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[PMID]:25200342
[Au] Autor:Edwards SK; Baron J; Moore CR; Liu Y; Perlman DH; Hart RP; Xie P
[Ti] Título:Mutated in colorectal cancer (MCC) is a novel oncogene in B lymphocytes.
[So] Source:J Hematol Oncol;7:56, 2014 Sep 09.
[Is] ISSN:1756-8722
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Identification of novel genetic risk factors is imperative for a better understanding of B lymphomagenesis and for the development of novel therapeutic strategies. TRAF3, a critical regulator of B cell survival, was recently recognized as a tumor suppressor gene in B lymphocytes. The present study aimed to identify novel oncogenes involved in malignant transformation of TRAF3-deficient B cells. METHODS: We used microarray analysis to identify genes differentially expressed in TRAF3-/- mouse splenic B lymphomas. We employed lentiviral vector-mediated knockdown or overexpression to manipulate gene expression in human multiple myeloma (MM) cell lines. We analyzed cell apoptosis and proliferation using flow cytometry, and performed biochemical studies to investigate signaling mechanisms. To delineate protein-protein interactions, we applied affinity purification followed by mass spectrometry-based sequencing. RESULTS: We identified mutated in colorectal cancer (MCC) as a gene strikingly up-regulated in TRAF3-deficient mouse B lymphomas and human MM cell lines. Aberrant up-regulation of MCC also occurs in a variety of primary human B cell malignancies, including non-Hodgkin lymphoma (NHL) and MM. In contrast, MCC expression was not detected in normal or premalignant TRAF3-/- B cells even after treatment with B cell stimuli, suggesting that aberrant up-regulation of MCC is specifically associated with malignant transformation of B cells. In elucidating the functional roles of MCC in malignant B cells, we found that lentiviral shRNA vector-mediated knockdown of MCC induced apoptosis and inhibited proliferation in human MM cells. Experiments of knockdown and overexpression of MCC allowed us to identify several downstream targets of MCC in human MM cells, including phospho-ERK, c-Myc, p27, cyclin B1, Mcl-1, caspases 8 and 3. Furthermore, we identified 365 proteins (including 326 novel MCC-interactors) in the MCC interactome, among which PARP1 and PHB2 were two hubs of MCC signaling pathways in human MM cells. CONCLUSIONS: Our results indicate that in sharp contrast to its tumor suppressive role in colorectal cancer, MCC functions as an oncogene in B cells. Our findings suggest that MCC may serve as a diagnostic marker and therapeutic target in B cell malignancies, including NHL and MM.
[Mh] Termos MeSH primário: Linfócitos B/patologia
Transformação Celular Neoplásica/genética
Genes MCC/genética
Oncogenes/genética
[Mh] Termos MeSH secundário: Animais
Apoptose/genética
Linhagem Celular Tumoral
Proliferação Celular/genética
Imunoprecipitação da Cromatina
Citometria de Fluxo
Seres Humanos
Immunoblotting
Imunoprecipitação
Linfoma não Hodgkin/genética
Camundongos
Camundongos Knockout
Mieloma Múltiplo/genética
Análise de Sequência com Séries de Oligonucleotídeos
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Fator 3 Associado a Receptor de TNF/deficiência
Espectrometria de Massas em Tandem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (TNF Receptor-Associated Factor 3)
[Em] Mês de entrada:1505
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140910
[St] Status:MEDLINE
[do] DOI:10.1186/s13045-014-0056-6


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[PMID]:25183869
[Au] Autor:Young T; Poobalan Y; Tan EK; Tao S; Ong S; Wehner P; Schwenty-Lara J; Lim CY; Sadasivam A; Lovatt M; Wang ST; Ali Y; Borchers A; Sampath K; Dunn NR
[Ad] Endereço:Institute of Medical Biology, Agency for Science, Technology and Research (A*STAR), 8A Biomedical Grove, #06-06 Immunos, Singapore 138648.
[Ti] Título:The PDZ domain protein Mcc is a novel effector of non-canonical Wnt signaling during convergence and extension in zebrafish.
[So] Source:Development;141(18):3505-16, 2014 Sep.
