 years (range 39-91 years) underwent whole body skin examination.
  • Sixty-seven per cent of patients were found to have additional lesions requiring treatment, 46% sin cancers (30 patients basal cell carcinomas, five squamous cell carcinomas, seven basal and squamous cell carcinomas, two lentigo maligna, two adenexal tumours) and 21% solar keratoses.
  • Sixty-eight patients had a past history of skin cancer excision.
  • CONCLUSIONS: In the Australian patient population, the need for whole body skin examination is essential to avoid missing concurrent lesions.
  • [MeSH-major] Physical Examination / methods. Skin Neoplasms / diagnosis
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Australia / epidemiology. Diagnosis, Differential. Female. Humans. Incidence. Male. Middle Aged. Reproducibility of Results. Retrospective Studies. Surveys and Questionnaires

  • MedlinePlus Health Information. consumer health - Health Checkup.
  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19878165.001).
  • [ISSN] 1445-2197
  • [Journal-full-title] ANZ journal of surgery
  • [ISO-abbreviation] ANZ J Surg
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Australia
  •  go-up   go-down


25. Varga Z, Mallon E: Histology and immunophenotype of invasive lobular breast cancer. daily practice and pitfalls. Breast Dis; 2008-2009;30:15-9
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.
  • [Title] Histology and immunophenotype of invasive lobular breast cancer. daily practice and pitfalls.
  • Invasive lobular carcinomas (ILC) represent the most common subtype of invasive breast cancer and account for about 5-15% of all breast cancer cases.
  • Invasive lobular carcinoma is often accompanied by in situ lesions, by lobular neoplasia (LN).
  • Invasive lobular carcinomas display diverse histologic patterns varying from classical through solid to pleomorphic subtypes.
  • The majority of invasive lobular carcinomas are hormone receptor positive, overexpression and/or amplification of the Her2 gene is lower than in carcinomas of invasive ductal type.
  • Loss of heterozygosity of the 16q chromosomal regions and the consequent lack of E-Cadherin expression are common findings in invasive lobular carcinomas.
  • Intra-operative evaluation of resection margins in ILC is often unsatisfactory due to the diffuse nature of the tumor.
  • [MeSH-major] Breast Neoplasms / pathology. Carcinoma, Lobular / pathology
  • [MeSH-minor] Carcinoma, Ductal, Breast / immunology. Carcinoma, Ductal, Breast / pathology. Diagnosis, Differential. Female. Humans. Immunohistochemistry. Neoplasm Grading. Prognosis


26. Cheng CY, Mei HC, Tsao CF, Liao YR, Huang HH, Chung YC: Diversity of the bacterial community in a bioreactor during ammonia gas removal. Bioresour Technol; 2010 Jan;101(1):434-7
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.
  • Polymerase chain reaction analysis in combination with denaturing gradient gel electrophoresis (DGGE) was used to determine changes in the composition of the bacterial community of a bioreactor during ammonia removal.
  • However, the occurrence and predominance of specific bacterial species varied with the concentrations of NH(3) introduced into the bioreactor.
  • The complexity of the bacterial species generally decreased with increasing inlet NH(3) concentration.
  • The strains identified in this study are potential candidate strains for the purification of waste gases containing high concentrations of NH(3).

  • Hazardous Substances Data Bank. Ammonia .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19716695.001).
  • [ISSN] 1873-2976
  • [Journal-full-title] Bioresource technology
  • [ISO-abbreviation] Bioresour. Technol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Gases; 0 / Industrial Waste; 7664-41-7 / Ammonia
  •  go-up   go-down


27. Flanagan AM, Rafferty G, O'Neill A, Rynne L, Kelly J, McCann J, Carty MP: The human POLH gene is not mutated, and is expressed in a cohort of patients with basal or squamous cell carcinoma of the skin. Int J Mol Med; 2007 Apr;19(4):589-96
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.
  • [Title] The human POLH gene is not mutated, and is expressed in a cohort of patients with basal or squamous cell carcinoma of the skin.
  • Skin cancer, the most common cancer in the general population, is strongly associated with exposure to the ultraviolet component of sunlight.
  • To investigate the relationship between DNA damage processing and skin tumour development, we determined the POLH status of a cohort of skin cancer patients.
  • In the absence of active poleta in xeroderma pigmentosum variant (XPV) patients, mutations accumulate at sites of UV-induced DNA damage, providing the initiating step in skin carcinogenesis.
  • Forty patients diagnosed with skin cancer were genotyped for polymorphisms in the POLH protein-coding sequence, using glycosylase-mediated polymorphism detection (GMPD) and direct DNA sequencing of POLH PCR products derived from white blood cell genomic DNA.
  • No POLH mutations were identified in genomic DNA from skin tumours derived from 15 of these patients.
  • As determined by RT-PCR, POLH mRNA was expressed in all normal and skin tumour tissue examined.
  • Poleta protein was also detectable by Western blotting, in two matched normal and skin tumour extracts.
  • An alternatively spliced form of POLH mRNA, lacking exon 2, was more readily detected in skin tissue than in white blood cells from the same patient.
  • Real-time PCR was used to quantify POLH expression in matched normal and skin tumour-derived mRNA from a series of patients diagnosed with either basal or squamous cell carcinoma.
  • Compared to matched normal skin tissue from the same patient, 1 of 7 SCC, and 4 of 10 BCC tumours examined showed at least a 2-fold reduction in POLH expression, while 1 of 7 SCC, and 3 of 10 BCC tumours showed at least a 2-fold increase in POLH expression.
  • Differences in gene expression, rather than sequence changes may be the main mechanism by which POLH status varies between normal and skin tumours in the population under investigation.
  • Knowledge of the POLH status in skin tumours could contribute to an understanding of the role of this gene in the development of the most common cancer in the general population.
  • [MeSH-major] Carcinoma, Squamous Cell / genetics. DNA-Directed DNA Polymerase / genetics. Gene Expression. Skin Neoplasms / genetics

  • Genetic Alliance. consumer health - Carcinoma, Squamous Cell.
  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • COS Scholar Universe. author profiles.
  • 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
  • (PMID = 17334634.001).
  • [ISSN] 1107-3756
  • [Journal-full-title] International journal of molecular medicine
  • [ISO-abbreviation] Int. J. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / RNA, Messenger; EC 2.7.7.7 / DNA-Directed DNA Polymerase; EC 2.7.7.7 / Rad30 protein
  •  go-up   go-down


28. Chew YK, Noorizan Y, Khir A, Brito-Mutunayagam S, Prepagaran N: The use of paramedian forehead flap reconstruction after wide excision of basal cell carcinoma of the nose. Med J Malaysia; 2008 Oct;63(4):339-40
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.
  • [Title] The use of paramedian forehead flap reconstruction after wide excision of basal cell carcinoma of the nose.
  • Basal cell carcinoma (BCC) is an indolent, slow-growing malignant skin tumour.
  • The nose is a common site for malignant skin tumours, such as basal cell carcinoma and squamous cell carcinoma because it is exposed to the sun.
  • Excision of the BCC will leave the nose with a soft tissue defect which requires reconstruction.
  • This report illustrates a case of BCC of nose whereby a wide excision and reconstruction was performed with a paramedian forehead flap.
  • [MeSH-major] Carcinoma, Basal Cell / surgery. Nose Neoplasms / surgery. Rhinoplasty / methods. Surgical Flaps

  • MedlinePlus Health Information. consumer health - Nasal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19385500.001).
  • [ISSN] 0300-5283
  • [Journal-full-title] The Medical journal of Malaysia
  • [ISO-abbreviation] Med. J. Malaysia
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Malaysia
  •  go-up   go-down


29. Bori R, Cserni G: Basal phenotype in breast carcinoma occurring in women aged 35 or younger. Pathol Oncol Res; 2009 Mar;15(1):41-5
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.
  • [Title] Basal phenotype in breast carcinoma occurring in women aged 35 or younger.
  • Breast cancer in the young is considered a special clinical presentation of the disease.
  • Sixty-nine breast cancer cases diagnosed at or before the age of 35 were analyzed for common morphological and immunophenotypical features of basal-like carcinomas.
  • Sixteen carcinomas displayed the immunophenotypical characteristics (estrogen receptor and HER2 negativity and positivity for at least one of the following basal markers: cytokeratin 5 or 14, epidermal growth factor receptor, p63) of basal-like carcinomas, and most of them demonstrated characteristic histological features (pushing borders, lymphocytic peritumoral infiltrate, central hypocellular zone or necrosis, high mitotic rate) too.
  • The presence of a basal-like phenotype can be important as concerns systemic treatment issues and could theoretically be associated with a higher rate of BRCA1 mutations in the young, because of the overlap of BRCA1 mutation associated breast carcinomas and the basal-like phenotype.
  • [MeSH-major] Breast Neoplasms / pathology. Carcinoma, Basal Cell / pathology
  • [MeSH-minor] Adult. Female. Humans. Immunoenzyme Techniques. Keratins / metabolism. Phenotype. Tissue Array Analysis. Tumor Suppressor Proteins / metabolism. Young Adult


30. Boehm I: Apoptosis in physiological and pathological skin: implications for therapy. Curr Mol Med; 2006 Jun;6(4):375-94
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.
  • [Title] Apoptosis in physiological and pathological skin: implications for therapy.
  • Dysregulated apoptosis is associated with various pathological conditions, including inflammation, and cancer.
  • Acanthosis, the hallmark of psoriatic skin, is an example for diminished epidermal apoptosis.
  • Experimental evidence suggests a role for Bcl-2 and CD95L in the inhibition of programmed cell death in UV-induced skin cancer or malignant melanoma cells.
  • Thus, it leads to survival of malignant cell clones.
  • The slow growth of basal cell carcinomas is due to an increased apoptosis to mitosis ratio.
  • Malignant melanoma cells characteristically show different anti-apoptotic strategies which underscore its aggressive behavior and its refractory towards classic therapeutic regimens.
  • Additionally, induction of apoptosis in tumor infiltrating immune cells seems to be a strategy by which the tumor escapes from an immunological attack (tumor counter-attack).
  • [MeSH-major] Apoptosis. Skin / cytology. Skin / pathology. Skin Diseases / pathology. Skin Diseases / therapy
  • [MeSH-minor] Animals. Cell Differentiation. Humans. Keratinocytes / cytology

  • MedlinePlus Health Information. consumer health - Skin Conditions.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16900661.001).
  • [ISSN] 1566-5240
  • [Journal-full-title] Current molecular medicine
  • [ISO-abbreviation] Curr. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Number-of-references] 205
  •  go-up   go-down


31. Ying MG, Chen Q, Ye YB, Chen HJ, Chen X, Zheng HY, Wu F: [Application of serum proteomic mass spectrum analysis in breast cancer]. Zhonghua Zhong Liu Za Zhi; 2010 Sep;32(9):698-702
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.
  • [Title] [Application of serum proteomic mass spectrum analysis in breast cancer].
  • OBJECTIVE: To analyze the characteristics of serum proteins mass spectra in healthy controls, benign breast tumors, and CA15-3 negative or CA15-3 positive breast cancer patients by surface enhanced laser desorption ionization time of flight mass spectrometry (SELDI-TOF-MS).
  • METHODS: Tissue samples of 113 cases of breast cancer (93 case of CA15-3 negative, 20 case of CA15-3 positive), 103 cases of benign breast tumor and 92 cases of healthy controls were examined and analyzed by SELDI and protein chip (CM10) techniques.
  • RESULTS: Twelve significantly different protein peaks were found in serum samples between breast cancer patients and healthy controls.
  • Eleven significantly different peaks were found between benign breast tumor patients and healthy controls.
  • By combined analysis of those three different protein mass spectra, the peak 15 952 was found to be significantly different between breast cancer group and healthy controls, and the peak 7985 was significantly different among breast cancer group, benign breast tumor group and health controls.
  • The blind test with the differential proteins for the serum samples of 93 cases of CA15-3 negative breast cancer and 36 cases of benign breast tumors showed that the sensitivity was 80.6% and specificity was 91.7%.
  • The blind test in 20 cases of CA15-3 positive breast cancer and 36 cases of benign breast tumors showed that the sensitivity was 75.0% and specificity was 91.7%.
  • Four significantly different protein peaks were found between the benign breast tumor patients and CA15-3 negative breast cancer patients.
  • CONCLUSION: Significantly different protein peaks can be screened out in breast cancer, benign breast tumor patients and healthy controls by SELDI-TOF-MS analysis.
  • [MeSH-major] Blood Proteins / metabolism. Breast Neoplasms / diagnosis. Carcinoma, Ductal, Breast / diagnosis. Fibroadenoma / diagnosis. Proteomics / methods
  • [MeSH-minor] Adenoma / blood. Adenoma / diagnosis. Adenoma / metabolism. Adult. Aged. Biomarkers, Tumor / blood. Case-Control Studies. Female. Humans. Middle Aged. Mucin-1 / metabolism. Protein Array Analysis. Sensitivity and Specificity. Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization

  • Genetic Alliance. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 21122387.001).
  • [ISSN] 0253-3766
  • [Journal-full-title] Zhonghua zhong liu za zhi [Chinese journal of oncology]
  • [ISO-abbreviation] Zhonghua Zhong Liu Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Blood Proteins; 0 / Mucin-1
  •  go-up   go-down


32. Larson PS, Schlechter BL, King CL, Yang Q, Glass CN, Mack C, Pistey R, de Las Morenas A, Rosenberg CL: CDKN1C/p57kip2 is a candidate tumor suppressor gene in human breast cancer. BMC Cancer; 2008 Mar 06;8:68
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] CDKN1C/p57kip2 is a candidate tumor suppressor gene in human breast cancer.
  • BACKGROUND: CDKN1C (also known as p57KIP2) is a cyclin-dependent kinase inhibitor previously implicated in several types of human cancer.
  • Its family members (CDKN1A/p21CIP1 and B/p27KIP1) have been implicated in breast cancer, but information about CDKN1C's role is limited.
  • We hypothesized that decreased CDKN1C may be involved in human breast carcinogenesis in vivo.
  • METHODS: We determined rates of allele imbalance or loss of heterozygosity (AI/LOH) in CDKN1C, using an intronic polymorphism, and in the surrounding 11p15.5 region in 82 breast cancers.
  • Similarly, CDKN1C protein staining was seen in 19/20 (95%) cases' normal epithelium but in only 7/14 (50%) cases' CIS (p < 0.004) and 5/18 (28%) cases' IC (p < 0.00003).
  • Decreased CDKN1C was not clearly associated with tumor grade, histology, ER, PR or HER2 status.
  • CONCLUSION: CDKN1C is expressed in normal epithelium of most breast cancer cases, mainly in the myothepithelial layer.
  • This expression decreases, at both the mRNA and protein level, in the large majority of breast cancers, and does not appear to be mediated by AI/LOH at the gene.
  • Thus, CDKN1C may be a breast cancer tumor suppressor.


33. Vachon CM, Brandt KR, Ghosh K, Scott CG, Maloney SD, Carston MJ, Pankratz VS, Sellers TA: Mammographic breast density as a general marker of breast cancer risk. Cancer Epidemiol Biomarkers Prev; 2007 Jan;16(1):43-9
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] Mammographic breast density as a general marker of breast cancer risk.
  • Mammographic breast density is a strong risk factor for breast cancer but whether breast density is a general marker of susceptibility or is specific to the location of the eventual cancer is unknown.
  • A study of 372 incident breast cancer cases and 713 matched controls was conducted within the Mayo Clinic mammography screening practice.
  • Mammograms on average 7 years before breast cancer were digitized, and quantitative measures of percentage density and dense area from each side and view were estimated.
  • Location of breast cancer and potential confounders were abstracted from medical records.
  • There were increasing trends in breast cancer risk with increasing quartiles of percentage density and dense area, irrespective of the side of the breast with cancer (P(trends) < 0.001).
  • Percentage density from the ipsilateral side [craniocaudal (CC): odds ratios (ORs), 1.0 (ref), 1.7, 3.1, and 3.1; mediolateral oblique (MLO): ORs, 1.0 (ref), 1.5, 2.2, and 2.8] and the contralateral side [CC: ORs, 1.0 (ref), 1.8, 2.2, and 3.7; MLO: ORs, 1.0 (ref), 1.6, 1.9, and 2.5] similarly predicted case-control status (C-statistics, 0.64-65).
  • Accounting for overall percentage density, density in the region where the cancer subsequently developed was not a significant risk factor [CC: 1.0 (ref), 1.3, 1.0, and 1.2; MLO: 1.0 (ref), 1.1, 1.0, and 1.1 for increasing quartiles].
  • Results did not change when examining mammograms 3 years on average before the cancer.
  • Overall mammographic density seems to represent a general marker of breast cancer risk that is not specific to breast side or location of the eventual cancer.
  • [MeSH-major] Breast Neoplasms / radiography. Mammography
  • [MeSH-minor] Case-Control Studies. Female. Humans. Mass Screening. Minnesota. Odds Ratio. Radiographic Image Enhancement. Risk Factors. Time Factors

  • Genetic Alliance. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Mammography.
  • COS Scholar Universe. author profiles.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17220330.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA97396
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  •  go-up   go-down


34. Koh WP, Yuan JM, Van Den Berg D, Lee HP, Yu MC: Polymorphisms in angiotensin II type 1 receptor and angiotensin I-converting enzyme genes and breast cancer risk among Chinese women in Singapore. Carcinogenesis; 2005 Feb;26(2):459-64
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.
  • [Title] Polymorphisms in angiotensin II type 1 receptor and angiotensin I-converting enzyme genes and breast cancer risk among Chinese women in Singapore.
  • Angiotensin II is converted from its precursor by angiotensin I-converting enzyme (ACE) and has been shown to mediate growth in breast cancer cell lines via ligand-induced activity through the angiotensin II type 1 receptor (AGTR1).
  • Earlier we showed that women with the low activity genotype of the ACE gene have a statistically significantly ( approximately 50%) reduced breast cancer risk compared with those possessing the high activity ACE genotype.
  • To further test the hypothesis that angiotensin II participates in breast carcinogenesis through AGTR1, we examined genetic polymorphisms in the 5'-region of the AGTR1 gene (A-168G, C-535T and T-825A) in relation to risk of breast cancer in 258 breast cancer cases and 670 female controls within the Singapore Chinese Health Study.
  • Relative to the homozygotes, individual genotypes with one or two copies of the respective allelic variants (putative low risk genotypes) were each associated with an approximately 30% reduction in risk of breast cancer.
  • Risk of breast cancer decreased with increasing number of low risk AGTR1 genotypes after adjustment for potential confounders.
  • Our findings suggest that pharmacological inhibition of the angiotensin II effect by blockade of ACE and/or AGTR1 could be potential targets for the prevention and treatment of breast cancer.
  • [MeSH-major] Breast Neoplasms / genetics. Genetic Predisposition to Disease. Peptidyl-Dipeptidase A / genetics. Polymorphism, Single Nucleotide / genetics. Receptor, Angiotensin, Type 1 / genetics
  • [MeSH-minor] Aged. Alleles. Case-Control Studies. China. Female. Humans. Middle Aged. Singapore