[Is] ISSN:1477-9129
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:During vertebrate gastrulation, a complex set of mass cellular rearrangements shapes the embryonic body plan and appropriately positions the organ primordia. In zebrafish and Xenopus, convergence and extension (CE) movements simultaneously narrow the body axis mediolaterally and elongate it from head to tail. This process is governed by polarized cell behaviors that are coordinated by components of the non-canonical, ß-catenin-independent Wnt signaling pathway, including Wnt5b and the transmembrane planar cell polarity (PCP) protein Vangl2. However, the intracellular events downstream of Wnt/PCP signals are not fully understood. Here, we show that zebrafish mutated in colorectal cancer (mcc), which encodes an evolutionarily conserved PDZ domain-containing putative tumor suppressor, is required for Wnt5b/Vangl2 signaling during gastrulation. Knockdown of mcc results in CE phenotypes similar to loss of vangl2 and wnt5b, whereas overexpression of mcc robustly rescues the depletion of wnt5b, vangl2 and the Wnt5b tyrosine kinase receptor ror2. Biochemical experiments establish a direct physical interaction between Mcc and the Vangl2 cytoplasmic tail. Lastly, CE defects in mcc morphants are suppressed by downstream activation of RhoA and JNK. Taken together, our results identify Mcc as a novel intracellular effector of non-canonical Wnt5b/Vangl2/Ror2 signaling during vertebrate gastrulation.
[Mh] Termos MeSH primário: Gastrulação/fisiologia
Genes MCC/genética
Morfogênese/fisiologia
Via de Sinalização Wnt/fisiologia
Peixe-Zebra/embriologia
[Mh] Termos MeSH secundário: Animais
Western Blotting
Polaridade Celular/fisiologia
Imunoprecipitação
Hibridização In Situ
Luciferases
Proteínas de Membrana/metabolismo
Microscopia Confocal
Domínios PDZ/genética
Reação em Cadeia da Polimerase
Receptores Órfãos Semelhantes a Receptor Tirosina Quinase/metabolismo
Proteínas Wnt/metabolismo
Proteína Wnt-5a
Proteínas de Peixe-Zebra/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Membrane Proteins); 0 (Wnt Proteins); 0 (Wnt-5a Protein); 0 (Wnt5a protein, zebrafish); 0 (Zebrafish Proteins); 0 (vangl2 protein, zebrafish); EC 1.13.12.- (Luciferases); EC 2.7.10.1 (Receptor Tyrosine Kinase-like Orphan Receptors)
[Em] Mês de entrada:1410
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140904
[St] Status:MEDLINE
[do] DOI:10.1242/dev.114033


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[PMID]:22542170
[Au] Autor:Poursoltan P; Currey N; Pangon L; van Kralingen C; Selinger CI; Mahar A; Cooper WA; Kennedy CW; McCaughan BC; Trent R; Kohonen-Corish MR
[Ad] Endereço:Department of Molecular and Clinical Genetics, Royal Prince Alfred Hospital, Missenden Road, Camperdown, Sydney, NSW 2050, Australia.
[Ti] Título:Loss of heterozygosity of the Mutated in Colorectal Cancer gene is not associated with promoter methylation in non-small cell lung cancer.
[So] Source:Lung Cancer;77(2):272-6, 2012 Aug.
[Is] ISSN:1872-8332
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:'Mutated in Colorectal Cancer' (MCC) is emerging as a multifunctional protein that affects several cellular processes and pathways. Although the MCC gene is rarely mutated in colorectal cancer, it is frequently silenced through promoter methylation. Previous studies have reported loss of heterozygosity (LOH) of the closely linked MCC and APC loci in both colorectal and lung cancers. APC promoter methylation is a marker of poor survival in non-small cell lung cancer (NSCLC). However, MCC methylation has not been previously studied in lung cancer. Therefore, we wanted to determine if MCC is silenced through promoter methylation in lung cancer and whether this methylation is associated with LOH of the MCC locus or methylation of the APC gene. Three polymorphic markers for the APC/MCC locus were analysed for LOH in 64 NSCLC specimens and matching normal tissues. Promoter methylation of both genes was determined using methylation specific PCR in primary tumours. LOH of the three markers was found in 41-49% of the specimens. LOH within the MCC locus was less common in adenocarcinoma (ADC) (29%) than in squamous cell carcinoma (SCC) (72%; P=0.006) or large cell carcinoma (LCC) (75%; P=0.014). However, this LOH was not accompanied by MCC promoter methylation, which was found in only two cancers (3%). In contrast, 39% of the specimens showed APC methylation, which was more common in ADC (58%) than in SCC (13%). Western blotting revealed that MCC was expressed in a subset of lung tissue specimens but there was marked variation between patients rather than between cancer and matching non-cancer tissue specimens. In conclusion, we have shown that promoter methylation of the APC gene does not extend to the neighbouring MCC gene in lung cancer, but LOH is found at both loci. The variable levels of MCC expression were not associated with promoter methylation and may be regulated through other cellular mechanisms.
[Mh] Termos MeSH primário: Carcinoma Pulmonar de Células não Pequenas/genética
Metilação de DNA
Genes MCC
Perda de Heterozigosidade
Neoplasias Pulmonares/genética
Regiões Promotoras Genéticas
[Mh] Termos MeSH secundário: Adenocarcinoma/genética
Carcinoma de Células Grandes/genética
Carcinoma Pulmonar de Células não Pequenas/metabolismo
Carcinoma de Células Escamosas/genética
Linhagem Celular Tumoral
Regulação Neoplásica da Expressão Gênica
Genes APC
Seres Humanos
Neoplasias Pulmonares/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Mês de entrada:1211
[Cu] Atualização por classe:120713
[Lr] Data última revisão:
120713
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:120501
[St] Status:MEDLINE
[do] DOI:10.1016/j.lungcan.2012.04.001


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[PMID]:20707908
[Au] Autor:Ji X; Tang J; Halberg R; Busam D; Ferriera S; Peña MM; Venkataramu C; Yeatman TJ; Zhao S
[Ad] Endereço:Department of Biochemistry and Molecular Biology, Institute of Bioinformatics, University of Georgia, Athens 30602, GA, USA.
[Ti] Título:Distinguishing between cancer driver and passenger gene alteration candidates via cross-species comparison: a pilot study.
[So] Source:BMC Cancer;10:426, 2010 Aug 13.
[Is] ISSN:1471-2407
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: We are developing a cross-species comparison strategy to distinguish between cancer driver- and passenger gene alteration candidates, by utilizing the difference in genomic location of orthologous genes between the human and other mammals. As an initial test of this strategy, we conducted a pilot study with human colorectal cancer (CRC) and its mouse model C57BL/6J ApcMin/+, focusing on human 5q22.2 and 18q21.1-q21.2. METHODS: We first performed bioinformatics analysis on the evolution of 5q22.2 and 18q21.1-q21.2 regions. Then, we performed exon-targeted sequencing, real time quantitative polymerase chain reaction (qPCR), and real time quantitative reverse transcriptase PCR (qRT-PCR) analyses on a number of genes of both regions with both human and mouse colon tumors. RESULTS: These two regions (5q22.2 and 18q21.1-q21.2) are frequently deleted in human CRCs and encode genuine colorectal tumor suppressors APC and SMAD4. They also encode genes such as MCC (mutated in colorectal cancer) with their role in CRC etiology unknown. We have discovered that both regions are evolutionarily unstable, resulting in genes that are clustered in each human region being found scattered at several distinct loci in the genome of many other species. For instance, APC and MCC are within 200 kb apart in human 5q22.2 but are 10 Mb apart in the mouse genome. Importantly, our analyses revealed that, while known CRC driver genes APC and SMAD4 were disrupted in both human colorectal tumors and tumors from ApcMin/+ mice, the questionable MCC gene was disrupted in human tumors but appeared to be intact in mouse tumors. CONCLUSIONS: These results indicate that MCC may not actually play any causative role in early colorectal tumorigenesis. We also hypothesize that its disruption in human CRCs is likely a mere result of its close proximity to APC in the human genome. Expanding this pilot study to the entire genome may identify more questionable genes like MCC, facilitating the discovery of new CRC driver gene candidates.