  • Genetic Alliance. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15498791.001).
  • [ISSN] 0143-3334
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA55069; United States / NCI NIH HHS / CA / R01 CA80205; United States / NCI NIH HHS / CA / R35 CA53890
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Receptor, Angiotensin, Type 1; EC 3.4.15.1 / Peptidyl-Dipeptidase A
  •  go-up   go-down


35. Lin HY, Cheng CY, Hsu WM, Kao WH, Chou P: Incidence of eyelid cancers in Taiwan: a 21-year review. Ophthalmology; 2006 Nov;113(11):2101-7
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.
  • DESIGN: Retrospective population-based cancer registry data review.
  • PARTICIPANTS: A total of 1166 primary eyelid cancers coded to International Classification of Diseases 8 or 9, site 172.1 (malignant melanoma of eyelid) and 173.1 (other malignant neoplasm of eyelid) were retrieved from the Taiwan National Cancer Registry between January 1979 and December 1999.
  • We further examined the effects of age, period of diagnosis, and birth cohort on incidence trends using age-period-cohort analysis.
  • RESULTS: The mean age at diagnosis of eyelid cancers was 62.6+/-14.1 years.
  • The most common eyelid malignancy was basal cell carcinoma (BCC; 65.1%), followed by squamous cell carcinoma (12.6%), and sebaceous cell carcinoma (7.9%).
  • The increasing rates were mainly driven by an increase in the incidence of BCC.
  • Cohort effects were found to play a major role in terms of model fit for the incidence trends of BCC.
  • Basal cell carcinoma dominates the incidence trends, and the significant cohort effects give a warning of increasing risk of BCC in younger birth cohorts.
  • [MeSH-major] Carcinoma, Basal Cell / epidemiology. Eyelid Neoplasms / epidemiology
  • [MeSH-minor] Adenocarcinoma, Sebaceous / epidemiology. Adolescent. Adult. Aged. Aged, 80 and over. Carcinoma, Squamous Cell / epidemiology. Child. Child, Preschool. Female. Humans. Male. Middle Aged. Registries. Retrospective Studies. Sebaceous Gland Neoplasms / epidemiology. Taiwan / epidemiology

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16962174.001).
  • [ISSN] 1549-4713
  • [Journal-full-title] Ophthalmology
  • [ISO-abbreviation] Ophthalmology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down


36. Mateju M, Stribrna J, Zikan M, Kleibl Z, Janatova M, Kormunda S, Novotny J, Soucek P, Petruzelka L, Pohlreich P: Population-based study of BRCA1/2 mutations: family history based criteria identify minority of mutation carriers. Neoplasma; 2010;57(3):280-5
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.
  • The two major susceptibility genes, BRCA1 and BRCA2, are involved in hereditary breast and ovarian cancer syndrome.
  • Generally accepted inclusion criteria for BRCA1/2 mutation testing are based either upon family history of breast or ovarian cancer or young age at cancer diagnosis.
  • In order to analyze the impact of BRCA1/2 mutations on breast cancer development in the Czech population and to confront the clinical and histopathological data of mutation carriers with current criteria for mutation testing we examined the frequency of mutations in unselected breast cancer cases.
  • Mutational analysis of BRCA1/2 genes performed in 679 unselected female breast cancer patients included all recurrent deleterious alterations previously identified in the Prague area and truncating mutations in the whole exon 11 of BRCA1.
  • A total of 16 breast cancer patients (2.4%) carried a mutation.
  • Family history of ovarian cancer was a strong predictor of a BRCA1/2 mutation (OR = 8.3; p = 0.01), however, family history of breast cancer was not indicative of carrier status.
  • A significant association between medullary breast cancer and mutation status was observed.
  • Ten breast cancer patients with confirmed BRCA1/2 germ-line mutation exhibited no clinical characteristics that would predict their carrier status.
  • Our results indicate that analysis of locally prevalent BRCA1/2 mutations in all breast cancer patients might extend substantially the percentage of identified mutation carriers.
  • [MeSH-major] Breast Neoplasms / genetics. Genes, BRCA1. Genes, BRCA2. Heterozygote Detection. Mutation

  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • 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
  • (PMID = 20353281.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Slovakia
  •  go-up   go-down


37. Perrett CM, Tan SK, Cerio R, Goldsmith PC, McGregor JM, Proby CM, Harwood CA: Treatment of basal cell carcinoma with topical methylaminolaevulinate photodynamic therapy in an organ-transplant recipient. Clin Exp Dermatol; 2006 Jan;31(1):146-7
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.
  • [Title] Treatment of basal cell carcinoma with topical methylaminolaevulinate photodynamic therapy in an organ-transplant recipient.
  • [MeSH-major] Aminolevulinic Acid / analogs & derivatives. Carcinoma, Basal Cell / drug therapy. Liver Transplantation. Nose Neoplasms / drug therapy. Photochemotherapy / methods. Photosensitizing Agents / administration & dosage
  • [MeSH-minor] Administration, Topical. Female. Humans. Middle Aged. Skin Neoplasms / drug therapy. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Liver Transplantation.
  • MedlinePlus Health Information. consumer health - Nasal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16309518.001).
  • [ISSN] 0307-6938
  • [Journal-full-title] Clinical and experimental dermatology
  • [ISO-abbreviation] Clin. Exp. Dermatol.
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Photosensitizing Agents; 0 / methyl 5-aminolevulinate; 88755TAZ87 / Aminolevulinic Acid
  •  go-up   go-down


38. Sharma NL, Mehta KI, Mahajan VK, Kanga AK, Sharma VC, Tegta GR: Cutaneous sporotrichosis of face: polymorphism and reactivation after intralesional triamcinolone. Indian J Dermatol Venereol Leprol; 2007 May-Jun;73(3):188-90
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.
  • We describe a culture-proven case of cutaneous sporotrichosis of the face mimicking lupus vulgaris initially and basal cell carcinoma later, who did not tolerate potassium iodide and failed to respond to treatment with fluconazole.

  • Genetic Alliance. consumer health - Sporotrichosis.
  • MedlinePlus Health Information. consumer health - Facial Injuries and Disorders.
  • Hazardous Substances Data Bank. TRIAMCINOLONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17558054.001).
  • [ISSN] 0973-3922
  • [Journal-full-title] Indian journal of dermatology, venereology and leprology
  • [ISO-abbreviation] Indian J Dermatol Venereol Leprol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] India
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Antifungal Agents; 1ZK20VI6TY / Triamcinolone
  •  go-up   go-down


39. Pennington BE, Leffell DJ: Mohs micrographic surgery: established uses and emerging trends. Oncology (Williston Park); 2005 Aug;19(9):1165-71; discussion 1171-2, 1175
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.
  • This is accomplished through the sequential removal of thin layers of tissue in which the entire peripheral and deep margins are examined for residual tumor.
  • This approach appears to be superior to conventional surgical excision in the treatment of basal cell carcinoma (BCC) and squamous cell carcinoma (SCC), the two most common cancers of the skin.
  • Its efficacy in treating BCC and SCC has led clinicians to explore the role of Mohs micrographic surgery in the management of less common cutaneous neoplasms, such as melanoma, Merkel cell carcinoma, dermatofibrosarcoma protuberans, extramammary Paget's disease, and microcystic adnexal carcinoma.
  • [MeSH-minor] Adenoma / surgery. Carcinoma, Basal Cell / surgery. Carcinoma, Merkel Cell / surgery. Carcinoma, Squamous Cell / surgery. Dermatofibrosarcoma / surgery. Humans. Melanoma / surgery. Paget Disease, Extramammary / surgery. Skin Neoplasms / surgery

  • COS Scholar Universe. author profiles.
  • 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
  • (PMID = 16255133.001).
  • [ISSN] 0890-9091
  • [Journal-full-title] Oncology (Williston Park, N.Y.)
  • [ISO-abbreviation] Oncology (Williston Park, N.Y.)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


40. Hafner C: [Targeted therapy of basal cell carcinoma through inhibition of the hedgehog signaling pathway]. Hautarzt; 2010 Apr;61(4):356-8
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.
  • [Title] [Targeted therapy of basal cell carcinoma through inhibition of the hedgehog signaling pathway].
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Carcinoma, Basal Cell / drug therapy. Drug Delivery Systems / methods. Hedgehog Proteins / antagonists & inhibitors. Signal Transduction / drug effects. Skin Neoplasms / drug therapy

  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cell. 1996 Jun 14;85(6):841-51 [8681379.001]
  • [Cites] N Engl J Med. 2005 Nov 24;353(21):2262-9 [16306523.001]
  • [Cites] N Engl J Med. 2009 Sep 17;361(12 ):1173-8 [19726761.001]
  • [Cites] N Engl J Med. 2009 Sep 17;361(12 ):1164-72 [19726763.001]
  • [Cites] Science. 2009 Oct 23;326(5952):572-4 [19726788.001]
  • (PMID = 20309511.001).
  • [ISSN] 1432-1173
  • [Journal-full-title] Der Hautarzt; Zeitschrift fur Dermatologie, Venerologie, und verwandte Gebiete
  • [ISO-abbreviation] Hautarzt
  • [Language] ger
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Hedgehog Proteins
  •  go-up   go-down


41. Ghaderi R, Haghighi F: Immunohistochemistry assessment of p53 protein in Basal cell carcinoma. Iran J Allergy Asthma Immunol; 2005 Dec;4(4):167-71
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] Immunohistochemistry assessment of p53 protein in Basal cell carcinoma.
  • The most frequently mutated tumor suppressor gene found in human cancer is p53.
  • In a normal situation, p53 is activated upon the induction of DNA damage to either arrest the cell cycle or else induce apoptosis.
  • Our aim was to investigate p53 protein alteration in cases of basal cell carcinoma (BCC) and compare it with the control group.
  • We investigated P53 gene expression in 41 cases of basal cell carcinoma and 20 patients with benign skin disease as control group.
  • The Data were analyzed using SPSS package, T and Chi-Square tests.Twenty eight out of 41 basal cell carcinoma and 3 out of 20 control were p53-mutated, and there was a statistically significant difference in cases of BCC in comparison with controls (x2 test; p= 0.0001).Taken together, showing alteration of p53 protein, our findings could add to the knowledge that might contribute to the self-maintenance of cancer cells and development of basal cell carcinoma.

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17301441.001).
  • [ISSN] 1735-1502
  • [Journal-full-title] Iranian journal of allergy, asthma, and immunology
  • [ISO-abbreviation] Iran J Allergy Asthma Immunol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Iran
  •  go-up   go-down


42. Lott DG, Akst LM, Greene D, Roberts JK: T-cell primary cutaneous anaplastic large cell lymphoma mimicking appearance of large basal cell carcinoma. Otolaryngol Head Neck Surg; 2006 Jul;135(1):170-1
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.
  • [Title] T-cell primary cutaneous anaplastic large cell lymphoma mimicking appearance of large basal cell carcinoma.
  • [MeSH-major] Carcinoma, Basal Cell / pathology. Lymphoma, T-Cell, Cutaneous / pathology. Skin Neoplasms / pathology
  • [MeSH-minor] Aged. Biopsy. Diagnosis, Differential. Follow-Up Studies. Humans. Male


43. Mizuno S, Isaji S, Ogawa T, Tabata M, Yamagiwa K, Yokoi H, Uemoto S: Approach to fine-needle aspiration cytology-negative cases of breast cancer. Asian J Surg; 2005 Jan;28(1):13-7
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] Approach to fine-needle aspiration cytology-negative cases of breast cancer.
  • OBJECTIVE: To clarify the clinical usefulness of fine-needle aspiration (FNA) cytology of breast tumours and the management of FNA cytology-negative cases suspected of or equivocal for malignancy.
  • We calculated the sensitivity, specificity and accuracy of FNA cytology for the diagnosis of malignancy.
  • We also compared clinical and radiological findings between false-negative and true-negative cases.
  • There were seven false-negative cases and one false-positive case.
  • Findings that aroused suspicion of malignancy were more frequent in the false-negative cases, especially from mammography and magnetic resonance imaging (MRI).
  • CONCLUSION: FNA cytology was an accurate preoperative diagnostic procedure for the evaluation of breast masses.
  • In FNA cytology-negative cases, repeated FNA, core needle biopsy or excisional biopsy needs to be performed based on MRI findings.

  • Genetic Alliance. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15691791.001).
  • [ISSN] 1015-9584
  • [Journal-full-title] Asian journal of surgery
  • [ISO-abbreviation] Asian J Surg
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] China
  •  go-up   go-down


44. Lee SA, Haiman CA, Burtt NP, Pooler LC, Cheng I, Kolonel LN, Pike MC, Altshuler D, Hirschhorn JN, Henderson BE, Stram DO: A comprehensive analysis of common genetic variation in prolactin (PRL) and PRL receptor (PRLR) genes in relation to plasma prolactin levels and breast cancer risk: the multiethnic cohort. BMC Med Genet; 2007 Dec 01;8:72
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] A comprehensive analysis of common genetic variation in prolactin (PRL) and PRL receptor (PRLR) genes in relation to plasma prolactin levels and breast cancer risk: the multiethnic cohort.
  • BACKGROUND: Studies in animals and humans clearly indicate a role for prolactin (PRL) in breast epithelial proliferation, differentiation, and tumorigenesis.
  • Prospective epidemiological studies have also shown that women with higher circulating PRL levels have an increase in risk of breast cancer, suggesting that variability in PRL may also be important in determining a woman's risk.
  • METHODS: We evaluated genetic variation in the PRL and PRL receptor (PRLR) genes as predictors of plasma PRL levels and breast cancer risk among African-American, Native Hawaiian, Japanese-American, Latina, and White women in the Multiethnic Cohort Study (MEC).
  • We sequenced the coding regions of PRL and PRLR in 95 advanced breast cancer cases (19 of each racial/ethnic group) to uncover putative functional variation.
  • A total of 33 and 60 haplotype "tag" SNPs (tagSNPs) that allowed for high predictability (Rh2 > or = 0.70) of the common haplotypes in PRL and PRLR, respectively, were then genotyped in a multiethnic breast cancer case-control study of 1,615 invasive breast cancer cases and 1,962 controls in the MEC.
  • RESULTS: We observed no significant associations between PRL and PRLR haplotypes or individual SNPs in relation to breast cancer risk.
  • However, this association was not significant (p = 0.002) using our type I error criteria to correct for multiple testing, nor was this SNP associated with breast cancer risk (p = 0.58).
  • CONCLUSION: In this comprehensive analysis covering 59 kb of the PRL locus and 210 kb of the PRLR locus, we found no significant association between common variation in these candidate genes and breast cancer risk or plasma PRL levels.
  • The LD characterization of PRL and PRLR in this multiethnic population provide a framework for studying these genes in relation to other disease outcomes that have been associated with PRL, as well as for larger studies of plasma PRL levels.

  • Genetic Alliance. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • COS Scholar Universe. author profiles.
  • Guide to Pharmacology. gene/protein/disease-specific - Prolactin-releasing peptide receptor - overview and references .
  • Guide to Pharmacology. gene/protein/disease-specific - PrRP receptor - data and references .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Endocrinology. 1999 Nov;140(11):5447-50 [10537179.001]
  • [Cites] Clin Chem. 1989 Dec;35(12):2313-6 [2591049.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2000 Jun;9(6):575-9 [10868691.001]
  • [Cites] Arthritis Rheum. 2001 Oct;44(10):2358-66 [11665977.001]
  • [Cites] J Biol Chem. 2001 Nov 2;276(44):41086-94 [11518703.001]
  • [Cites] Lupus. 2001;10(10):676-83 [11721693.001]
  • [Cites] Mol Endocrinol. 2002 Jan;16(1):45-57 [11773438.001]
  • [Cites] Endocrinology. 2002 Jun;143(6):2139-42 [12021177.001]
  • [Cites] Hum Hered. 2002;53(2):79-91 [12037407.001]
  • [Cites] Science. 2002 Jun 21;296(5576):2225-9 [12029063.001]
  • [Cites] Trends Endocrinol Metab. 2002 Aug;13(6):245-50 [12128285.001]
  • [Cites] Science. 2002 Dec 20;298(5602):2381-5 [12493913.001]
  • [Cites] J Mol Endocrinol. 2003 Feb;30(1):31-47 [12580759.001]
  • [Cites] Endocr Rev. 2003 Feb;24(1):1-27 [12588805.001]
  • [Cites] Breast Cancer Res Treat. 2003 May;79(2):241-52 [12825859.001]
  • [Cites] Hum Hered. 2003;55(1):27-36 [12890923.001]
  • [Cites] Hum Mol Genet. 2003 Oct 15;12(20):2679-92 [12944421.001]
  • [Cites] Am J Pathol. 1995 Mar;146(3):695-705 [7534043.001]
  • [Cites] Mol Biol Evol. 1995 Sep;12(5):921-7 [7476138.001]
  • [Cites] J Clin Endocrinol Metab. 1997 Nov;82(11):3692-9 [9360527.001]
  • [Cites] Cytogenet Cell Genet. 1990;53(2-3):161-5 [2369845.001]
  • [Cites] J Biol Chem. 1990 Sep 25;265(27):16412-21 [1697858.001]
  • [Cites] Med J Aust. 1990 Oct 15;153(8):469-73 [2215338.001]
  • [Cites] Cancer. 1991 Sep 15;68(6):1401-5 [1873792.001]
  • [Cites] Int J Epidemiol. 1992 Apr;21(2):214-21 [1428472.001]
  • [Cites] Epidemiol Rev. 1993;15(1):48-65 [8405212.001]
  • [Cites] Cancer Detect Prev. 1994;18(2):79-85 [8025899.001]
  • [Cites] Mol Endocrinol. 1994 May;8(5):635-42 [8058071.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Feb;83(2):667-74 [9467590.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Feb 16;96(4):1246-51 [9990009.001]
  • [Cites] J Clin Endocrinol Metab. 1999 Mar;84(3):1153-6 [10084611.001]
  • [Cites] Cancer Res. 1959 May;19(4):402-12 [13652125.001]
  • [Cites] Genet Epidemiol. 2004 Dec;27(4):365-74 [15372618.001]
  • [Cites] Nat Genet. 2004 Dec;36(12):1312-8 [15543147.001]
  • [Cites] Nature. 2005 Oct 27;437(7063):1299-320 [16255080.001]
  • [Cites] Nat Genet. 2005 Nov;37(11):1217-23 [16244653.001]
  • [Cites] Ann Hum Genet. 2005 Nov;69(Pt 6):623-38 [16266402.001]
  • [Cites] J Clin Endocrinol Metab. 2006 Apr;91(4):1513-9 [16434456.001]
  • [Cites] J Clin Oncol. 2007 Apr 20;25(12):1482-8 [17372279.001]
  • [Cites] Cancer Causes Control. 2003 Sep;14(7):599-607 [14575357.001]
  • [Cites] J Steroid Biochem Mol Biol. 2004 Jan;88(1):69-77 [15026085.001]
  • [Cites] Curr Med Res Opin. 2004 Apr;20(4):533-40 [15119991.001]
  • [Cites] J Natl Cancer Inst. 2004 Jun 16;96(12):936-45 [15199113.001]
  • [Cites] Cancer Res. 2004 Sep 15;64(18):6814-9 [15375001.001]
  • [Cites] Hum Mol Genet. 2004 Oct 15;13(20):2431-41 [15317758.001]
  • [Cites] Cancer Res. 1973 Nov;33(11):2939-46 [4795906.001]
  • [Cites] Cancer Res. 1977 Apr;37(4):951-63 [191183.001]
  • [Cites] Cancer Res. 1977 Dec;37(12):4650-4 [922745.001]
  • [Cites] Eur J Cancer. 1977 Jul;13(7):677-84 [598393.001]
  • [Cites] Cancer. 1981 Dec 15;48(12):2687-91 [7306924.001]
  • [Cites] Br J Cancer. 1983 Feb;47(2):269-75 [6824571.001]
  • [Cites] EMBO J. 1984 Feb;3(2):429-37 [6325171.001]
  • [Cites] J Natl Cancer Inst. 1986 Sep;77(3):617-20 [3462405.001]
  • [Cites] Am J Epidemiol. 2000 Feb 15;151(4):346-57 [10695593.001]
  • (PMID = 18053149.001).
  • [ISSN] 1471-2350
  • [Journal-full-title] BMC medical genetics
  • [ISO-abbreviation] BMC Med. Genet.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA54281; United States / NIAID NIH HHS / AI / T32 AI060530; United States / NCI NIH HHS / CA / CA63464; United States / NCI NIH HHS / CA / R01 CA063464; United States / NCI NIH HHS / CA / R01 CA054281; United States / NCI NIH HHS / CA / U01 CA063464; United States / NCI NIH HHS / CA / R37 CA054281
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Receptors, Prolactin; 9002-62-4 / Prolactin
  • [Other-IDs] NLM/ PMC2219987
  •  go-up   go-down