[Mh] Termos MeSH primário: Neoplasias Colorretais/genética
Neoplasias Colorretais/patologia
Regulação Neoplásica da Expressão Gênica
Genes APC/fisiologia
Genes MCC/fisiologia
Genoma Humano
[Mh] Termos MeSH secundário: Animais
Sequência de Bases
Cromossomos Humanos Par 18/genética
Cromossomos Humanos Par 5/genética
Biologia Computacional
Evolução Molecular
Genes DCC/fisiologia
Seres Humanos
Camundongos
Dados de Sequência Molecular
Projetos Piloto
Proteína Smad4/genética
Especificidade da Espécie
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Smad4 Protein)
[Em] Mês de entrada:1102
[Cu] Atualização por classe:141203
[Lr] Data última revisão:
141203
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:100817
[St] Status:MEDLINE
[do] DOI:10.1186/1471-2407-10-426


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[PMID]:19702696
[Au] Autor:Hebbar M; Fournier P; Romano O
[Ad] Endereço:Department of Medical Oncology, University Hospital, Lille, France. m-hebbar@chru-lille.fr
[Ti] Título:KRAS mutational status assessment in patients with metastatic colorectal cancer: are the clinical implications so clear?
[So] Source:Eur J Cancer Care (Engl);19(2):167-71, 2010 Mar.
[Is] ISSN:1365-2354
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The CRYSTAL study demonstrated an advantage in terms of objective response and progression-free survival for the FOLFIRI-cetuximab combination compared with first-line FOLFIRI for patients with metastatic colorectal cancer. The results of an ancillary biological study with screening for a KRAS gene mutation in 540 patients were reported at the 2008 American Society of Clinical Oncology congress. The analysis confirmed the value of adding cetuximab only in the absence of KRAS mutation. These results led to recommend restriction of the use of cetuximab in Europe to patients with a tumour bearing wild-type KRAS. How should this apparent simplification be integrated into clinical practice? The FOLFIRI-cetuximab combination is certainly a useful supplementary first-line option although its place in relation to other high-dose regimens (high-dose FOLFIRI, FOLFOXIRI or FOLFOX-7), conventional chemotherapy plus bevacizumab, or even a fluoropyrimidine alone in the case of unresectable metastases, has yet to be specified. For subsequent lines, no study has prospectively assessed the value of the chemotherapy--anti-epidermal growth factor receptor combination as a function of KRAS status. Should the absence of objective response constantly observed in retrospective analyses in patients with a tumour presenting a KRAS mutation definitively exclude these patients while stable disease (and potentially a slight gain in survival) may be obtained?
[Mh] Termos MeSH primário: Neoplasias Colorretais/genética
Proteínas Proto-Oncogênicas/genética
Proteínas ras/genética
[Mh] Termos MeSH secundário: Anticorpos Monoclonais/administração & dosagem
Anticorpos Monoclonais Humanizados
Protocolos de Quimioterapia Combinada Antineoplásica/administração & dosagem
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Camptotecina/administração & dosagem
Camptotecina/análogos & derivados
Cetuximab
Neoplasias Colorretais/tratamento farmacológico
Neoplasias Colorretais/secundário
Intervalo Livre de Doença
Fluoruracila/administração & dosagem
Genes MCC
Seres Humanos
Leucovorina/administração & dosagem
Proteínas Proto-Oncogênicas p21(ras)
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Antibodies, Monoclonal, Humanized); 0 (KRAS protein, human); 0 (Proto-Oncogene Proteins); EC 3.6.5.2 (Proto-Oncogene Proteins p21(ras)); EC 3.6.5.2 (ras Proteins); PQX0D8J21J (Cetuximab); Q573I9DVLP (Leucovorin); U3P01618RT (Fluorouracil); XT3Z54Z28A (Camptothecin)
[Em] Mês de entrada:1009
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:N
[Da] Data de entrada para processamento:090826
[St] Status:MEDLINE
[do] DOI:10.1111/j.1365-2354.2009.01134.x


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[PMID]:17260021
[Au] Autor:Kohonen-Corish MR; Sigglekow ND; Susanto J; Chapuis PH; Bokey EL; Dent OF; Chan C; Lin BP; Seng TJ; Laird PW; Young J; Leggett BA; Jass JR; Sutherland RL
[Ad] Endereço:Cancer Research Program, Garvan Institute of Medical Research, Sydney, New South Wales, Australia. m.corish@garvan.org.au
[Ti] Título:Promoter methylation of the mutated in colorectal cancer gene is a frequent early event in colorectal cancer.
[So] Source:Oncogene;26(30):4435-41, 2007 Jun 28.
[Is] ISSN:0950-9232
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The mutated in colorectal cancer (MCC) gene is in close linkage with the adenomatous polyposis coli (APC) gene on chromosome 5, in a region of frequent loss of heterozygosity in colorectal cancer. The role of MCC in carcinogenesis, however, has not been extensively analysed, and functional studies are emerging, which implicate it as a candidate tumor suppressor gene. The aim of this study was to examine loss of MCC expression due to promoter hypermethylation and its clinicopathologic significance in colorectal cancer. Correspondence of MCC methylation with gene silencing was demonstrated using bisulfite sequencing, reverse transcription-polymerase chain reaction and Western blotting. MCC methylation was detected in 45-52% of 187 primary colorectal cancers. There was a striking association with CDKN2A methylation (P<0.0001), the CpG island methylator phenotype (P<0.0001) and the BRAF V600E mutation (P<0.0001). MCC methylation was also more common (P=0.0084) in serrated polyps than in adenomas. In contrast, there was no association with APC methylation or KRAS mutations. This study demonstrates for the first time that MCC methylation is a frequent change during colorectal carcinogenesis. Furthermore, MCC methylation is significantly associated with a distinct spectrum of precursor lesions, which are suggested to give rise to cancers via the serrated neoplasia pathway.
[Mh] Termos MeSH primário: Neoplasias Colorretais/genética
Metilação de DNA
Genes MCC
Regiões Promotoras Genéticas
[Mh] Termos MeSH secundário: Adenoma/genética
Neoplasias Colorretais/etiologia
Neoplasias Colorretais/patologia
Ilhas de CpG
Seres Humanos
Pólipos Intestinais/genética
Mutação
Fenótipo
Proteínas Proto-Oncogênicas B-raf/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
EC 2.7.11.1 (BRAF protein, human); EC 2.7.11.1 (Proto-Oncogene Proteins B-raf)
[Em] Mês de entrada:0708
[Cu] Atualização por classe:161025
[Lr] Data última revisão:
161025
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:070130
[St] Status:MEDLINE


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[PMID]:15842799
[Au] Autor:Cong WM; Zhang SH; Xian ZH; Wu WQ; Wu MC
[Ad] Endereço:Department of Pathology, Oriental Hepatobiliary Surgery Hospital, Second Military Medical University Shanghai 200438, China. wmcong@smmu.edu.cn
[Ti] Título:[Study on loss of heterozygosity and microsatellite instability in hepatocellular carcinoma].
[So] Source:Zhonghua Bing Li Xue Za Zhi;34(2):71-4, 2005 Feb.
[Is] ISSN:0529-5807
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:OBJECTIVE: To investigate the role of loss of heterozygosity (LOH) in tumor suppressor genes (TSG) and microsatellite instability (MSI) in hepatocarcinogenesis, as well as their correlation with clinicopathologic features. METHODS: LOH in 6 TSG (APC, DCC, MCC, OGG1, p53 and RB1) was detected in 36 informative cases of hepatocellular carcinoma (HCC), among 92 surgically resected HCC. Thirteen polymorphic microsatellite markers were also studied in 15 of these cases by microdissection-based PCR amplification and direct DNA sequencing. The correlation between genetic alterations and clinicopathologic features was analyzed. RESULTS: The overall incidence of LOH in HCC was 41.7% (15/36). There was no LOH in MCC gene. 46.2% (6/13) microsatellites showed LOH in 9 of the 15 cases of HCC (60%). Certain clinicopathologic differences were observed between cases (number = 7) with LOH in APC, OGG1 and DCC ("type I") and cases (number = 8) with LOH in p53 and RB1 ("type II"). The mean tumor size of these two types was 2.9 (+/- 1.7) cm and 7.2 (+/- 3.4) cm, respectively (P < 0.01); and the mean survival was 72.0 (+/- 38.6) months, and 51.0 (+/- 30.4) months, respectively (P < 0.05). CONCLUSIONS: Compared with MSI pathway, LOH pathway plays a more important role in the development of HCC. A multistep hepatocarcinogenesis is likely, with LOH in APC, OGG1 and DCC ("type I") being an early event and LOH in p53 and RB1 ("type II") being a late event. On the other hand, MCC gene seems to play no role in the whole process.