45. Wettstein R, Erba P, Farhadi J, Kalbermatten DF, Arnold A, Haug M, Pierer G: Incomplete excision of basal cell carcinoma in the subunits of the nose. Scand J Plast Reconstr Surg Hand Surg; 2008;42(2):92-5
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.
  • [Title] Incomplete excision of basal cell carcinoma in the subunits of the nose.
  • Reconstructive procedures after resection of nasal basal cell carcinoma (BCC) vary depending on the subunit involved.
  • The aim of the present study was to assess the influence of the location of the BCC on the rate of incomplete excisions, so we made a retrospective analysis of all nasal BCC excised at our hospital between 2002 and 2005.
  • BCC were most likely to be incompletely excised on the nasal tip and alae, and both subunits required more elaborate reconstructions.
  • This, however, was not the result of poor estimation of the extent of the tumour and reluctance to excise more challenging areas widely for reconstruction, but to the method chosen to eradicate the tumour.

  • MedlinePlus Health Information. consumer health - Nasal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18335353.001).
  • [ISSN] 0284-4311
  • [Journal-full-title] Scandinavian journal of plastic and reconstructive surgery and hand surgery
  • [ISO-abbreviation] Scand J Plast Reconstr Surg Hand Surg
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] England
  •  go-up   go-down


51. Eyal A, Pelleg O, Embon L, Polturak E: Evidence for a high-temperature disorder-induced mobility in solid 4He. Phys Rev Lett; 2010 Jul 9;105(2):025301
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.
  • [Title] Evidence for a high-temperature disorder-induced mobility in solid 4He.
  • These were all observed both in the bcc and hcp phases of solid 4He.
  • The onset of this behavior is coincidental with the creation of crystalline disorder but does not depend strongly on the crystalline symmetry or on the temperature.

  • 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
  • (PMID = 20867713.001).
  • [ISSN] 1079-7114
  • [Journal-full-title] Physical review letters
  • [ISO-abbreviation] Phys. Rev. Lett.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


52. Tanori M, Mancuso M, Pasquali E, Leonardi S, Rebessi S, Di Majo V, Guilly MN, Giangaspero F, Covelli V, Pazzaglia S, Saran A: PARP-1 cooperates with Ptc1 to suppress medulloblastoma and basal cell carcinoma. Carcinogenesis; 2008 Oct;29(10):1911-9
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.
  • [Title] PARP-1 cooperates with Ptc1 to suppress medulloblastoma and basal cell carcinoma.
  • The patched (Ptc1) protein is a negative regulator of sonic hedgehog signaling, a genetic pathway whose perturbation causes developmental defects and predisposition to specific malignant tumors.
  • Humans and mice with mutated Ptc1 are prone to medulloblastoma and basal cell carcinoma (BCC), both tumors showing dependence on radiation damage for rapid onset and high penetrance.
  • In addition to increased formation and slowed down kinetics of disappearance of gamma-H2AX foci, we observed increased apoptosis in PARP-1-deficient granule cell progenitors after irradiation.
  • Double-mutant mice were also strikingly more susceptible to BCC, with >50% of animals developing multiple, large, infiltrative tumors within 30 weeks of age.
  • [MeSH-major] Carcinoma, Basal Cell / prevention & control. Medulloblastoma / prevention & control. Poly(ADP-ribose) Polymerases / physiology. Receptors, Cell Surface / physiology

  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18660545.001).
  • [ISSN] 1460-2180
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Histones; 0 / Receptors, Cell Surface; 0 / gamma-H2AX protein, mouse; 0 / patched receptors; EC 2.4.2.30 / Parp1 protein, mouse; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases
  •  go-up   go-down


53. Gilaberte Y, Serra-Guillén C, de las Heras ME, Ruiz-Rodríguez R, Fernández-Lorente M, Benvenuto-Andrade C, González-Rodríguez S, Guillén-Barona C: [Photodynamic therapy in dermatology]. Actas Dermosifiliogr; 2006 Mar;97(2):83-102
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.
  • In dermatology, PDT with topical 5-aminolevulinic acid or 5-methyl aminolevulinate is very effective in the treatment of actinic keratoses, basal cell carcinomas and Bowen's disease.
  • [MeSH-major] Photochemotherapy. Photosensitizing Agents / therapeutic use. Skin Diseases / drug therapy
  • [MeSH-minor] Aminolevulinic Acid / radiation effects. Aminolevulinic Acid / therapeutic use. Esthetics. Forecasting. Humans. Infrared Rays. Low-Level Light Therapy. Photochemistry. Photosensitivity Disorders / etiology. Precancerous Conditions / drug therapy. Rejuvenation. Skin Diseases, Infectious / drug therapy. Skin Neoplasms / drug therapy. Ultraviolet Rays

  • MedlinePlus Health Information. consumer health - Skin Conditions.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16595110.001).
  • [ISSN] 0001-7310
  • [Journal-full-title] Actas dermo-sifiliográficas
  • [ISO-abbreviation] Actas Dermosifiliogr
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Photosensitizing Agents; 88755TAZ87 / Aminolevulinic Acid
  • [Number-of-references] 120
  •  go-up   go-down


54. Laque T, Farjalla VF, Rosado AS, Esteves FA: Spatiotemporal variation of bacterial community composition and possible controlling factors in tropical shallow lagoons. Microb Ecol; 2010 May;59(4):819-29
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.
  • Bacterial community composition (BCC) has been extensively related to specific environmental conditions.
  • Tropical coastal lagoons present great temporal and spatial variation in their limnological conditions, which, in turn, should influence the BCC.
  • Here, we sought for the limnological factors that influence, in space and time, the BCC in tropical coastal lagoons (Rio de Janeiro State, Brazil).
  • BCC was evaluated by bacteria-specific PCR-DGGE methods.
  • Great variations were observed in limnological conditions and BCC on both temporal and spatial scales.
  • Changes in the BCC of Visgueiro lagoon throughout the year were best related to salinity and concentrations of NO (3) (-) , dissolved phosphorus and chlorophyll-a, while changes in BCC between lagoons were best related to salinity and dissolved phosphorus concentration.
  • Salinity has a direct impact on the integrity of the bacterial cell, and it was previously observed that phosphorus is the main limiting nutrient to bacterial growth in these lagoons.
  • Therefore, we conclude that great variations in limnological conditions of coastal lagoons throughout time and space resulted in different BCCs and salinity and nutrient concentration, particularly dissolved phosphorus, are the main limnological factors influencing BCC in these tropical coastal lagoons.

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. PHOSPHORUS, ELEMENTAL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Microb Ecol. 2000 Aug;40(2):125-138 [11029081.001]
  • [Cites] Microb Ecol. 2009 Jul;58(1):140-52 [18953593.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Dec 18;104(51):20404-9 [18077371.001]
  • [Cites] Environ Microbiol. 2009 Apr;11(4):867-76 [19040452.001]
  • [Cites] Extremophiles. 2008 Jul;12(4):595-604 [18427718.001]
  • [Cites] Appl Environ Microbiol. 1997 Sep;63(9):3367-73 [9292986.001]
  • [Cites] Ecol Lett. 2006 Jul;9(7):805-12 [16796570.001]
  • [Cites] Ecology. 2007 Sep;88(9):2162-73 [17918395.001]
  • [Cites] Environ Microbiol. 2007 Nov;9(11):2765-74 [17922760.001]
  • [Cites] Environ Microbiol. 2006 Apr;8(4):755-8 [16584487.001]
  • [Cites] Antonie Van Leeuwenhoek. 1998 Jan;73(1):127-41 [9602286.001]
  • [Cites] Appl Environ Microbiol. 2003 Jul;69(7):3701-9 [12839735.001]
  • [Cites] FEMS Microbiol Ecol. 2000 Apr 1;32(2):143-155 [10817867.001]
  • [Cites] Microb Ecol. 2009 May;57(4):657-66 [18985269.001]
  • [Cites] Appl Environ Microbiol. 2005 Dec;71(12):8201-6 [16332803.001]
  • [Cites] Appl Environ Microbiol. 2005 Jan;71(1):227-39 [15640192.001]
  • [Cites] Braz J Biol. 2007 Aug;67(3):475-83 [18094830.001]
  • [Cites] Environ Sci Pollut Res Int. 2009 Jul;16(5):531-8 [19462194.001]
  • [Cites] Ecology. 2006 Aug;87(8):2068-79 [16937646.001]
  • [Cites] Environ Microbiol. 2006 Apr;8(4):720-31 [16584483.001]
  • [Cites] FEMS Microbiol Ecol. 2007 Nov;62(2):142-60 [17892477.001]
  • [Cites] Braz J Biol. 2008 Nov;68(4 Suppl):967-81 [19197469.001]
  • [Cites] FEMS Microbiol Ecol. 2008 Mar;63(3):328-37 [18205816.001]
  • [Cites] Braz J Biol. 2002 Feb;62(1):51-62 [12185923.001]
  • [Cites] Appl Environ Microbiol. 1993 Mar;59(3):695-700 [7683183.001]
  • [Cites] Appl Environ Microbiol. 2007 Nov;73(21):6776-89 [17827310.001]
  • (PMID = 20217404.001).
  • [ISSN] 1432-184X
  • [Journal-full-title] Microbial ecology
  • [ISO-abbreviation] Microb. Ecol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Nitrates; 1406-65-1 / Chlorophyll; 27YLU75U4W / Phosphorus; YF5Q9EJC8Y / chlorophyll a
  •  go-up   go-down


55. Marasà L, Marasà S, Sciancalepore G: Collagen IV, laminin, fibronectin, vitronectin. Comparative study in basal cell carcinoma. Correlation between basement membrane molecules expression and invasive potential. G Ital Dermatol Venereol; 2008 Jun;143(3):169-73
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.
  • [Title] Collagen IV, laminin, fibronectin, vitronectin. Comparative study in basal cell carcinoma. Correlation between basement membrane molecules expression and invasive potential.
  • AIM: Basal cell carcinoma (BCC) is a malignant carcinoma arising by cells of epidermal basal layer and adnexal epithelium.
  • It appears intimately connected with a stromale component that holds a relevant role for tumour's evolution.
  • METHODS: Particularly formalin-fixed, paraffin-embedded tissue from 40 cases of BCC, 20 recurring and 20 not recurring, had been studied, with immunohistochemical techniques to value the distribution of intrinsic and extrinsic components of basal membrane.
  • RESULTS: The immunohistochemical examination showed collagen IV and laminin continuous positivity in peripheral cells, seating around neoplastic nests of 62.5% not recurring BCC.
  • The same antigens exhibited discontinuous positivity in cells with non distinguished borders, seating around nests of 85% micronodular recurring BCC.
  • Fibronectin in fact appeared hyper-expressed in peritumoral stroma of 80% recurring BCC, vitronectin appeared less expressed than normally in peritumoral stroma of 95% recurring BCC.
  • CONCLUSION: A correlation between basal membrane's break and carcinoma's recurrence has been noticed.
  • This shows the utility of other prognostic factors helping the valuation of malignant progression.
  • [MeSH-major] Basement Membrane / chemistry. Carcinoma, Basal Cell / chemistry. Carcinoma, Basal Cell / pathology. Collagen Type IV / analysis. Fibronectins / analysis. Laminin / analysis. Skin Neoplasms / chemistry. Skin Neoplasms / pathology. Vitronectin / analysis
  • [MeSH-minor] Humans. Immunohistochemistry. Neoplasm Invasiveness

  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18833058.001).
  • [ISSN] 0392-0488
  • [Journal-full-title] Giornale italiano di dermatologia e venereologia : organo ufficiale, Società italiana di dermatologia e sifilografia
  • [ISO-abbreviation] G Ital Dermatol Venereol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Collagen Type IV; 0 / Fibronectins; 0 / Laminin; 0 / Vitronectin
  •  go-up   go-down


56. Alessi E, Venegoni L, Fanoni D, Berti E: Cytokeratin profile in basal cell carcinoma. Am J Dermatopathol; 2008 Jun;30(3):249-55
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.
  • [Title] Cytokeratin profile in basal cell carcinoma.
  • Origin of basal cell carcinoma (BCC) is still unclear.
  • We studied the cytokeratin (CK) profile in BCC using monoclonal antibodies against 12 CKs to further investigate the suggested origin of the tumor from follicular matrix cells or from follicular outer root sheath cells and to determine if BCC subtypes can be identified on the basis of their CK profiles.
  • Cases of pilomatricoma and samples of fetal skin served as controls to establish the CK profile in matrical cells and developing follicles during intrauterine life, that of the epidermis and cutaneous adnexa in adult life having been determined in a previous study.
  • The most significant findings were as follows: (a) CK 5 and CK 17 positivity in all the BCCs studied;.
  • (b) CK 7, CK 8, CK 18, and CK 19 positivity in 30/52, 33/52, 42/52, and 14/52 BCCs, respectively;.
  • (c) CK 14 negativity in almost all the BCCs studied; and (d) lack of CK 1 expression only in 2/2 morpheiform BCCs and 4/10 nodular BCCs.
  • The study suggests a tumorous differentiation toward follicular outer root sheath cells and, in most cases, also toward the glandular components of the pilosebaceous-apocrine unit.
  • No significant difference in the CK profile among the BCC subtypes studied was found.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Carcinoma, Basal Cell / metabolism. Keratins / metabolism. Skin Neoplasms / metabolism
  • [MeSH-minor] Cell Transformation, Neoplastic. Fetus. Gestational Age. Hair Diseases / metabolism. Hair Diseases / pathology. Hair Follicle / metabolism. Hair Follicle / pathology. Humans. Keratinocytes / metabolism. Keratinocytes / pathology. Pilomatrixoma / metabolism. Pilomatrixoma / pathology. Skin / chemistry. Skin / embryology

  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • COS Scholar Universe. author profiles.
  • 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
  • (PMID = 18496426.001).
  • [ISSN] 1533-0311
  • [Journal-full-title] The American Journal of dermatopathology
  • [ISO-abbreviation] Am J Dermatopathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 68238-35-7 / Keratins
  •  go-up   go-down


57. Brennan D, Mahoney MG: Increased expression of Dsg2 in malignant skin carcinomas: A tissue-microarray based study. Cell Adh Migr; 2009 Apr-Jun;3(2):148-54
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] Increased expression of Dsg2 in malignant skin carcinomas: A tissue-microarray based study.
  • Desmoglein 2 (Dsg2), a transmembrane cadherin of the desmosomal cell-cell adhesion structure, is downregulated with epithelial differentiation.
  • We recently demonstrated that overexpression of Dsg2 in epidermal keratinocytes deregulates multiple signaling pathways associated with increased growth rate, anchorage-independent cell survival, and the development of skin tumors.
  • While changes in Dsg2 expression have been observed in neoplastic lesions, the correlation of expression levels and localization of Dsg2 and the state of tumor development has not been fully established.
  • Using these antibodies in immunostaining of tissue microarrays, we show a dramatic upregulation of Dsg2 expression in certain human epithelial malignancies including basal cell carcinomas (BCC; n = 12), squamous cell carcinomas (SCC; n = 57), carcinomas of sebaceous and sweat glands (n = 12), and adenocarcinomas (n = 3).
  • Dsg2 expression was completely absent in malignant fibrosarcomas (n = 16) and melanomas (n = 15).
  • While Dsg2 expression was consistently strong in BCC, it varied in SCC with a minor correlation between a decrease of Dsg2 expression and tumor differentiation.