[Mh] Termos MeSH primário: Carcinoma Hepatocelular/genética
Genes Supressores de Tumor
Neoplasias Hepáticas/genética
Perda de Heterozigosidade
Instabilidade de Microssatélites
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Carcinoma Hepatocelular/patologia
Feminino
Genes APC
Genes DCC
Genes MCC
Genes p53
Seres Humanos
Lactente
Neoplasias Hepáticas/patologia
Masculino
Meia-Idade
[Pt] Tipo de publicação:ENGLISH ABSTRACT; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Mês de entrada:0704
[Cu] Atualização por classe:160818
[Lr] Data última revisão:
160818
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:050422
[St] Status:MEDLINE


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[PMID]:12901725
[Au] Autor:Sikdar N; Paul RR; Panda CK; Banerjee SK; Roy B
[Ad] Endereço:Anthropology and Human Genetics Unit, Biological Sciences Division, Indian Statistical Institute, 203 B. T. Road, Kolkata 700 08, India.
[Ti] Título:Loss of heterozygosity at APC and MCC genes of oral cancer and leukoplakia tissues from Indian tobacco chewers.
[So] Source:J Oral Pathol Med;32(8):450-4, 2003 Sep.
[Is] ISSN:0904-2512
[Cp] País de publicação:Denmark
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Loss of heterozygosity (LOH) at tumor suppressor genes, such as adenomatous polyposis coli (APC) and mutated in colon cancer (MCC) genes, is one of the early events in carcinogenesis of oral tissue in Caucasian and Chinese patients. We wanted to check whether it is also true in Indian oral pre-cancer and cancer patients. METHODS: Loss of heterozygosity at APC and MCC genes was investigated in 57 and 40 unrelated primary oral leukoplakia (a pre-cancerous lesion) and squamous cell carcinomas (SCC), respectively, by polymerase chain reaction. RESULTS: In these samples, most of the leukoplakia patients had tobacco smoking habit whereas majority of cancer patients had tobacco chewing habit. LOH at APC gene was observed in 4 of 16 (25%) and 1 of 29 (3%) informative tumor and leukoplakia DNAs from tobacco chewers, respectively. LOH at MCC gene was not detected either in tumor or in leukoplakia DNAs. CONCLUSION: This infrequent LOH at APC gene of pre-cancer and cancer tissues suggests that it may not be an early event in oral carcinogenesis in these patients.
[Mh] Termos MeSH primário: Genes APC
Genes MCC/genética
Leucoplasia Bucal/genética
Perda de Heterozigosidade/genética
Neoplasias Bucais/genética
Tabaco sem Fumaça/efeitos adversos
[Mh] Termos MeSH secundário: Adulto
Idoso
Areca/efeitos adversos
Carcinoma de Células Escamosas/genética
DNA de Neoplasias/genética
Feminino
Genótipo
Seres Humanos
Índia
Masculino
Meia-Idade
Mutação/genética
Lesões Pré-Cancerosas/genética
Fumar/efeitos adversos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (DNA, Neoplasm)
[Em] Mês de entrada:0311
[Cu] Atualização por classe:061115
[Lr] Data última revisão:
061115
[Sb] Subgrupo de revista:D; IM
[Da] Data de entrada para processamento:030807
[St] Status:MEDLINE


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[PMID]:12586804
[Au] Autor:Bilchik AJ; Nora DT; Sobin LH; Turner RR; Trocha S; Krasne D; Morton DL
[Ad] Endereço:Division of Surgical Oncology, John Wayne Cancer Institute at Saint John's Health Center, 2200 Santa Monica Boulevard, Santa Monica, CA 90404, USA. bilchika@jwci.org
[Ti] Título:Effect of lymphatic mapping on the new tumor-node-metastasis classification for colorectal cancer.
[So] Source:J Clin Oncol;21(4):668-72, 2003 Feb 15.
[Is] ISSN:0732-183X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Sensitive detection methods and accurate reporting are necessary to determine the prognostic significance of micrometastases (MM) and isolated tumor cells (ITCs) in lymph nodes that drain colorectal cancers (CRCs). This study examined the role of lymphatic mapping (LM) in the application of the new tumor-node-metastasis (TNM) classification for MM and ITC. PATIENTS AND METHODS: All patients at the John Wayne Cancer Institute underwent LM immediately before standard resection of primary CRC between 1996 and 2001. Sentinel nodes (SNs) were identified using blue dye and/or radiotracer and were examined by hematoxylin-eosin (H&E) staining, cytokeratin immunohistochemistry, and multilevel sectioning. The comparison group comprised 370 patients whose primary CRCs were resected without LM during the same period at the same institution. RESULTS: LM was successfully performed in 115 of 120 (96%) patients and correctly predicted the tumor status of the nodal basin in 110 of 115 (96%) patients. Thirty-seven patients (32%) were lymph node-positive by H&E, ITC and MM were found in 23 patients (29.4%) whose lymph nodes were negative by H&E. Tumor deposits were found in the SN only in 29 patients (50%). Nodal involvement was identified for 14.3%, 30%, 74.6%, and 83.3% of T1, T2, T3, and T4 tumors, respectively, in the study group, and for 6.8%, 8.5%, 49.3%, and 41.8% of T1, T2, T3, and T4 tumors, respectively, in the comparison group. The study group had a higher percentage of nodal metastases (53% v 36%; P <.01) and a higher incidence of MM and ITC (29.4% v 1.9%; P <.0001). The mean number of lymph nodes found in the study group (14) was also significantly more than the number found in the comparison group (10; P <.00001). CONCLUSION: Conventional examination of lymph nodes for CRC is inadequate for the detection of MM and ITC as described in the new TNM classification. Thus, LM and focused SN analysis should be considered to fully stage CRC.
[Mh] Termos MeSH primário: Neoplasias Colorretais/patologia
Biópsia de Linfonodo Sentinela/métodos
[Mh] Termos MeSH secundário: Idoso
Neoplasias Colorretais/classificação
Neoplasias Colorretais/cirurgia
Feminino
Genes MCC
Seres Humanos
Metástase Linfática
Masculino
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, P.H.S.
[Em] Mês de entrada:0303
[Cu] Atualização por classe:161102
[Lr] Data última revisão:
161102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:030215
[St] Status:MEDLINE


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[PMID]:12094695
[Au] Autor:Ozawa S; Kitagawa Y; Kitajima M
[Ad] Endereço:Department of Surgery, School of Medicine, Keio University, Tokyo, Japan.
[Ti] Título:[Molecular alterations in esophageal cancer].
[So] Source:Nihon Geka Gakkai Zasshi;103(6):457-62, 2002 Jun.
[Is] ISSN:0301-4894
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Ab] Resumo:The clinicopathological characteristics of esophageal cancer have gradually been clarified using molecular biologic methods developed over the past 20 years. For example, amplification of the c-erb B gene is a prognostic factor and predictive of lymph node involvement, while the amplification of the cyclin D1 gene is also a prognostic factor and predictive of distant organ metastasis. Alteration of the p16 gene is also a prognostic factor and predicts lymph node involvement. As telomerase activity is almost a unique phenomenon of cancer cells, highly sensitive detection of esophageal cancer cells in the peripheral blood can be performed. Recently, such new methods as comparative genomic hybridization analysis and cDNA microarray analysis have been used to determine meaningful genetic changes. For therapeutic purposes, although tailor-made therapy has been proposed for several years, the validity of these approaches should be confirmed in a well-designed clinical trial. As molecular targeted therapies, tyrosine kinase inhibitors of epidermal growth factor receptor (EGFR) and monoclonal antibodies against EGFR are being studied in clinical trials in Western countries. A clinical trial of p53 gene therapy against esophageal cancer is also promising.
[Mh] Termos MeSH primário: Neoplasias Esofágicas/genética
[Mh] Termos MeSH secundário: Ciclina D1/genética
DNA/genética
Genes DCC
Genes MCC
Genes Supressores de Tumor
Genes p53
Genes ras
Seres Humanos
Proteínas Oncogênicas v-erbB/genética
Ploidias
[Pt] Tipo de publicação:ENGLISH ABSTRACT; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Oncogene Proteins v-erbB); 136601-57-5 (Cyclin D1); 9007-49-2 (DNA)
[Em] Mês de entrada:0207
[Cu] Atualização por classe:110726
[Lr] Data última revisão:
110726
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:020704
[St] Status:MEDLINE



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