  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Invest Dermatol. 2007 Sep;127(9):2191-206 [17495963.001]
  • [Cites] Br J Cancer. 2007 Jun 18;96(12):1783-7 [17519903.001]
  • [Cites] Clin Cancer Res. 2007 Dec 1;13(23):7003-11 [18056176.001]
  • [Cites] Mod Pathol. 2008 Mar;21(3):271-81 [18084253.001]
  • [Cites] Adv Exp Med Biol. 2008;624:283-95 [18348464.001]
  • [Cites] Adv Anat Pathol. 2008 Jul;15(4):234-40 [18580099.001]
  • [Cites] Br J Cancer. 2000 Jan;82(1):65-73 [10638968.001]
  • [Cites] Ann Surg Oncol. 2000 Apr;7(3):204-9 [10791851.001]
  • [Cites] Cancer Res. 2000 Jul 1;60(13):3397-403 [10910046.001]
  • [Cites] Arch Pathol Lab Med. 2000 Aug;124(8):1147-51 [10923074.001]
  • [Cites] Pathol Res Pract. 2001;197(2):85-91 [11261822.001]
  • [Cites] Hybrid Hybridomics. 2002 Feb;21(1):37-44 [11991815.001]
  • [Cites] Exp Dermatol. 2002 Apr;11(2):115-25 [11994138.001]
  • [Cites] J Cutan Pathol. 2003 Nov;30(10):621-30 [14744087.001]
  • [Cites] J Clin Oncol. 2004 Apr 1;22(7):1242-52 [15051772.001]
  • [Cites] Differentiation. 1996 May;60(2):99-108 [8641550.001]
  • [Cites] J Cell Sci. 1996 May;109 ( Pt 5):1143-54 [8743961.001]
  • [Cites] Acta Derm Venereol. 1996 Nov;76(6):417-20 [8982400.001]
  • [Cites] Exp Cell Res. 1998 Feb 25;239(1):50-9 [9511724.001]
  • [Cites] Br J Cancer. 1998 Apr;77(8):1275-9 [9579833.001]
  • [Cites] J Pathol. 1998 Apr;184(4):369-81 [9664902.001]
  • [Cites] Biol Reprod. 1998 Aug;59(2):388-94 [9687312.001]
  • [Cites] Differentiation. 2004 Oct;72(8):434-49 [15606502.001]
  • [Cites] Int J Cancer. 2005 May 1;114(5):779-90 [15609307.001]
  • [Cites] Anticancer Res. 2005 Jan-Feb;25(1A):183-91 [15816537.001]
  • [Cites] J Pathol. 2005 Oct;207(2):199-206 [16025435.001]
  • [Cites] Exp Dermatol. 2006 Feb;15(2):101-9 [16433681.001]
  • [Cites] J Cell Sci. 2007 Mar 1;120(Pt 5):758-71 [17284515.001]
  • [Cites] Int Rev Cytol. 2007;264:65-163 [17964922.001]
  • (PMID = 19458482.001).
  • [ISSN] 1933-6926
  • [Journal-full-title] Cell adhesion & migration
  • [ISO-abbreviation] Cell Adh Migr
  • [Language] ENG
  • [Grant] United States / NIAMS NIH HHS / AR / R21 AR055251; United States / NIAMS NIH HHS / AR / AR055251
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Desmoglein 2
  • [Other-IDs] NLM/ PMC2679873
  •  go-up   go-down


58. Gufler H, Franke FE, Rau WS: High-resolution MRI of basal cell carcinomas of the face using a microscopy coil. AJR Am J Roentgenol; 2007 May;188(5):W480-4
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.
  • [Title] High-resolution MRI of basal cell carcinomas of the face using a microscopy coil.
  • OBJECTIVE: The objective of this article is to evaluate the diagnostic accuracy of high-resolution MRI using a microscopy surface coil to stage basal cell carcinomas of the face.
  • CONCLUSION: High-resolution MRI using a microscopy surface coil is a promising method to determine the extension of basaliomas of the facial region and to exclude infiltration of bone by the tumor.
  • [MeSH-major] Carcinoma, Basal Cell / diagnosis. Magnetic Resonance Imaging / methods. Skin Neoplasms / diagnosis

  • MedlinePlus Health Information. consumer health - MRI Scans.
  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17449748.001).
  • [ISSN] 1546-3141
  • [Journal-full-title] AJR. American journal of roentgenology
  • [ISO-abbreviation] AJR Am J Roentgenol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


59. Schweiger ES, Kwasniak L, Tonkovic-Capin V: A patient with neviod basal cell carcinoma syndrome treated successfully with photodynamic therapy: case report and review of the literature. J Drugs Dermatol; 2010 Feb;9(2):167-8
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.
  • [Title] A patient with neviod basal cell carcinoma syndrome treated successfully with photodynamic therapy: case report and review of the literature.
  • Nevoid basal cell carcinoma syndrome (NBCCS) is a genetic disorder characterized by multiple basal cell carcinomas (BCCs) in addition to skeletal abnormalities and other neoplasms.
  • Difficulty lies in treating the large number of BCCs that develop in these patients.
  • The authors report a case of a patient with NBCCS treated successfully with photodynamic therapy (PDT) using 20% 5-aminolevulinc acid and blue light.
  • The authors also review the literature and summarize past case reports and series using PDT to treat patient with NBCCS.
  • Based on their experience and the reports of others, the authors assert that PDT should become the first-line therapy in the treatment of multiple BCCs in patients with NBCCS.
  • [MeSH-major] Basal Cell Nevus Syndrome / drug therapy. Photochemotherapy. Skin Neoplasms / drug therapy

  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20214182.001).
  • [ISSN] 1545-9616
  • [Journal-full-title] Journal of drugs in dermatology : JDD
  • [ISO-abbreviation] J Drugs Dermatol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 11
  •  go-up   go-down


60. Alessi SS, Sanches JA, Oliveira WR, Messina MC, Pimentel ER, Festa Neto C: Treatment of cutaneous tumors with topical 5% imiquimod cream. Clinics (Sao Paulo); 2009;64(10):961-6
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.
  • MATERIALS AND METHODS: Here, we present our experience in the treatment of 123 cutaneous tumors of various types, including basal cell carcinoma (BCC), squamous cell carcinoma (SCC), Bowen's disease, erythroplasia of Queyrat, Paget's disease, and trichoepithelioma, with 5% imiquimod cream from 2003 to 2008 in the Cutaneous Oncology Group of the Dermatology Department of Hospital das Clinicas.
  • Patients were divided into two separate groups according to their diagnosis and comorbidities; these comorbidities included epidermodysplasia verruciformis, xeroderma pigmentosum, albinism, basal cell nevus syndrome, Brooke-Spiegler syndrome, HIV, chronic lymphocytic leukemia, B-cell lymphoma, and kidney transplantation.
  • These specific patients demonstrated cure rates of 83.5% for superficial BCC and 50% for Bowen's disease.
  • Aggressive BCC and superficial and nodular BCC did not present a good response to treatment.
  • Trichoepitheliomas and nodular BCC showed a partial response, and erythroplasia of Queyrat showed a complete response.
  • For these patients, the cure rates were 85.7% for superficial and nodular BCC, 88% for superficial BCC, 57% for Bowen's disease, 50% for nodular BCC, and 50% for aggressive BCC.
  • One SCC lesion demonstrated a complete response, and tumors caused by Paget's disease and erythroplasia of Queyrat presented a partial response.
  • Having a cutaneous comorbidity, high-risk tumors such as mixed aggressive BCC (sclerodermiform or micronodular), nodular BCC, or Bowen's disease, and presenting no local reaction to imiquimod were considered as risk factors for a worse prognosis.
  • [MeSH-major] Adjuvants, Immunologic / administration & dosage. Aminoquinolines / administration & dosage. Antineoplastic Agents / administration & dosage. Skin Neoplasms / drug therapy

  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • Hazardous Substances Data Bank. Imiquimod .
  • 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] J Am Acad Dermatol. 1999 Dec;41(6):1002-7 [10570388.001]
  • [Cites] J Am Acad Dermatol. 2001 May;44(5):807-13 [11312429.001]
  • [Cites] Dermatol Surg. 2002 May;28(5):427-9 [12030878.001]
  • [Cites] Arch Dermatol. 2002 Sep;138(9):1165-71 [12224977.001]
  • [Cites] J Dermatolog Treat. 2002 Sep;13(3):123-7 [12227875.001]
  • [Cites] J Am Acad Dermatol. 2002 Oct;47(4 Suppl):S240-8 [12271286.001]
  • [Cites] J Drugs Dermatol. 2008 May;7(5):447-51 [18505136.001]
  • [Cites] Dermatol Surg. 2003 Oct;29(10):1027-34 [12974699.001]
  • [Cites] Dermatol Surg. 2003 Dec;29(12):1181-6 [14725659.001]
  • [Cites] J Am Acad Dermatol. 2004 May;50(5):722-33 [15097956.001]
  • [Cites] Br J Dermatol. 2005 May;152(5):939-47 [15888150.001]
  • [Cites] Eur J Dermatol. 2005 Sep-Oct;15(5):374-81 [16172048.001]
  • [Cites] J Drugs Dermatol. 2007 May;6(5):507-13 [17679185.001]
  • [Cites] Br J Dermatol. 2002 Dec;147(6):1227-36 [12452875.001]
  • (PMID = 19841702.001).
  • [ISSN] 1980-5322
  • [Journal-full-title] Clinics (São Paulo, Brazil)
  • [ISO-abbreviation] Clinics (Sao Paulo)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Aminoquinolines; 0 / Antineoplastic Agents; 99011-02-6 / imiquimod
  • [Other-IDs] NLM/ PMC2763070
  • [Keywords] NOTNLM ; Basal cell carcinoma / Imiquimod / Immunomodulator / Immunotherapy / Non-melanoma skin cancer
  •  go-up   go-down


61. Pálmer HG, Anjos-Afonso F, Carmeliet G, Takeda H, Watt FM: The vitamin D receptor is a Wnt effector that controls hair follicle differentiation and specifies tumor type in adult epidermis. PLoS One; 2008 Jan 23;3(1):e1483
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] The vitamin D receptor is a Wnt effector that controls hair follicle differentiation and specifies tumor type in adult epidermis.
  • Many epidermal genes induced by beta-catenin, including the stem cell marker keratin 15, contain vitamin D response elements (VDREs) and several are induced independently of TCF/Lef.
  • Human trichofolliculomas (hair follicle tumours) are characterized by high nuclear beta-catenin and VDR, whereas infiltrative basal cell carcinomas (BCCs) have high beta-catenin and low VDR levels.
  • In mice, EB1089 prevents beta-catenin induced trichofolliculomas, while in the absence of VDR beta-catenin induces tumours resembling BCCs.


62. Entezari A, Van De Ville D, Möeller T: Practical box splines for reconstruction on the body centered cubic lattice. IEEE Trans Vis Comput Graph; 2008 Mar-Apr;14(2):313-28
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.
  • We introduce a family of box splines for efficient, accurate and smooth reconstruction of volumetric data sampled on the Body Centered Cubic (BCC) lattice, which is the favorable volumetric sampling pattern due to its optimal spectral sphere packing property.
  • First, we construct a box spline based on the four principal directions of the BCC lattice that allows for a linear C(0) reconstruction.
  • We further demonstrate that approximation in the shift-invariant space---generated by BCC-lattice shifts of these box splines---is {twice} as efficient as using the tensor-product B-spline solutions on the Cartesian lattice (with comparable smoothness and approximation order, and with the same sampling density).
  • Practical evidence is provided demonstrating that not only the BCC lattice is generally a more accurate sampling pattern, but also allows for extremely efficient reconstructions that outperform tensor-product Cartesian reconstructions.

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18192712.001).
  • [ISSN] 1077-2626
  • [Journal-full-title] IEEE transactions on visualization and computer graphics
  • [ISO-abbreviation] IEEE Trans Vis Comput Graph
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


63. Jensen AØ, Olesen AB, Dethlefsen C, Sørensen HT: Do incident and new subsequent cases of non-melanoma skin cancer registered in a Danish prospective cohort study have different 10-year mortality? Cancer Detect Prev; 2007;31(5):352-8
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.
  • [Title] Do incident and new subsequent cases of non-melanoma skin cancer registered in a Danish prospective cohort study have different 10-year mortality?
  • BACKGROUND: The Danish Gerda Frentz Cohort (GFC) was created for registering all incident and new subsequent cases of non-melanoma skin cancer (NMSC) among patients seen by Danish dermatologists in 1995.
  • We have recently found, in this cohort, a lower 10-year mortality than in the general population in patients with basal cell carcinoma (BCC).
  • Differences in mortality between incident and new subsequent cases, incomplete registration or selection bias may be responsible for this finding.
  • METHODS: We aimed to quantify differences in mortality between incident and new subsequent cases of NMSC in the GFC and to compare mortality among incident cases recorded in the GFC and those recorded in the Danish Cancer Registry (DCR).
  • We followed 10,830 skin cancer patients and 106,696 age-, gender- and residence-matched population controls through 2006 and computed their cumulative mortality and mortality rate ratio (MRR).
  • RESULTS: One-, 5-, and 10-year cumulative mortality of incident and new subsequent cases of BCC and SCC in the GFC were similar.
  • Likewise, MRR for incident BCC (MRR=0.91; 95% CI 0.84-0.98) and incident SCC (MRR=1.29; 95% CI 1.05-1.56) among patients registered in the GFC were similar to their counterparts in the DCR (MRR=0.96; 95% CI 0.91-1.00 and MRR=1.36; 95% CI 1.22-1.52).
  • CONCLUSION: Mortality of incident and new subsequent cases of NMSC was similar and thus did not explain the reduced mortality of BCC patients.
  • [MeSH-major] Carcinoma, Basal Cell / mortality. Carcinoma, Squamous Cell / mortality. Skin Neoplasms / mortality

  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • COS Scholar Universe. author profiles.
  • 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
  • (PMID = 18031945.001).
  • [ISSN] 1525-1500
  • [Journal-full-title] Cancer detection and prevention
  • [ISO-abbreviation] Cancer Detect. Prev.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  •  go-up   go-down


64. Zhou G, Ventura M, Gu M, Matthews A, Kivshar Y: Photonic bandgap properties of void-based body-centered-cubic photonic crystals in polymer. Opt Express; 2005 Jun 13;13(12):4390-5
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.
  • We report on the fabrication and characterization of void-based body-centered-cubic (bcc) photonic crystals in a solidified transparent polymer by the use of a femtosecond laser-driven microexplosion method.
  • The change in the refractive index in the region surrounding the void dots that form the bcc structures is verified by presenting confocal microscope images, and the bandgap properties are characterized by using a Fourier transform infrared spectrometer.
  • We observe multiple stop gaps with a suppression rate of the main gap of 47% for a bcc structure with a lattice constant of 2.77 microm, where the first and second stop gaps are located at 3.7 microm and 2.2 microm, respectively.

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19495354.001).
  • [ISSN] 1094-4087
  • [Journal-full-title] Optics express
  • [ISO-abbreviation] Opt Express
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


65. Watkins J: Dermatology and the community nurse: actinic (solar) keratosis. Br J Community Nurs; 2010 Jan;15(1):6, 8, 10-1
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.
  • They are then able to check other sun-exposed areas such as the face, ears, scalp, back and limbs to discover any other lesions or more serious problems of basal cell carcinoma, squamous cell carcinoma or malignant melanoma the would require referral, sometimes urgently, to a dermatologist for full assessment and treatment.
  • In any case, sound advice about further protection from the sun, both for themselves and their families may help to reduce the likelihood of further problems.
  • [MeSH-major] Keratosis / nursing. Skin Neoplasms / nursing. Sunlight / adverse effects
  • [MeSH-minor] Community Health Nursing. Diagnosis, Differential. Humans. Nursing Diagnosis. Protective Clothing. Risk Factors. Sunscreening Agents

  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20216512.001).
  • [ISSN] 1462-4753
  • [Journal-full-title] British journal of community nursing
  • [ISO-abbreviation] Br J Community Nurs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Sunscreening Agents
  • [Number-of-references] 13
  •  go-up   go-down


66. Dawe RS: Treatment options for non-melanoma skin cancer. G Ital Dermatol Venereol; 2009 Aug;144(4):453-8
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.
  • [Title] Treatment options for non-melanoma skin cancer.
  • Non melanoma skin cancers (basal cell carcinoma and squamous cell carcinoma) are becoming more common.
  • The choice as to how to treat a particular tumour depends not only on features of the tumour but characteristics of the patient and his or her preferences.
  • [MeSH-major] Carcinoma, Basal Cell / therapy. Carcinoma, Squamous Cell / therapy. Skin Neoplasms / therapy

  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19755949.001).
  • [ISSN] 0392-0488
  • [Journal-full-title] Giornale italiano di dermatologia e venereologia : organo ufficiale, Società italiana di dermatologia e sifilografia
  • [ISO-abbreviation] G Ital Dermatol Venereol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Italy
  • [Number-of-references] 38
  •  go-up   go-down


67. Godhi SS, Kukreja P: Keratocystic odontogenic tumor: a review. J Maxillofac Oral Surg; 2009 Jun;8(2):127-31
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] Keratocystic odontogenic tumor: a review.
  • There are many types of cysts of the jaws, but what makes the odontogenic keratocyst unusual are its characteristic histopathological and clinical features, including potentially aggressive behaviour, high recurrence rate, and an association with the nevoid basal cell carcinoma syndrome.
  • The 2005 WHO classification now uses the term 'keratocystic odontogenic tumor'.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Br J Oral Surg. 1975 Nov;13(2):111-27 [1059480.001]
  • [Cites] Oral Surg Oral Med Oral Pathol. 1991 Sep;72(3):265-9 [1717918.001]
  • [Cites] Int J Oral Maxillofac Surg. 1991 Feb;20(1):9-11 [2019786.001]
  • [Cites] Br J Oral Maxillofac Surg. 1987 Aug;25(4):271-9 [3476151.001]
  • [Cites] Nature. 2000 Aug 31;406(6799):1005-9 [10984056.001]
  • [Cites] Int J Oral Maxillofac Surg. 2001 Feb;30(1):14-25 [11289615.001]
  • [Cites] J Oral Maxillofac Surg. 2001 Jul;59(7):720-5; discussion 726-7 [11429726.001]
  • [Cites] Oral Oncol. 2002 Apr;38(3):219-26 [11978543.001]
  • [Cites] Oral Oncol. 2002 Jul;38(5):407-15 [12110333.001]
  • [Cites] Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2002 Aug;94(2):151-6 [12221380.001]
  • [Cites] Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2005 Jan;99(1):71-8 [15599351.001]
  • [Cites] J Oral Maxillofac Surg. 2006 Mar;64(3):379-83 [16487797.001]
  • [Cites] J Indian Soc Pedod Prev Dent. 2007 Jul-Sep;25(3):137-9 [17951931.001]
  • [Cites] J Can Dent Assoc. 2008 Mar;74(2):165-165h [18353202.001]
  • [Cites] J Craniomaxillofac Surg. 1989 Jul;17(5):226-33 [2668340.001]
  • [Cites] Int J Oral Maxillofac Surg. 1988 Feb;17(1):25-8 [3127485.001]
  • [Cites] J Craniomaxillofac Surg. 1988 May;16(4):184-95 [3290262.001]
  • [Cites] J Maxillofac Surg. 1981 Nov;9(4):228-36 [6172530.001]
  • [Cites] J Oral Maxillofac Surg. 1994 Sep;52(9):960-3 [8064460.001]
  • [Cites] J Oral Maxillofac Surg. 1994 Sep;52(9):964-6 [8064461.001]
  • [Cites] Laryngoscope. 1998 Feb;108(2):280-3 [9473082.001]
  • [Cites] Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2000 Nov;90(5):553-8 [11077375.001]
  • [Cites] Oral Oncol. 2002 Jun;38(4):323-31 [12076694.001]
  • [Cites] Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2002 Nov;94(5):543-53 [12424446.001]
  • [Cites] Acta Pathol Microbiol Scand. 1963;58:283-94 [14044666.001]
  • [Cites] J Oral Maxillofac Surg. 2004 Jun;62(6):651-5; discussion 655-6 [15170272.001]
  • [Cites] J Oral Maxillofac Surg. 2005 Feb;63(2):267-71 [15690300.001]
  • [Cites] Ann Acad Med Singapore. 2005 Jan;34(1):130-3 [15726232.001]
  • [Cites] J Oral Maxillofac Surg. 2005 May;63(5):635-9 [15883937.001]
  • [Cites] J Oral Maxillofac Surg. 2005 Nov;63(11):1667-73 [16243185.001]
  • [Cites] Med Hypotheses. 2006;67(5):1242-4 [16806729.001]
  • [Cites] Oral Maxillofac Surg Clin North Am. 2003 Aug;15(3):383-92 [18088690.001]
  • [Cites] Oral Maxillofac Surg Clin North Am. 2003 Aug;15(3):407-14 [18088692.001]
  • [Cites] J Oral Maxillofac Surg. 2008 May;66(5):1025-36 [18423297.001]
  • [Cites] Int Endod J. 2008 Sep;41(9):800-6 [18637853.001]
  • [Cites] Dentomaxillofac Radiol. 2008 Oct;37(7):412-4 [18812605.001]
  • [Cites] Oral Surg Oral Med Oral Pathol. 1994 May;77(5):494-7 [7518070.001]
  • [Cites] Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1998 Jul;86(1):42-7 [9690244.001]
  • [Cites] Br J Oral Maxillofac Surg. 1985 Jun;23(3):195-203 [3159419.001]
  • [Cites] Br J Oral Maxillofac Surg. 1985 Jun;23(3):204-9 [3159420.001]
  • [Cites] Br J Oral Maxillofac Surg. 1988 Feb;26(1):52-7 [3278734.001]
  • [Cites] Proc R Soc Med. 1971 May;64(5):547-50 [4930728.001]
  • [Cites] Br Dent J. 1970 Mar 3;128(5):225-31 [5270271.001]
  • [Cites] Int J Oral Surg. 1984 Dec;13(6):506-10 [6210260.001]
  • [Cites] Proc Finn Dent Soc. 1980;76(3):129-74 [7443696.001]
  • (PMID = 23139489.001).
  • [ISSN] 0972-8279
  • [Journal-full-title] Journal of maxillofacial and oral surgery
  • [ISO-abbreviation] J Maxillofac Oral Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Other-IDs] NLM/ PMC3453933
  • [Keywords] NOTNLM ; Cyst / Odontogenic tumor
  •  go-up   go-down


68. Watson A, Kent P, Alam M, Paller AS, Umbach DM, Yoon JW, Iannaccone PM, Walterhouse DO: GLI1 genotypes do not predict basal cell carcinoma risk: a case control study. Mol Cancer; 2009 Nov 30;8:113
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] GLI1 genotypes do not predict basal cell carcinoma risk: a case control study.
  • BACKGROUND: Susceptibility to basal cell carcinoma results from complex interactions between ultraviolet radiation exposure and genetic factors.
  • We determined whether GLI1 polymorphisms were risk factors for developing basal cell carcinoma, either alone or in combination with patterns of past sun exposure, and whether there were functional differences among different GLI1 haplotypes.
  • RESULTS: GLI1 genotypes at c.2798 and c.3298 from 201 basal cell carcinoma patients were compared to 201 age and sex-matched controls.
  • Neither genotype nor haplotype frequencies differed between cases and controls.
  • However, the odds of developing basal cell carcinoma on the trunk compared to the head/neck appeared somewhat lower with carriers of the c.3298GC than the CC genotype.
  • There was no evidence for interactions between skin type, childhood sunburning, average adult sun exposure, adult sunbathing, or intermittency of sun exposure and GLI1 haplotype.
  • Additionally, we found no significant differences in transcription activation or cell transforming ability among the four GLI1 haplotypes.
  • CONCLUSION: These results suggest that different GLI1 genotypes alone or in combination with past sun exposure patterns as assessed in this study do not affect basal cell carcinoma risk.

  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Biol Chem. 1998 Feb 6;273(6):3496-501 [9452474.001]
  • [Cites] Nature. 1998 Jan 1;391(6662):90-2 [9422511.001]
  • [Cites] J Am Acad Dermatol. 2005 Mar;52(3 Pt 1):468-73 [15761425.001]
  • [Cites] Chin Med J (Engl). 2006 Feb 20;119(4):267-74 [16537020.001]
  • [Cites] J Invest Dermatol. 2006 Jul;126(7):1510-7 [16645598.001]
  • [Cites] Int J Cancer. 2008 Apr 15;122(8):1787-93 [18067130.001]
  • [Cites] Nat Genet. 2008 Jul;40(7):886-91 [18488027.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Mar 28;97(7):3438-43 [10725363.001]
  • [Cites] Am J Kidney Dis. 2000 Jul;36(1):167-76 [10873887.001]
  • [Cites] J Invest Dermatol. 2000 Aug;115(2):328-9 [10951255.001]
  • [Cites] Lancet. 2001 Aug 25;358(9282):641-2 [11530156.001]
  • [Cites] J Photochem Photobiol B. 2001 Oct;63(1-3):8-18 [11684447.001]
  • [Cites] Arch Dermatol. 1988 Jun;124(6):869-71 [3377516.001]
  • [Cites] Mol Cell Biol. 1991 Mar;11(3):1724-8 [1825351.001]
  • [Cites] Nat Genet. 1996 Sep;14(1):78-81 [8782823.001]
  • [Cites] J Invest Dermatol. 1997 Apr;108(4):519-22 [9077484.001]
  • [Cites] Nature. 1997 Oct 23;389(6653):876-81 [9349822.001]
  • [Cites] Cancer Lett. 2004 Dec 28;216(2):191-7 [15533595.001]
  • (PMID = 19948058.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] ENG
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / GLI1 protein, human; 0 / Transcription Factors
  • [Other-IDs] NLM/ PMC2789726
  •  go-up   go-down


69. Li N, Wolgamot G, Argenyi Z: Primary cutaneous neuroendocrine cell carcinoma (Merkel cell carcinoma) with prominent microcystic features, mimicking eccrine carcinoma. J Cutan Pathol; 2007 May;34(5):410-4
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.
  • [Title] Primary cutaneous neuroendocrine cell carcinoma (Merkel cell carcinoma) with prominent microcystic features, mimicking eccrine carcinoma.
  • Although primary cutaneous neuroendocrine cell carcinoma [Merkel cell carcinoma (MCC)] may show divergent features, including microcystic ('tubuloglandular'), squamous, eccrine and rhabdomyoblastic, a diffuse microcystic pattern is exceedingly rare.
  • In this study, we present two cases of MCC with prominent microcystic features, which precluded a definitive diagnosis in the initial punch biopsy.
  • Punch biopsies from both patients revealed an infiltrating neoplasm with prominent microcystic features that mimick tubuloglandular structures, lined by hyperchromatic basaloid cells, which were strongly positive for chromogranin and BerEP4, variably positive for CK7 and CK5/6 and negative for CK20, synaptophysin, S-100, epithelial membrane antigen (EMA), gross cystic disease fluid protein-15 (GCDFP-15), estrogen/progesterone receptors (ER/PR), thyroid transcription factor 1 (TTF1) and carcinoembryonic antigen (CEA).
  • The re-excision specimens showed a multifocal intra-epidermal component in one case and typical finely stippled nuclear chromatin in both cases.
  • Although the lack of CK20 staining is unusual, the histologic characteristics along with the remaining immunohistochemical studies favor the diagnosis of a primary cutaneous neuroendocrine cell carcinoma over the variants of eccrine carcinoma or basal cell carcinoma with neuroendocrine differentiation.
  • Our cases illustrate that prominent microcystic features, mimicking glandular differentiation, may occur in MCC and pose a diagnostic challenge in small biopsy specimens.
  • [MeSH-major] Carcinoma, Merkel Cell / pathology. Neoplasms, Adnexal and Skin Appendage / pathology. Skin Neoplasms / pathology
  • [MeSH-minor] Adult. Biomarkers, Tumor / analysis. Diagnosis, Differential. Eccrine Glands / pathology. Humans. Immunohistochemistry. Male. Neck / pathology

  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • COS Scholar Universe. author profiles.
  • 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
  • (PMID = 17448197.001).
  • [ISSN] 0303-6987
  • [Journal-full-title] Journal of cutaneous pathology
  • [ISO-abbreviation] J. Cutan. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  •  go-up   go-down


70. Postmenopausal hormone therapy and breast cancer. Prescrire Int; 2009 Apr;18(100):66-7
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.
  • [Title] Postmenopausal hormone therapy and breast cancer.
  • (1) According to the WHI trial, postmenopausal hormone replacement therapy exposes women to an additional risk of breast cancer of about 8 cases a year per 10 000 treated women;.
  • (2) In the United States, a comparison of the breast cancer incidence rates in 2001 and 2004 showed an overall annual decrease of 8.6%, attributable to the reduction in the use of hormone replacement therapy in postmenopausal women.
  • (3) In summary, if prescribers had waited for the results of the WHI trial, many cases of breast cancer would probably have been avoided.
  • [MeSH-major] Breast Neoplasms / chemically induced. Estrogen Replacement Therapy / adverse effects. Estrogens / adverse effects. Hormone Replacement Therapy / adverse effects. Progestins / adverse effects

  • Genetic Alliance. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Hormone Replacement Therapy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19585723.001).
  • [ISSN] 1167-7422
  • [Journal-full-title] Prescrire international
  • [ISO-abbreviation] Prescrire Int
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Estrogens; 0 / Progestins
  •  go-up   go-down


71. Degen A, Satzger I, Voelker B, Kapp A, Hauschild A, Gutzmer R: Does basal cell carcinoma belong to the spectrum of sorafenib-induced epithelial skin cancers? Dermatology; 2010;221(3):193-6
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.
  • [Title] Does basal cell carcinoma belong to the spectrum of sorafenib-induced epithelial skin cancers?
  • Multiple cutaneous side effects are well described but recent reports indicated a possible association of epithelial skin cancer growth during sorafenib therapy.
  • To our knowledge, few cases of actinic keratoses and variants of squamous cell carcinomas associated with sorafenib have been published.
  • We report 2 patients who developed a basal cell carcinoma (BCC) while treated with sorafenib.
  • Interestingly BCC is a tumor which has not been described yet in association with sorafenib therapy.
  • After termination of sorafenib treatment, no new BCCs or other epithelial skin cancers occurred.
  • There is accumulating evidence in the literature that sorafenib and possibly other targeted agents are associated with an increased occurrence of epithelial skin cancers.
  • These observations are summarized here and complemented by the new observation that also BCCs might be associated with sorafenib therapy.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Benzenesulfonates / adverse effects. Carcinoma, Basal Cell / chemically induced. Protein Kinase Inhibitors / adverse effects. Pyridines / adverse effects. Skin Neoplasms / chemically induced
  • [MeSH-minor] Aged. Carcinoma, Renal Cell / drug therapy. Carcinoma, Renal Cell / secondary. Female. Humans. Male. Melanoma / drug therapy. Melanoma / secondary. Niacinamide / analogs & derivatives. Phenylurea Compounds

  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • Hazardous Substances Data Bank. NICOTINAMIDE .
  • 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
  • (PMID = 20720388.001).
  • [ISSN] 1421-9832
  • [Journal-full-title] Dermatology (Basel, Switzerland)
  • [ISO-abbreviation] Dermatology (Basel)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzenesulfonates; 0 / Phenylurea Compounds; 0 / Protein Kinase Inhibitors; 0 / Pyridines; 25X51I8RD4 / Niacinamide; 9ZOQ3TZI87 / sorafenib
  •  go-up   go-down


72. Kim YM, Kwak KH, Lim JO, Baek WY: Reduction of allodynia by intrathecal transplantation of microencapsulated porcine chromaffin cells. Artif Organs; 2009 Mar;33(3):240-9
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.
  • Bovine chromaffin cells (BCCs) are well known to have analgesic effect to reduce acute or chronic pain when transplanted in the subarachnoid space and have been considered as an alternative therapy for pain management.
  • In the present study, we investigated whether microencapsulated porcine adrenal medullary chromaffin cells (PCCs) also have analgesic effect to reduce allodynia caused by neuropathic pain in chronic constriction injury model of rat.
  • In in vitro tests, the microencapsulated PCCs were investigated whether they have an ability to release catecholamines responding to nicotine stimulation.
  • The levels of catecholamines released from the microencapsulated PCCs were significantly higher than from microencapsulated BCCs.
  • In in vivo tests, implantation of microencapsulated PCCs reduced both mechanical and cold allodynia in chronic constriction injury model of a rat whereas the microencapsulated BCCs reduced only cold allodynia under the same conditions.
  • [MeSH-major] Cell- and Tissue-Based Therapy / methods. Chromaffin Cells / cytology. Chromaffin Cells / transplantation. Pain

  • MedlinePlus Health Information. consumer health - Pain.
  • Hazardous Substances Data Bank. NICOTINE .
  • 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
  • (PMID = 19245523.001).
  • [ISSN] 1525-1594
  • [Journal-full-title] Artificial organs
  • [ISO-abbreviation] Artif Organs
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Catecholamines; 25104-18-1 / Polylysine; 6M3C89ZY6R / Nicotine
  •  go-up   go-down


73. Ruiter R, Visser LE, Eijgelsheim M, Rodenburg EM, Hofman A, Coebergh JW, Nijsten T, Stricker BH: High-ceiling diuretics are associated with an increased risk of basal cell carcinoma in a population-based follow-up study. Eur J Cancer; 2010 Sep;46(13):2467-72
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.
  • [Title] High-ceiling diuretics are associated with an increased risk of basal cell carcinoma in a population-based follow-up study.
  • INTRODUCTION: In Caucasians, basal cell carcinoma (BCC) is among the most frequently diagnosed cancers and its incidence is increasing.
  • Known risk factors for the development of BCC are age, sun exposure, and certain skin characteristics.
  • Despite photosensitizing abilities of diuretic agents, little is known about a possible association with BCC.
  • The diagnoses of BCC were obtained through general practitioners, and by linkage with a registry of histo- and cytopathology.
  • Cumulative use of diuretics at the date of diagnosis was categorized into quartiles for users of high-ceiling diuretics, potassium sparing agents and thiazides.
  • The association between these drugs and BCC was assessed by Cox proportional hazard modeling with adjustment for age, gender and potential confounders.
  • RESULTS: Use of high-ceiling diuretics in the highest quartile (>3.7 years cumulative exposure) was associated with an increased hazard of BCC of 62% compared to no use (HR 1.6; 95% CI 1.1-2.4).
  • Patients who used high-ceiling diuretics and had a high tendency of getting sunburned had a higher risk of diagnosis than non-users who do not easily get sunburned.
  • Neither the use of potassium sparing agents, nor the use of thiazides was associated with BCC.
  • CONCLUSION: In our study, cumulative use of high-ceiling diuretics was associated with an increased risk of diagnosis of BCC.
  • [MeSH-major] Carcinoma, Basal Cell / chemically induced. Photosensitizing Agents / adverse effects. Skin Neoplasms / chemically induced. Sodium Potassium Chloride Symporter Inhibitors / adverse effects

  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2010. Published by Elsevier Ltd.
  • (PMID = 20605443.001).
  • [ISSN] 1879-0852
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Photosensitizing Agents; 0 / Sodium Potassium Chloride Symporter Inhibitors
  •  go-up   go-down


74. Cheng HL, Su SJ, Huang LW, Hsieh BS, Hu YC, Hung TC, Chang KL: Arecoline induces HA22T/VGH hepatoma cells to undergo anoikis - involvement of STAT3 and RhoA activation. Mol Cancer; 2010;9:126
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.
  • BACKGROUND: Our previous study showed that, in basal cell carcinoma cells, arecoline reduces levels of the tumor cell survival factor interleukin-6 (IL-6), increases levels of tumor suppressor factor p53, and elicits cell cycle arrest, followed by apoptosis.
  • In preliminarily studies, we observed that arecoline induces detachment of the human-derived hepatoma cell line HA22T/VGH from the extracellular matrix.
  • METHODS: HA22T/VGH cells or primary cultured rat hepatocytes were treated with arecoline, then changes in morphology, viability, apoptosis, and the expression of surface beta1-integrin, apoptosis-related proteins, and IL-6 were examined.
  • RESULTS: A low concentration of arecoline (<or= 100 microg/ml) caused cytoskeletal changes in HA22T/VGH cells, but not hepatocytes, and this was accompanied by decreased beta1-integrin expression and followed by apoptosis, indicating that HA22T/VGH cells undergo anoikis after arecoline treatment.
  • [MeSH-major] Anoikis / drug effects. Antineoplastic Agents / pharmacology. Arecoline / pharmacology. Carcinoma, Hepatocellular / metabolism. Enzyme Activation / drug effects. Liver Neoplasms / metabolism
  • [MeSH-minor] Animals. Blotting, Western. Cell Adhesion / drug effects. Cell Line, Tumor. Cell Separation. DNA Fragmentation / drug effects. Flow Cytometry. Fluorescent Antibody Technique. Humans. In Situ Nick-End Labeling. Rats. Rats, Sprague-Dawley. Reverse Transcriptase Polymerase Chain Reaction. STAT3 Transcription Factor / drug effects. STAT3 Transcription Factor / metabolism. Signal Transduction / drug effects. Signal Transduction / physiology. rhoA GTP-Binding Protein / drug effects. rhoA GTP-Binding Protein / metabolism

  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • 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 .
  • 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] Cytometry. 2000 Jun 1;40(2):151-60 [10805935.001]
  • [Cites] Ann N Y Acad Sci. 2009 Feb;1155:206-21 [19250206.001]
  • [Cites] Science. 2000 Oct 6;290(5489):144-7 [11021801.001]
  • [Cites] Nat Cell Biol. 2001 Apr;3(4):339-45 [11283606.001]
  • [Cites] Nat Cell Biol. 2001 Apr;3(4):346-52 [11283607.001]
  • [Cites] Nat Cell Biol. 2001 Apr;3(4):361-7 [11283609.001]
  • [Cites] Nat Genet. 2001 May;28(1):29-35 [11326271.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Jul 31;98(16):9014-9 [11470914.001]
  • [Cites] Mol Biol Cell. 2001 Sep;12(9):2711-20 [11553710.001]
  • [Cites] Mol Biol Cell. 2001 Oct;12(10):3282-94 [11598209.001]
  • [Cites] Methods. 2001 Dec;25(4):402-8 [11846609.001]
  • [Cites] Biochem J. 2002 Oct 15;367(Pt 2):549-59 [12126481.001]
  • [Cites] J Cell Biol. 2003 Jan 20;160(2):255-65 [12538643.001]
  • [Cites] Life Sci. 2003 Mar 7;72(16):1871-82 [12586224.001]
  • [Cites] Nutr Cancer. 2003;45(1):113-23 [12791511.001]
  • [Cites] Trends Biochem Sci. 2003 Jun;28(6):284-93 [12826400.001]
  • [Cites] Carcinogenesis. 2003 Aug;24(8):1301-15 [12807728.001]
  • [Cites] Mol Cell. 2004 Feb 13;13(3):341-55 [14967142.001]
  • [Cites] Chin J Physiol. 2004 Jun 30;47(2):89-94 [15481791.001]
  • [Cites] Cell Mol Biol Incl Cyto Enzymol. 1981;27(6):687-94 [7343093.001]
  • [Cites] Carcinogenesis. 1984 Apr;5(4):501-3 [6705148.001]
  • [Cites] Cancer Res. 1989 Oct 1;49(19):5294-8 [2766297.001]
  • [Cites] Trends Pharmacol Sci. 1989 Dec;Suppl:85-8 [2694530.001]
  • [Cites] Psychopharmacol Bull. 1991;27(3):315-9 [1775605.001]
  • [Cites] Mutat Res. 1992 Apr;278(4):271-6 [1373864.001]
  • [Cites] J Cancer Res Clin Oncol. 1992;118(4):283-8 [1577847.001]
  • [Cites] FASEB J. 1993 Nov;7(14):1407-13 [8224613.001]
  • [Cites] J Cell Biol. 1994 Feb;124(4):619-26 [8106557.001]
  • [Cites] J Dent Res. 1994 May;73(5):1043-9 [8006230.001]
  • [Cites] Annu Rev Immunol. 1997;15:797-819 [9143707.001]
  • [Cites] J Cell Biol. 1997 Aug 25;138(4):901-11 [9265655.001]
  • [Cites] Genes Dev. 1997 Sep 15;11(18):2295-322 [9308960.001]
  • [Cites] Curr Opin Cell Biol. 1997 Oct;9(5):701-6 [9330874.001]
  • [Cites] J Biol Chem. 1999 Jun 25;274(26):18675-85 [10373480.001]
  • [Cites] J Biol Chem. 1999 Jul 30;274(31):21701-6 [10419481.001]
  • [Cites] Cell. 1999 Aug 6;98(3):295-303 [10458605.001]
  • [Cites] Oncogene. 1999 Aug 19;18(33):4654-62 [10467412.001]
  • [Cites] Food Chem Toxicol. 1999 Jul;37(7):751-6 [10496377.001]
  • [Cites] J Biol Chem. 2004 Dec 3;279(49):50676-83 [15375172.001]
  • [Cites] IARC Monogr Eval Carcinog Risks Hum. 2004;85:1-334 [15635762.001]
  • [Cites] J Biol Chem. 2005 Apr 29;280(17):17275-85 [15705584.001]
  • [Cites] Cancer Res. 2005 Jul 1;65(13):5828-34 [15994959.001]
  • [Cites] Cell Mol Immunol. 2005 Apr;2(2):92-100 [16191414.001]
  • [Cites] Toxicology. 2006 Mar 15;220(2-3):81-9 [16413651.001]
  • [Cites] Nat Struct Mol Biol. 2007 Mar;14(3):215-23 [17310253.001]
  • [Cites] Ann N Y Acad Sci. 2006 Dec;1091:151-69 [17341611.001]
  • [Cites] J Biol Chem. 2007 Mar 16;282(11):8069-78 [17234627.001]
  • [Cites] J Clin Pathol. 2007 Jun;60(6):642-8 [16901975.001]
  • [Cites] J Cell Biol. 2007 Jul 2;178(1):23-30 [17606864.001]
  • [Cites] J Cell Biol. 2007 Oct 8;179(1):23-31 [17908916.001]
  • [Cites] Cancer Cell. 2008 Jan;13(1):7-9 [18167335.001]
  • [Cites] Neurochem Int. 2008 Feb;52(3):376-83 [17719699.001]
  • [Cites] Mol Cancer. 2008;7:78 [18939995.001]
  • [Cites] Chin J Physiol. 2000 Mar 31;43(1):23-8 [10857465.001]
  • (PMID = 20507639.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / STAT3 Transcription Factor; 4ALN5933BH / Arecoline; EC 3.6.5.2 / rhoA GTP-Binding Protein
  • [Other-IDs] NLM/ PMC2895595
  •  go-up   go-down


75. de Haas ER, de Vijlder HC, van Reesema WS, van Everdingen JJ, Neumann HA: Quality of clinical practice guidelines in dermatological oncology. J Eur Acad Dermatol Venereol; 2007 Oct;21(9):1193-8
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.
  • METHODS: We searched MEDLINE, PubMed, EMBASE and Cochrane literature and relevant websites of guidelines development programmes and the national dermatological society to identify evidence-based dermatological guidelines especially in the treatment of to basal cell carcinoma, squamous cell carcinoma and melanoma.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17894704.001).
  • [ISSN] 0926-9959
  • [Journal-full-title] Journal of the European Academy of Dermatology and Venereology : JEADV
  • [ISO-abbreviation] J Eur Acad Dermatol Venereol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  •  go-up   go-down


76. De-Domingo B, González F, Lorenzo P: [Gorlin syndrome (nevoid basal cell carcinoma syndrome)]. Arch Soc Esp Oftalmol; 2008 May;83(5):321-4
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] [Gorlin syndrome (nevoid basal cell carcinoma syndrome)].
  • [Transliterated title] Síndrome de Gorlin (síndrome nevoide basocelular).
  • CLINICAL CASE: A 77 year-old male patient with Parkinson's disease and senile dementia had many facial basal cell carcinomas and an ectropion of the left eye.
  • DISCUSSION: Gorlin syndrome is an autosomal dominant condition characterized by basal cell carcinomas, and skeletal and neurological anomalies.
  • The presence of multiple basal cell carcinomas on the eyelids in a child or in a young patient should alert ophthalmologists to the possibility of this syndrome.
  • [MeSH-major] Basal Cell Nevus Syndrome / pathology. Eyelid Neoplasms / pathology

  • Genetic Alliance. consumer health - Nevoid basal cell carcinoma syndrome.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18464182.001).
  • [ISSN] 0365-6691
  • [Journal-full-title] Archivos de la Sociedad Española de Oftalmología
  • [ISO-abbreviation] Arch Soc Esp Oftalmol
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Spain
  •  go-up   go-down


77. Begnami MD, Quezado M, Pinto P, Linehan WM, Merino M: Adenoid cystic/basal cell carcinoma of the prostate: review and update. Arch Pathol Lab Med; 2007 Apr;131(4):637-40
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.
  • [Title] Adenoid cystic/basal cell carcinoma of the prostate: review and update.
  • CONTEXT: Although most prostate carcinomas are of the conventional acinar type, unusual variants have been reported.
  • Adenoid cystic/basal cell carcinoma of the prostate is a rare tumor with distinctive histopathologic features.
  • There are only a few publications in the literature concerning the diagnosis, treatment, and prognosis of this neoplasm.
  • OBJECTIVE: To review current literature together with the clinical, pathologic, and immunohistochemical features of adenoid cystic/basal cell carcinoma of the prostate and offer a practical approach to the diagnosis--including the differential diagnosis--of this neoplasm in surgical pathologic specimens.
  • DATA SOURCES: Adenoid cystic/basal cell carcinoma of the prostate is composed of infiltrating basaloid cells forming dilated acinar and cribriform spaces with luminal basementlike material.
  • Differentiation of adenoid cystic/basal cell carcinoma from basal cell hyperplasia and cribriform pattern of acinar adenocarcinoma may be difficult.
  • The use of cytokeratin 34betaE12 and prostate-specific antigen can help in difficult cases.
  • Most cases are indolent, but metastasis has been documented in a few cases.
  • CONCLUSIONS: Various histologic and immunohistochemical features are helpful in recognizing adenoid cystic/basal cell carcinoma of the prostate.
  • This is a rare subtype of prostate cancer and correct diagnosis is important because of the unique clinical and biological features and the implications for treatment and prognosis.
  • [MeSH-major] Carcinoma, Adenoid Cystic / pathology. Carcinoma, Basal Cell / pathology. Prostatic Neoplasms / pathology
  • [MeSH-minor] Diagnosis, Differential. Humans. Immunohistochemistry. Male


78. Hafner C, Becker B, Landthaler M, Vogt T: Expression profile of Eph receptors and ephrin ligands in human skin and downregulation of EphA1 in nonmelanoma skin cancer. Mod Pathol; 2006 Oct;19(10):1369-77
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] Expression profile of Eph receptors and ephrin ligands in human skin and downregulation of EphA1 in nonmelanoma skin cancer.
  • Beyond their well-defined meaning in developmental processes, these molecules also have important functions in adult human tissues and cancer.
  • However, the Eph/ephrin expression profile in human skin is only marginally studied.
  • We therefore investigated the mRNA expression of 21 Eph receptors and ephrin ligands in adult human skin in comparison to 13 other adult human tissues using quantitative real-time RT-PCR.
  • In addition, immunohistochemistry was established for some members (EphA1, EphA2 and EphA7) to confirm the results of the RT-PCR and to identify the expressing cells in the skin.
  • We found all investigated family members expressed in human skin, but at highly varying levels.
  • EphA1, EphB3 and ephrin-A3 turned out to be most prominently expressed in skin compared to other adult human tissues.
  • We therefore investigated the expression of EphA1 in nonmelanoma skin cancers derived from the epidermis (56 basal cell carcinomas and 32 squamous cell carcinomas).
  • As demonstrated by immunohistochemistry, both skin cancers displayed a significant downregulation of EphA1 compared to the normal epidermis.
  • In squamous cell carcinoma, the EphA1 downregulation was associated with increased tumor thickness, although this was not significant.
  • Our results indicate that Eph receptors and ephrin ligands are widely expressed in the adult human skin, particularly in the epidermis, and may play an important role in skin homeostasis.
  • EphA1 seems to be a marker of the differentiated normal epidermis and its downregulation in nonmelanoma skin cancer may contribute to carcinogenesis of these very frequent human tumors.
  • EphA1 represents a new potential prognostic marker and therapeutic target in nonmelanoma skin cancer.
  • [MeSH-major] Carcinoma, Squamous Cell / chemistry. Ephrins / analysis. Neoplasms, Basal Cell / chemistry. Receptor, EphA1 / analysis. Skin / chemistry. Skin Neoplasms / chemistry. Skin Neoplasms / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Down-Regulation. Ephrin-A3 / analysis. Female. Humans. Immunohistochemistry. Male. Middle Aged. Prognosis. RNA, Messenger / metabolism. Receptor, EphB3 / analysis. Reverse Transcriptase Polymerase Chain Reaction. Skin Ulcer / metabolism. Skin Ulcer / pathology

  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16862074.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ephrin-A3; 0 / Ephrins; 0 / RNA, Messenger; EC 2.7.10.1 / Receptor, EphA1; EC 2.7.10.1 / Receptor, EphB3
  •  go-up   go-down


79. Mogensen M, Jemec GB: Diagnosis of nonmelanoma skin cancer/keratinocyte carcinoma: a review of diagnostic accuracy of nonmelanoma skin cancer diagnostic tests and technologies. Dermatol Surg; 2007 Oct;33(10):1158-74
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.
  • [Title] Diagnosis of nonmelanoma skin cancer/keratinocyte carcinoma: a review of diagnostic accuracy of nonmelanoma skin cancer diagnostic tests and technologies.
  • BACKGROUND: Nonmelanoma skin cancer (NMSC) is the most prevalent cancer in the light-skinned population.
  • OBJECTIVE: The scope of this review is to present data on the current state-of-the-art diagnostic methods for keratinocyte carcinoma: basal cell carcinoma, squamous cell carcinoma, and actinic keratosis.
  • [MeSH-major] Skin Neoplasms / diagnosis
  • [MeSH-minor] Carcinoma, Basal Cell / diagnosis. Carcinoma, Basal Cell / pathology. Carcinoma, Basal Cell / ultrasonography. Carcinoma, Squamous Cell / diagnosis. Carcinoma, Squamous Cell / pathology. Carcinoma, Squamous Cell / ultrasonography. Dermoscopy. Diagnostic Tests, Routine. Humans. Keratosis / diagnosis. Keratosis / pathology. Keratosis / ultrasonography

  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17903149.001).
  • [ISSN] 1076-0512
  • [Journal-full-title] Dermatologic surgery : official publication for American Society for Dermatologic Surgery [et al.]
  • [ISO-abbreviation] Dermatol Surg
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 128
  •  go-up   go-down


80. Nasir S, Kayikcioglu A, Aydin MA, Tunçbilek G: Coverage of the cranium with latissimus dorsi in the recurrent basal cell carcinoma of Gorlin syndrome: for protection against clinical invasion. J Craniofac Surg; 2006 May;17(3):599-602
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.
  • [Title] Coverage of the cranium with latissimus dorsi in the recurrent basal cell carcinoma of Gorlin syndrome: for protection against clinical invasion.
  • Gorlin's syndrome is a genetic disorder of autosomal dominant inheritance with characterized primarily by five major findings: multiple basal cell carsinoma (BCC), jaw cysts, pits on the palms and soles, ectopic calcification of the falx cerebri and skeletal anomalies.
  • BCC is the most frequently accompanied tumor with this syndrome.
  • The risk of recurrent BCC with Gorlin's syndrome is higher than non-syndromic BCC.
  • The authors present a 25-year-old man affected by recurrent basal cell carcinoma on the scalp.
  • The patient was treated by excising the tumor and reconstructing latissimus dorsi musculocutaneous flap.
  • The fascial component of the scalp forms an additional layer between the skin and the cranium.
  • This structure creates an extra distance before the invasion into the cranium which needs to be penetrated by the skin tumor.
  • Muscle tissue transformed in scalp reconstruction imitates the fascia layer in forming an additional layer against the invasion of skin tumors such as recurrent BCC into the cranium.
  • Free flap reconstruction for recurrent scalp BCC can be best therapy model at Gorlin's syndrome.
  • [MeSH-major] Basal Cell Nevus Syndrome / surgery. Carcinoma, Basal Cell / surgery. Muscle, Skeletal / transplantation. Scalp / surgery. Skin Neoplasms / surgery. Skull / surgery
  • [MeSH-minor] Adult. Clinical Protocols. Fascia / transplantation. Follow-Up Studies. Humans. Male. Neoplasm Invasiveness. Neoplasm Recurrence, Local / surgery. Skin Transplantation / methods

  • Genetic Alliance. consumer health - Nevoid basal cell carcinoma syndrome.
  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16770207.001).
  • [ISSN] 1049-2275
  • [Journal-full-title] The Journal of craniofacial surgery
  • [ISO-abbreviation] J Craniofac Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


81. Pavicic WH, Laguens M, Richard SM: Analysis association between mitochondrial genome instability and xenobiotic metabolizing genes in human breast cancer. Mol Med; 2009 May-Jun;15(5-6):160-5
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] Analysis association between mitochondrial genome instability and xenobiotic metabolizing genes in human breast cancer.
  • The aim of this study was to determine the existence of association between the genetic polymorphisms of metabolizing genes GSTM-1, GSTT-1, and NAT-2, and the presence of mitochondrial genome instability (mtGI) in breast cancer cases.
  • Ninety-four pairs of tumoral/nontumoral breast cancer samples were analyzed.
  • GSTM-1 null genotype has shown a significant association with mtGI presence (chi(2) = 7.62; P = 0.006) in breast cancer cases; moreover, these genotypes also are related to an increased risk for mtDNA damage (odds ratio [OR] = 3.71 [1.41-9.88]; 95% Cornfield confidence interval [CI]).
  • The analysis of invasive breast cancer cases showed mtGI in 74.36% of ILC cases (29 of 39 samples), and in only 18.75% (9 out of 48) IDC cases; this result suggests a possible relation between mtDNA mutations and variations in molecular pathways of tumor development.
  • [MeSH-major] Arylamine N-Acetyltransferase / genetics. Breast Neoplasms / genetics. Genetic Predisposition to Disease. Genome, Mitochondrial / genetics. Genomic Instability. Glutathione Transferase / genetics

  • Genetic Alliance. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • 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] Carcinogenesis. 2000 Jan;21(1):49-54 [10607733.001]
  • [Cites] Am J Epidemiol. 2007 Aug 1;166(3):246-54 [17535831.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2000 Jun;9(6):567-73 [10868690.001]
  • [Cites] Cancer Res. 2000 Aug 1;60(15):4231-7 [10945635.001]
  • [Cites] Cancer Res. 2000 Sep 1;60(17):4667-77 [10987265.001]
  • [Cites] Mutat Res. 2001 Mar;488(1):9-23 [11223402.001]
  • [Cites] Mutat Res. 2001 Mar;488(1):77-85 [11223406.001]
  • [Cites] Mutat Res. 2001 Dec 12;484(1-2):103-6 [11733077.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2001 Dec;10(12):1239-48 [11751440.001]
  • [Cites] Cancer Res. 2002 Feb 15;62(4):972-6 [11861366.001]
  • [Cites] Cancer Invest. 2002;20(4):557-69 [12094550.001]
  • [Cites] Biochem J. 2002 Aug 15;366(Pt 1):45-55 [12020353.001]
  • [Cites] Cancer Lett. 2003 Jul 10;196(2):179-86 [12860276.001]
  • [Cites] Oncol Rep. 2003 Sep-Oct;10(5):1561-7 [12883742.001]
  • [Cites] Int J Cancer. 2004 Jan 10;108(2):228-31 [14639607.001]
  • [Cites] Nature. 1981 Apr 9;290(5806):457-65 [7219534.001]
  • [Cites] J Cancer Res Clin Oncol. 1990;116(5):499-502 [2229141.001]
  • [Cites] Carcinogenesis. 1990 Dec;11(12):2163-70 [2265468.001]
  • [Cites] J Cancer Res Clin Oncol. 1991;117(3):254-8 [2033093.001]
  • [Cites] Arch Biochem Biophys. 1994 Apr;310(1):82-8 [8161225.001]
  • [Cites] Pharmacogenetics. 1995 Feb;5(1):1-17 [7773298.001]
  • [Cites] Cytogenet Cell Genet. 1995;71(1):99-103 [7606938.001]
  • [Cites] Cancer Res. 1995 Aug 15;55(16):3483-5 [7627950.001]
  • [Cites] Am J Hum Genet. 1995 Sep;57(3):581-92 [7668286.001]
  • [Cites] Prog Clin Biol Res. 1997;396:53-61 [9108589.001]
  • [Cites] Carcinogenesis. 1997 Dec;18(12):2299-305 [9450473.001]
  • [Cites] Electrophoresis. 1997 Dec;18(15):2857-60 [9504821.001]
  • [Cites] J Natl Cancer Inst. 1998 Apr 1;90(7):512-8 [9539246.001]
  • [Cites] Chem Biol Interact. 1998 Apr 24;111-112:365-75 [9679567.001]
  • [Cites] Curr Opin Genet Dev. 1998 Jun;8(3):298-303 [9690990.001]
  • [Cites] Br J Cancer. 1999 Jan;79(2):346-53 [9888479.001]
  • [Cites] Mol Hum Reprod. 1999 Jul;5(7):636-41 [10381818.001]
  • [Cites] Carcinogenesis. 1999 Jul;20(7):1225-9 [10383893.001]
  • [Cites] Melanoma Res. 2004 Dec;14(6):501-8 [15577321.001]
  • [Cites] Carcinogenesis. 2005 Jan;26(1):145-52 [15375011.001]
  • [Cites] Gastroenterology. 2000 May;118(5):835-41 [10784582.001]
  • (PMID = 19287511.001).
  • [ISSN] 1528-3658
  • [Journal-full-title] Molecular medicine (Cambridge, Mass.)
  • [ISO-abbreviation] Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Mitochondrial; EC 2.3.1.5 / Arylamine N-Acetyltransferase; EC 2.3.1.5 / NAT2 protein, human; EC 2.5.1.- / glutathione S-transferase T1; EC 2.5.1.18 / Glutathione Transferase; EC 2.5.1.18 / glutathione S-transferase M1
  •  go-up   go-down


82. Shumaker PR, Lane K, Harford R: Linear unilateral basal cell nevus: a benign follicular hamartoma simulating multiple basal cell carcinomas. Cutis; 2006 Aug;78(2):122-4
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.
  • [Title] Linear unilateral basal cell nevus: a benign follicular hamartoma simulating multiple basal cell carcinomas.
  • We report a case of linear unilateral basal cell nevus (LBCN) occurring on the left lateral neck and left posterior shoulder of a 23-year-old woman.
  • LBCN is a rare benign follicular hamartoma that must be distinguished from the more aggressive unilateral and segmental variant of nevoid basal cell carcinoma syndrome (NBCCS) and the linear variant of BCC.
  • [MeSH-major] Carcinoma, Basal Cell / pathology. Hamartoma / pathology. Nevus / pathology. Skin Neoplasms / pathology
  • [MeSH-minor] Adult. Diagnosis, Differential. Female. Humans


83. Vestergård M, Henry F, Rangel-Castro JI, Michelsen A, Prosser JI, Christensen S: Rhizosphere bacterial community composition responds to arbuscular mycorrhiza, but not to reductions in microbial activity induced by foliar cutting. FEMS Microbiol Ecol; 2008 Apr;64(1):78-89
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.
  • Differences in bacterial community composition (BCC) between bulk and rhizosphere soil and between rhizospheres of different plant species are assumed to be strongly governed by quantitative and qualitative rhizodeposit differences.
  • However, data on the relationship between rhizodeposit amounts and BCC are lacking.
  • Other soil microorganisms, e.g. arbuscular mycorrhizal fungi (AMF), may also influence BCC.
  • These results show that a reduction in rhizosphere microbial activity is not necessarily accompanied by changes in BCC, whereas AMF presence inhibits proliferation of some bacterial taxa while stimulating others.

  • MedlinePlus Health Information. consumer health - Molds.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. Carbon dioxide .
  • 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
  • (PMID = 18312375.001).
  • [ISSN] 0168-6496
  • [Journal-full-title] FEMS microbiology ecology
  • [ISO-abbreviation] FEMS Microbiol. Ecol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Carbon Isotopes; 142M471B3J / Carbon Dioxide
  •  go-up   go-down


84. Garcia S, Dalès JP, Charafe-Jauffret E, Carpentier-Meunier S, Andrac-Meyer L, Jacquemier J, Andonian C, Lavaut MN, Allasia C, Bonnier P, Charpin C: Poor prognosis in breast carcinomas correlates with increased expression of targetable CD146 and c-Met and with proteomic basal-like phenotype. Hum Pathol; 2007 Jun;38(6):830-41
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.
  • [Title] Poor prognosis in breast carcinomas correlates with increased expression of targetable CD146 and c-Met and with proteomic basal-like phenotype.
  • Genomic studies have led to new taxonomic classifications of breast carcinomas.
  • Searching for new drug targets is particularly important for tumors of poor prognosis, such as breast tumors that lack estrogen receptors and HER2 amplification; in these tumors, certain molecules probably play a significant role in tumor spreading through the stromal microvasculature.
  • We investigated 930 breast carcinomas categorized according to patients' survival (range of follow-up = 4-10 years; median follow-up = 6.5 years) using (1) automated immunohistochemical procedures (Ventana, Cedex, France) with tissue microarrays (Alphelys, Plaisir, France) and (2) quantification of immunoprecipitates assessed by automated image analysis densitometry (SAMBA, Meylan, France).
  • Expression of c-Met and CD146 and that of signaling transducers PI3K, FAK, and FYN were compared in living and deceased patients.
  • Expression of some proteins recently reported to be characteristic of basal cell carcinomas was also assessed, namely, CK5-6, caveolin-1, carbonic anhydrase IX, p63, and CD117; these also constitute potential targets for therapies for aggressive tumors.
  • c-Met and CD146 are involved in tumor spreading, and our results suggest that they probably play an important role in patients' death, along with other proteins involved in hypoxia (carbonic anhydrase IX) and other cell functions or structures (caveolin-1, CD117, CK5-6, and p63) that are expressed in an aggressive subtype of basal cell carcinoma for which no specific therapy is available.
  • [MeSH-major] Antigens, CD146 / biosynthesis. Breast Neoplasms / metabolism. Breast Neoplasms / pathology. Neoplasms, Basal Cell / metabolism. Proto-Oncogene Proteins c-met / biosynthesis
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / analysis. Female. Focal Adhesion Kinase 1 / biosynthesis. Humans. Image Processing, Computer-Assisted. Immunohistochemistry. Immunoprecipitation. Middle Aged. Phenotype. Phosphatidylinositol 3-Kinases / biosynthesis. Prognosis. Proteomics. Proto-Oncogene Proteins c-fyn / biosynthesis. Tissue Array Analysis


85. Mapelli ET, Colombo L, Crespi E, Gualandri L, Menni S: Uncommon localization of basal cell carcinoma. Eur J Dermatol; 2010 Mar-Apr;20(2):224-5
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.
  • [Title] Uncommon localization of basal cell carcinoma.
  • [MeSH-major] Axilla / pathology. Carcinoma, Basal Cell / pathology. Skin Neoplasms / pathology

  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19919913.001).
  • [ISSN] 1167-1122
  • [Journal-full-title] European journal of dermatology : EJD
  • [ISO-abbreviation] Eur J Dermatol
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] France
  •  go-up   go-down


86. Basyuk E, Coulon V, Le Digarcher A, Coisy-Quivy M, Moles JP, Gandarillas A, Journot L: The candidate tumor suppressor gene ZAC is involved in keratinocyte differentiation and its expression is lost in basal cell carcinomas. Mol Cancer Res; 2005 Sep;3(9):483-92
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] The candidate tumor suppressor gene ZAC is involved in keratinocyte differentiation and its expression is lost in basal cell carcinomas.
  • ZAC is a zinc finger transcription factor that induces apoptosis and cell cycle arrest in various cell lines.
  • The corresponding gene is maternally imprinted and localized on chromosome 6q24-q25, a region harboring an unidentified tumor suppressor gene for a variety of solid neoplasms.
  • ZAC expression is lost or down-regulated in some breast, ovary, and pituitary tumors and in an in vitro model of ovary epithelial cell transformation.
  • In the present study, we examined ZAC expression in normal skin and found a high expression level in basal keratinocytes and a lower, more heterogeneous, expression in the first suprabasal differentiating layers of epidermis.
  • Interestingly, we found a dramatic loss of ZAC expression in basal cell carcinoma, a neoplasm characterized by a relatively undifferentiated morphology.
  • In contrast, ZAC expression was maintained in squamous cell carcinomas that retain the squamous differentiated phenotype.
  • [MeSH-major] Cell Cycle Proteins / metabolism. Cell Differentiation. Keratinocytes / cytology. Skin Neoplasms / metabolism. Transcription Factors / metabolism
  • [MeSH-minor] Carcinoma, Basal Cell / genetics. Carcinoma, Basal Cell / metabolism. Carcinoma, Basal Cell / pathology. Carcinoma, Squamous Cell / genetics. Carcinoma, Squamous Cell / metabolism. Carcinoma, Squamous Cell / pathology. Cells, Cultured. Genes, Tumor Suppressor. Humans. In Situ Hybridization. RNA Probes. Tumor Suppressor Proteins. Zinc Fingers

  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16179495.001).
  • [ISSN] 1541-7786
  • [Journal-full-title] Molecular cancer research : MCR
  • [ISO-abbreviation] Mol. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / PLAGL1 protein, human; 0 / RNA Probes; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins
  •  go-up   go-down


87. Boyd AS, Wu H, Shyr Y: Monster cells in malignant melanoma. Am J Dermatopathol; 2005 Jun;27(3):208-10
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.
  • [Title] Monster cells in malignant melanoma.
  • Cells with significantly enlarged nuclei have been described in basal cell carcinomas, dermatofibromas, and pleomorphic fibromas, to name a few.
  • Thirteen cases of melanoma containing monster cells were found.
  • The finding of monster cells is not an uncommon occurrence and is seen more often in nodular melanomas.
  • [MeSH-major] Melanoma / pathology. Skin Neoplasms / pathology

  • MedlinePlus Health Information. consumer health - Melanoma.
  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Am J Dermatopathol. 2006 Oct;28(5):462-3; author reply 463 [17012927.001]
  • (PMID = 15900123.001).
  • [ISSN] 0193-1091
  • [Journal-full-title] The American Journal of dermatopathology
  • [ISO-abbreviation] Am J Dermatopathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


88. Zur Hausen H: The search for infectious causes of human cancers: where and why. Virology; 2009 Sep 15;392(1):1-10
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.
  • Slightly more than 20% of the global cancer burden can presently be linked to infectious agents, including viruses, bacteria and parasites.
  • Emphasis is placed on hematopoietic malignancies, breast and colorectal cancers, but also basal cell carcinomas of the skin and lung cancers in non-smokers.
  • [MeSH-major] Infection / complications. Neoplasms / etiology
  • [MeSH-minor] Animals. Cluster Analysis. Epidemiologic Factors. Female. Helicobacter pylori / pathogenicity. Hepacivirus / pathogenicity. Hepatitis B virus / pathogenicity. Herpesvirus 4, Human / pathogenicity. Humans. Immunosuppression / adverse effects. Male. Models, Biological. Papillomaviridae / pathogenicity. Tumor Virus Infections / epidemiology. Tumor Virus Infections / etiology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19720205.001).
  • [ISSN] 1096-0341
  • [Journal-full-title] Virology
  • [ISO-abbreviation] Virology
  • [Language] eng
  • [Publication-type] Lectures
  • [Publication-country] United States
  •  go-up   go-down


89. Katoh Y, Katoh M: Integrative genomic analyses on GLI1: positive regulation of GLI1 by Hedgehog-GLI, TGFbeta-Smads, and RTK-PI3K-AKT signals, and negative regulation of GLI1 by Notch-CSL-HES/HEY, and GPCR-Gs-PKA signals. Int J Oncol; 2009 Jul;35(1):187-92
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.
  • GLI1 transcription is upregulated in a variety of human tumors, such as basal cell carcinoma, lung cancer, breast cancer, gastric cancer, pancreatic cancer, and esophageal cancer.

  • 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
  • (PMID = 19513567.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / ARHGAP9 protein, human; 0 / Adaptor Proteins, Signal Transducing; 0 / GLI1 protein, human; 0 / GTPase-Activating Proteins; 0 / Hedgehog Proteins; 0 / Immunoglobulin J Recombination Signal Sequence-Binding Protein; 0 / RBPJ protein, human; 0 / Receptors, G-Protein-Coupled; 0 / Receptors, Notch; 0 / Smad Proteins; 0 / Transcription Factors; 0 / Transforming Growth Factor beta; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gs
  •  go-up   go-down


90. Conroy H, Marshall NA, Mills KH: TLR ligand suppression or enhancement of Treg cells? A double-edged sword in immunity to tumours. Oncogene; 2008 Jan 7;27(2):168-80
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.
  • Toll-like receptor (TLR) agonists are potent activators of innate immune responses, activating dendritic cell (DC) maturation and inflammatory cytokine secretion by innate immune cells and as a consequence they promote adaptive immune response when coadministered with foreign antigens.
  • There is also some evidence from mouse models that TLR ligands can help to break tolerance to self-antigens and promote immune responses to tumour antigens.
  • Therefore, they have been exploited as adjuvants for tumour vaccines or as immunotherapeutics against cancer.
  • Clinical evaluation of TLR agonists has resulted in a licensed immunotherapeutic for basal cell carcinoma, but there have also been disappointing results from clinical trials, with one pharmaceutical company recently halting its clinical programme.
  • A major obstacle to the development of any active immunotherapeutic approach to cancer is the immunosuppressive environment of the growing tumour, including the induction of tolerogenic DCs and regulatory T (Treg) cells, which suppress the development of protective effector T-cell responses.
  • This is part of a normal mechanism for limiting collateral damage during infection or sterile inflammation, but can constrain their ability to induce protective antitumour immunity, especially in the immune suppressed environment of the tumour.
  • Alternatively, manipulating the TLR-activated innate immune responses to selectively blocking immunosuppressive arm, as well as that induced by the tumour, may hold the key to enhancing their efficacy as tumour immunotherapeutics and as adjuvants for cancer vaccines.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Immunity, Cellular / drug effects. Ligands. Neoplasms / immunology. T-Lymphocytes, Regulatory / drug effects. Toll-Like Receptors / agonists
  • [MeSH-minor] Animals. Cancer Vaccines / therapeutic use. Chemotherapy, Adjuvant. Dendritic Cells / immunology. Humans. Immunotherapy, Adoptive. Lymphocyte Activation / drug effects. Models, Biological

  • COS Scholar Universe. author profiles.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18176598.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cancer Vaccines; 0 / Ligands; 0 / Toll-Like Receptors
  • [Number-of-references] 133
  •  go-up   go-down


91. Ram R, Saadat P, Peng D, Vadmal M: Case report and literature review: primary cutaneous carcinosarcoma. Ann Clin Lab Sci; 2005;35(2):189-94
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.
  • [Title] Case report and literature review: primary cutaneous carcinosarcoma.
  • Carcinosarcomas are rare but aggressive neoplasms commonly described in organs such as the breast, urinary bladder, uterus, liver, and lungs.
  • Histopathologically, they are characterized by the presence of malignant epithelial and mesenchymal components.
  • Primary carcinosarcomas of the skin are uncommon.
  • To our knowledge, 20 cases of primary cutaneous carcinosarcoma have been described in the world literature.
  • Microscopically, the more common carcinoma component is a squamous cell carcinoma followed by basal cell carcinoma, whereas the most common sarcoma component is an osteosarcoma.
  • We report an example of this rare entity and speculate on its histogenesis in the skin.
  • [MeSH-major] Carcinosarcoma / pathology. Skin Neoplasms / pathology
  • [MeSH-minor] Aged. Carcinoma, Basal Cell / pathology. Carcinoma, Squamous Cell / pathology. Diagnosis, Differential. Humans. Male. Osteosarcoma / pathology

  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • 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
  • (PMID = 15943184.001).
  • [ISSN] 0091-7370
  • [Journal-full-title] Annals of clinical and laboratory science
  • [ISO-abbreviation] Ann. Clin. Lab. Sci.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


92. Soerjomataram I, Louwman WJ, Lemmens VE, Coebergh JW, de Vries E: Are patients with skin cancer at lower risk of developing colorectal or breast cancer? Am J Epidemiol; 2008 Jun 15;167(12):1421-9
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.
  • [Title] Are patients with skin cancer at lower risk of developing colorectal or breast cancer?
  • Ultraviolet exposure may reduce the risk of colorectal and breast cancer as the result of rising vitamin D levels.
  • Because skin cancer is positively related to sun exposure, the authors hypothesized a lower incidence of breast and colorectal cancer after skin cancer diagnosis.
  • They analyzed the incidence of colorectal and breast cancer diagnosed from 1972 to 2002 among 26,916 Netherlands skin cancer patients (4,089 squamous cell carcinoma (SCC), 19,319 basal cell carcinoma (BCC), and 3,508 cutaneous malignant melanoma (CMM)).
  • A markedly decreased risk of colorectal cancer was found for subgroups supposedly associated with the highest accumulated sun exposure: men (standardized incidence ratio (SIR) = 0.83, 95% confidence interval (CI): 0.71, 0.97); patients with SCC (SIR = 0.64, 95% CI: 0.43, 0.93); older patients at SCC diagnosis (SIR = 0.59, 95% CI: 0.37, 0.88); and patients with a SCC or BCC lesion on the head and neck area (SIR = 0.59, 95% CI: 0.36, 0.92 for SCC and SIR = 0.78, 95% CI: 0.63, 0.97 for BCC).
  • Patients with CMM exhibited an increased risk of breast cancer, especially advanced breast cancer (SIR = 2.20, 95% CI: 1.10, 3.94) and older patients at CMM diagnosis (SIR = 1.87, 95% CI: 1.14, 2.89).
  • Study results suggest a beneficial effect of continuous sun exposure against colorectal cancer.
  • The higher risk of breast cancer among CMM patients may be related to socioeconomic class, both being more common in the affluent group.
  • [MeSH-major] Breast Neoplasms / epidemiology. Colorectal Neoplasms / epidemiology. Skin Neoplasms / epidemiology. Ultraviolet Rays. Vitamin D / blood
  • [MeSH-minor] Carcinoma, Basal Cell / epidemiology. Carcinoma, Squamous Cell / epidemiology. Confidence Intervals. Female. Humans. Incidence. Male. Melanoma / epidemiology. Middle Aged. Netherlands / epidemiology. Odds Ratio. Risk Assessment. Risk Factors


93. Chan SY, Madan V, Lear JT, Helbert M: Highly active antiretroviral therapy-induced regression of basal cell carcinomas in a patient with acquired immunodeficiency and Gorlin syndrome. Br J Dermatol; 2006 Nov;155(5):1079-80
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.
  • [Title] Highly active antiretroviral therapy-induced regression of basal cell carcinomas in a patient with acquired immunodeficiency and Gorlin syndrome.
  • [MeSH-major] Acquired Immunodeficiency Syndrome / complications. Antiretroviral Therapy, Highly Active. Basal Cell Nevus Syndrome / complications
  • [MeSH-minor] Humans. Male. Middle Aged. Neoplasm Regression, Spontaneous. Treatment Outcome


94. Huang O, Chen C, Wu J, Chen S, Chen X, Liu G, Hu Z, Lu J, Wu J, Shao Z, Shen Z, Shen K: Retrospective analysis of 119 Chinese noninflammatory locally advanced breast cancer cases treated with intravenous combination of vinorelbine and epirubicin as a neoadjuvant chemotherapy: a median follow-up of 63.4 months. BMC Cancer; 2009;9:375
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] Retrospective analysis of 119 Chinese noninflammatory locally advanced breast cancer cases treated with intravenous combination of vinorelbine and epirubicin as a neoadjuvant chemotherapy: a median follow-up of 63.4 months.
  • BACKGROUND: This study is a retrospective evaluation of the efficacy of neoadjuvant chemotherapy (NC) with a vinorelbine (V) and epirubicin (E) intravenous combination regimen and is aimed at identification of predictive markers for the long-term outcome in noninflammatory locally advanced breast cancer (NLABC).
  • All patients were diagnosed with invasive breast cancer using 14 G core needle biopsy and treated with three cycles of VE before surgery.
  • Tissue sections cut from formalin-fixed paraffin-embedded blocks from biopsy specimens and postoperative tumor tissues were stained for the presence of estrogen receptor (ER), progesterone receptor (PgR), HER-2 (human epidermal growth factor receptor-2), and MIB-1(Ki-67).
  • All patients were evaluable for response: clinically complete response was documented in 27 patients (22.7%); 78 (65.6%) obtained partial response; stable disease was observed in 13 (10.9%); 1 patient (0.8%) had progressive disease.
  • Pathological complete response was found in 22 cases (18.5%).
  • Seventy-five patients were alive with no recurrence after a median follow-up of 63.4 months, the 5-year rates for disease-free survival and overall survival were 58.7% and 71.3%, respectively, after the start of NC.
  • Among patients with non-pCR, those with a pathological response at the tumor site with special involvement (i.e. skin, vessel and more than one quadrant) were at a higher risk of disease relapse and death (p < 0.001, p = 0.001, respectively).
  • CONCLUSION: This study suggests the promising use of a VE regimen as NC for Chinese NLABC after a median follow-up of 63.4 months.
  • Pathological response in the tumor site, pre-Ki-67 and post-Ki-67 expression, and pre-ER expression were the important variables that predicted long-term outcome.
  • [MeSH-major] Breast Neoplasms / drug therapy. Epirubicin / administration & dosage. Neoadjuvant Therapy. Vinblastine / analogs & derivatives

  • Genetic Alliance. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • Hazardous Substances Data Bank. EPIRUBICIN .
  • Hazardous Substances Data Bank. VINORELBINE .
  • Hazardous Substances Data Bank. VINBLASTINE .
  • 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] J Clin Oncol. 2000 Jun;18(12):2385-94 [10856098.001]
  • [Cites] J Clin Oncol. 2001 Nov 15;19(22):4224-37 [11709566.001]
  • [Cites] J Natl Cancer Inst Monogr. 2001;(30):96-102 [11773300.001]
  • [Cites] Anticancer Res. 2001 Nov-Dec;21(6A):4135-9 [11911307.001]
  • [Cites] Am J Clin Oncol. 2002 Jun;25(3):303-7 [12040294.001]
  • [Cites] J Clin Oncol. 2002 Sep 1;20(17):3628-36 [12202663.001]
  • [Cites] Endocr Relat Cancer. 2003 Mar;10(1):91-8 [12653672.001]
  • [Cites] Surg Clin North Am. 2003 Aug;83(4):803-19 [12875597.001]
  • [Cites] J Clin Oncol. 2003 Nov 15;21(22):4165-74 [14559892.001]
  • [Cites] Breast. 2003 Feb;12(1):42-50 [14659354.001]
  • [Cites] Clin Cancer Res. 2004 Oct 1;10(19):6622-8 [15475452.001]
  • [Cites] N Engl J Med. 1978 Dec 14;299(24):1330-4 [714108.001]
  • [Cites] Cancer. 1980 Dec 15;46(12 Suppl):2829-34 [7448729.001]
  • [Cites] Am Surg. 1996 Feb;62(2):162-5 [8554195.001]
  • [Cites] Anticancer Res. 1996 Sep-Oct;16(5B):3105-10 [8920776.001]
  • [Cites] Br J Cancer. 1998 Feb;77(4):621-6 [9484820.001]
  • [Cites] Mod Pathol. 1998 Feb;11(2):155-68 [9504686.001]
  • [Cites] Breast Cancer Res Treat. 1998 Mar;48(1):11-20 [9541185.001]
  • [Cites] Breast Cancer Res Treat. 1998 Mar;48(2):107-16 [9596482.001]
  • [Cites] Lancet. 1998 May 16;351(9114):1451-67 [9605801.001]
  • [Cites] Clin Ter. 1998 Jan-Feb;149(921):61-74 [9621491.001]
  • [Cites] J Clin Oncol. 1998 Aug;16(8):2672-85 [9704717.001]
  • [Cites] J Chemother. 1998 Aug;10(4):326-30 [9720473.001]
  • [Cites] Breast Cancer Res Treat. 1999 Jan;53(1):51-9 [10206072.001]
  • [Cites] J Clin Oncol. 1999 May;17(5):1474-81 [10334533.001]
  • [Cites] Acta Oncol. 1999;38(5):597-601 [10427948.001]
  • [Cites] Ann Oncol. 1999 Aug;10(8):937-42 [10509155.001]
  • [Cites] Ann Oncol. 1999 Aug;10(8):993-6 [10509165.001]
  • [Cites] Br J Cancer. 2004 Dec 13;91(12):2012-7 [15558072.001]
  • [Cites] J Natl Cancer Inst. 2005 Feb 2;97(3):188-94 [15687361.001]
  • [Cites] J Clin Oncol. 2005 Apr 10;23(11):2477-92 [15767642.001]
  • [Cites] Oncologist. 2005 Apr;10(4):242-9 [15821244.001]
  • [Cites] Anticancer Res. 2005 Mar-Apr;25(2B):1343-8 [15865089.001]
  • [Cites] Clin Cancer Res. 2005 Dec 15;11(24 Pt 1):8715-21 [16361558.001]
  • [Cites] J Clin Oncol. 2005 Dec 20;23(36):9304-11 [16361629.001]
  • [Cites] Clin Breast Cancer. 2006 Feb;6(6):511-7 [16595034.001]
  • [Cites] J Clin Oncol. 2006 May 1;24(13):2019-27 [16606972.001]
  • [Cites] Zhonghua Wai Ke Za Zhi. 2006 Jun 1;44(11):745-7 [16836921.001]
  • [Cites] Breast Cancer Res. 2006;8(3):R31 [16790076.001]
  • [Cites] J Clin Oncol. 2008 Feb 10;26(5):786-90 [18258987.001]
  • [Cites] Zhonghua Yi Xue Za Zhi. 2008 Jan 8;88(2):73-6 [18353206.001]
  • (PMID = 19845944.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Receptors, Estrogen; 3Z8479ZZ5X / Epirubicin; 5V9KLZ54CY / Vinblastine; Q6C979R91Y / vinorelbine
  • [Other-IDs] NLM/ PMC2770573
  •  go-up   go-down


95. Zhang XB, Zhang SQ, Li CX, Huang ZM, Luo YW: Acitretin systemic and retinoic acid 0.1% cream supression of basal cell carcinoma. Dermatol Reports; 2010 Jan 18;2(1):e4
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] Acitretin systemic and retinoic acid 0.1% cream supression of basal cell carcinoma.
  • Retinoids have been used for years as monotherapy and/or in combination for treatment and suppression of cutaneous malignancies in patients with basal cell nevus syndrome, xeroderma pigmentosum, or cutaneous T-cell lymphoma (CTCL) basal cell carcinoma (BCC).
  • We report 4 cases with BCC confirmed by histopathology who were treated by short-term systemic acitretin combined with retinoic acid 0.1% cream.
  • The 4 cases with BCC showed good response to the treatment without severe adverse effects during treatment and follow-up.
  • The finding suggests that acitretin may be an appropriate treatment option for elderly patients who require less invasive treatment for BCC.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 25386240.001).
  • [ISSN] 2036-7392
  • [Journal-full-title] Dermatology reports
  • [ISO-abbreviation] Dermatol Reports
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Other-IDs] NLM/ PMC4211482
  • [Keywords] NOTNLM ; acitretin / basal cell carcinoma.
  •  go-up   go-down


96. Schulz KK, Walling HW: Fractional photothermolysis improves a depressed alar scar following Mohs micrographic surgery. J Drugs Dermatol; 2010 Jan;9(1):66-7
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.
  • We present the case of a 49-year-old woman with a depressed 0.7 x 0.5 cm alar scar resulting from Mohs micrographic surgery for basal cell carcinoma with secondary intention healing.
  • [MeSH-minor] Carcinoma, Basal Cell / surgery. Face / pathology. Female. Humans. Middle Aged. Skin Neoplasms / surgery

  • MedlinePlus Health Information. consumer health - After Surgery.
  • MedlinePlus Health Information. consumer health - Scars.
  • 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
  • (PMID = 20120428.001).
  • [ISSN] 1545-9616
  • [Journal-full-title] Journal of drugs in dermatology : JDD
  • [ISO-abbreviation] J Drugs Dermatol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


97. Malimas T, Yukphan P, Takahashi M, Muramatsu Y, Kaneyasu M, Potacharoen W, Tanasupawat S, Nakagawa Y, Tanticharoen M, Yamada Y: Gluconobacter japonicus sp. nov., an acetic acid bacterium in the Alphaproteobacteria. Int J Syst Evol Microbiol; 2009 Mar;59(Pt 3):466-71
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 five strains weakly produced dihydroxyacetone from glycerol, but not 2,5-diketo-d-gluconate or a water-soluble brown pigment from d-glucose and contained ubiquinone-10.
  • The type strain is NBRC 3271(T) (=BCC 14458(T)=strain 7(T), K. Kondo).

  • Hazardous Substances Data Bank. ACETIC ACID .
  • SILVA. SILVA SSU Database .
  • StrainInfo. culture/stock collections - online strain list (subscription/membership/fee required).
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19244423.001).
  • [ISSN] 1466-5026
  • [Journal-full-title] International journal of systematic and evolutionary microbiology
  • [ISO-abbreviation] Int. J. Syst. Evol. Microbiol.
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ AB178400/ AB178408/ AB253434/ AB253435/ AB253436
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Bacterial; 0 / DNA, Ribosomal Spacer; 0 / RNA, Ribosomal, 16S; 0 / RNA, Ribosomal, 23S; Q40Q9N063P / Acetic Acid
  •  go-up   go-down


98. Hernández-Machin B, Borrego L, Gil-García M, Hernández BH: Office-based radiation therapy for cutaneous carcinoma: evaluation of 710 treatments. Int J Dermatol; 2007 May;46(5):453-9
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.
  • [Title] Office-based radiation therapy for cutaneous carcinoma: evaluation of 710 treatments.
  • Skin cancers are the most common malignancies and, historically, ionizing radiation has played an important role in their treatment.
  • The authors sought to evaluate the effectiveness and safety of office-based elective radiation therapy for cutaneous carcinoma.
  • A retrospective study of 604 basal cell carcinomas (BCCs) and 106 squamous cell carcinomas (SCCs) irradiated between 1971-96 was performed.
  • The percentage of patients who developed tumor recurrence during the follow-up period was calculated using Kaplan-Meier survival curves.
  • The recurrence rates for BCC and SCC were 11.5 and 16.5 per 1000 patient-years, respectively.
  • The 5-year cure rates were 94.4% for BCC and 92.7% for SCC, and the 15-year cure rates were 84.8% and 78.6%, respectively.
  • Tumor location on the nasolabial fold (OR 4.4; 95% IC, 1.3-14.7) and tumor size > or = 10 mm (OR 2.14; 95% IC, 1.03-4.45) were independent predictors of BCC recurrence.
  • This study suggested that radiation therapy is an effective treatment for BCC and SCC and should be considered as a first option in many cases.
  • [MeSH-major] Carcinoma, Basal Cell / radiotherapy. Carcinoma, Squamous Cell / radiotherapy. Skin Neoplasms / radiotherapy
  • [MeSH-minor] Aged. Female. Follow-Up Studies. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Neoplasm Recurrence, Local. Radiation Dosage. Radiotherapy / methods. Radiotherapy / statistics & numerical data. Retrospective Studies. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • 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
  • (PMID = 17472670.001).
  • [ISSN] 0011-9059
  • [Journal-full-title] International journal of dermatology
  • [ISO-abbreviation] Int. J. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


99. Bilici A, Ozguroglu M, Mihmanli I, Turna H, Adaletli I: A case-control study of non-alcoholic fatty liver disease in breast cancer. Med Oncol; 2007;24(4):367-71
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.
  • [Title] A case-control study of non-alcoholic fatty liver disease in breast cancer.
  • BACKGROUND: Patients with breast cancer sometimes present with increased liver enzymes during follow-up period that may be consistent with hepatic steatosis.
  • This effect known as non-alcoholic fatty liver disease may be associated with the malignancy itself, drugs or some other well-known risk factors that may induce steatosis.
  • We studied the influences of primary disease and treatment on steatosis in patients with breast cancer.
  • Group 1: 40 newly diagnosed, previously untreated breast cancer; Group 2: 45 cases of breast cancer treated with systemic therapy; Group 3: 40 cases of ovarian cancer; Group 4: 40 healthy women.
  • However, grade 2 and 3 steatosis were more frequent in breast cancer patients (group 1 and 2), compared with mild steatosis in ovarian cancer patients and healthy women.
  • Although a good correlation was found between tamoxifen use and chemotherapy on development of non-alcoholic fatty liver disease, no association of hepatic steatosis with transaminase levels was found, which might be of help for earlier detection of steatosis.
  • CONCLUSION: Hepatic steatosis, excluding patients with grade 1 steatosis, which may be a normal variant, were more readily detected in patients with breast cancer.
  • Non-alcoholic fatty liver disease in patients with breast cancer may be associated with the primary tumor itself or some well-known risk factors such as obesity, hyperlipidemia, and diabetes mellitus, which needs to be explored.
  • [MeSH-major] Breast Neoplasms / complications. Fatty Liver / epidemiology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Alanine Transaminase / blood. Alkaline Phosphatase / blood. Aspartate Aminotransferases / blood. Case-Control Studies. Female. Humans. L-Lactate Dehydrogenase / blood. Middle Aged. Risk Factors. Ultrasonography. gamma-Glutamyltransferase / blood

  • Genetic Alliance. consumer health - Liver cancer.
  • Genetic Alliance. consumer health - Liver Disease.
  • Genetic Alliance. consumer health - Non-alcoholic steatohepatitis (NASH).
  • Genetic Alliance. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Lipid Res. 1989 Aug;30(8):1137-45 [2504861.001]
  • [Cites] Ann Oncol. 1998 Oct;9(10 ):1123-6 [9834826.001]
  • [Cites] J Biol Chem. 1980 Nov 10;255(21):10464-71 [6253476.001]
  • [Cites] Oncol Rep. 2000 Nov-Dec;7(6):1299-304 [11032933.001]
  • [Cites] Gastroenterology. 1994 Oct;107(4):1103-9 [7523217.001]
  • [Cites] Int J Obes Relat Metab Disord. 2001 Feb;25(2):296-8 [11410835.001]
  • [Cites] Clin Radiol. 1991 Jun;43(6):393-6 [2070579.001]
  • [Cites] Cancer Chemother Pharmacol. 1989;23(3):194-5 [2924377.001]
  • [Cites] Ann Intern Med. 1997 Sep 1;127(5):410; author reply 411 [9273835.001]
  • [Cites] Breast Cancer Res Treat. 2006 May;97(2):223-4 [16322887.001]
  • [Cites] Br Med J (Clin Res Ed). 1984 Aug 4;289(6440):288 [6430441.001]
  • [Cites] Lancet. 1998 Mar 7;351(9104):725 [9504521.001]
  • [Cites] Semin Liver Dis. 2001;21(1):27-41 [11296694.001]
  • [Cites] Int J Oncol. 2000 Dec;17 (6):1119-23 [11078796.001]
  • [Cites] Acta Oncol. 1995;34(7):971-2 [7492393.001]
  • [Cites] Acta Med Scand. 1986;220(1):83-8 [3766211.001]
  • [Cites] Ann Intern Med. 1997 Jan 15;126(2):137-45 [9005748.001]
  • [Cites] Gastroenterology. 1999 Jun;116(6):1413-9 [10348825.001]
  • [Cites] Semin Liver Dis. 2001;21(1):3-16 [11296695.001]
  • [Cites] Oncol Rep. 2003 Jan-Feb;10 (1):97-100 [12469151.001]
  • [Cites] J Clin Endocrinol Metab. 1999 May;84(5):1513-7 [10323371.001]
  • [Cites] Eur J Gastroenterol Hepatol. 2004 Jun;16(6):593-8 [15167162.001]
  • [Cites] Mayo Clin Proc. 2000 Jul;75(7):733-9 [10907390.001]
  • [Cites] J Hepatol. 1998 Sep;29(3):495-501 [9765002.001]
  • [Cites] Gastroenterol Jpn. 1992 Aug;27(4):521-8 [1526433.001]
  • [Cites] J Ultrasound Med. 1984 Jan;3(1):9-14 [6694259.001]
  • [Cites] J Hepatol. 1995 Jul;23 (1):95-7 [8530816.001]
  • [Cites] Int J Obes. 1984;8(2):97-106 [6373641.001]
  • [Cites] Am J Gastroenterol. 2000 Jan;95(1):277-9 [10638597.001]
  • [Cites] Intern Med. 2002 May;41(5):345-50 [12058881.001]
  • [Cites] Ann Intern Med. 1995 Aug 1;123(3):236 [7598311.001]
  • [Cites] Br J Cancer. 1998 Jun;77(11):2008-11 [9667683.001]
  • [Cites] Semin Liver Dis. 2001;21(1):17-26 [11296693.001]
  • [Cites] J Hepatol. 1997 Jul;27(1):108-13 [9252082.001]
  • [Cites] Cancer. 1995 May 15;75(10 ):2592-6 [7736406.001]
  • [Cites] Lancet. 1999 Jan 2;353(9146):36-7 [10023952.001]
  • [Cites] Neoplasma. 2002;49(1):61-4 [12044063.001]
  • (PMID = 17917083.001).
  • [ISSN] 1357-0560
  • [Journal-full-title] Medical oncology (Northwood, London, England)
  • [ISO-abbreviation] Med. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 1.1.1.27 / L-Lactate Dehydrogenase; EC 2.3.2.2 / gamma-Glutamyltransferase; EC 2.6.1.1 / Aspartate Aminotransferases; EC 2.6.1.2 / Alanine Transaminase; EC 3.1.3.1 / Alkaline Phosphatase
  •  go-up   go-down


100. Laner-Plamberger S, Kaser A, Paulischta M, Hauser-Kronberger C, Eichberger T, Frischauf AM: Cooperation between GLI and JUN enhances transcription of JUN and selected GLI target genes. Oncogene; 2009 Apr 2;28(13):1639-51
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.
  • Sustained Hedgehog (HH) signaling is implicated in basal cell carcinoma of the skin and other types of cancer.
  • Here we show that GLI1 and GLI2, the main transcriptional activators of the HH pathway, directly regulate expression of the activator protein 1 (AP-1) family member JUN, a transcription factor controlling keratinocyte proliferation and skin homeostasis.
  • Some of these cooperatively activated genes are involved in cell-cycle progression, which is consistent with a significant reduction of the proliferative potential of GLI in the absence of JUN.
  • These results suggest a novel connection between HH/GLI pathway activity and JUN, which may contribute to the oncogenic activity of HH/GLI signaling in skin.
  • [MeSH-minor] Base Sequence. Binding Sites. Cell Proliferation. Cells, Cultured. Hedgehog Proteins / genetics. Hedgehog Proteins / physiology. Humans. Keratinocytes / metabolism. Keratinocytes / physiology. Phosphorylation. Promoter Regions, Genetic. Protein Binding / physiology. Protein Kinases / metabolism. Signal Transduction / genetics. Up-Regulation / genetics






Advertisement