Analysis by comparative genomic hybridization of gastric cancer with peritoneal dissemination and/or positive peritoneal cytology

Morohara, Koji; Nakao, Kentaro; Tajima, Yusuke; Nishino, Nobukazu; Yamazaki, Kaoru; Kaetsu, Tsutomu; Suzuki, Satoshi; Tsunoda, Akira; Kawamura, Masatoshi; Aida, Tadateru; Tachikawa, Tetsuhiko; Kusano, Mitsuo

doi:10.1016/j.cancergencyto.2005.01.007

Cited by 18 publications

(14 citation statements)

References 21 publications

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“…For most loci, the MCR represents a significantly narrowed focal region(s) within large regions or whole chromosomal arms of loss of heterozygosity (LOH) previously described in glioblastoma. There is strong cancer relevance within these narrowed loci, with many being associated with multiple diverse cancers; some examples include loss of 3q12 in small-cell lung cancer (32), leukemia (33), and nasopharyngeal carcinoma (34); loss of 4q34 in gastric cancer (35), hepatocellular cancer (36), and primitive neuroectodermal tumor (37); and loss of 15q21 in bladder cancer (38) and rhabdomyosarcoma (39). Thus, it is likely that these candidate tumor suppressor genes in primary glioblastoma bear relevance to other cancer types.…”

Section: Comparison Of Primary and Secondary Glioblastoma Genomic Promentioning

confidence: 99%

Marked Genomic Differences Characterize Primary and Secondary Glioblastoma Subtypes and Identify Two Distinct Molecular and Clinical Secondary Glioblastoma Entities

et al. 2006

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Section: Comparison Of Primary and Secondary Glioblastoma Genomic Promentioning

confidence: 99%

Marked Genomic Differences Characterize Primary and Secondary Glioblastoma Subtypes and Identify Two Distinct Molecular and Clinical Secondary Glioblastoma Entities

et al. 2006

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“…The sample is then cooled and mixed with 9 ll of reaction buffer and 1 ll of enzyme mix, before overnight (18 h) incubation at 30°C. After amplification, Phi29 DNA polymerase is heat-inactivated by 10 min incubation at 65°C (Morohara et al 2005). …”

Section: Genomiphimentioning

confidence: 99%

Gastric and intestinal phenotypic cell marker expressions in gastric differentiated-type carcinomas: association with E-cadherin expression and chromosomal changes

Morohara

Tajima

Nakao

et al. 2006

J Cancer Res Clin Oncol

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Gastric and intestinal phenotypic cell markers are widely expressed in gastric carcinomas, irrespective of their histological type. In the present study, the relations between the phenotypic marker expression of the tumour, histological findings, expression of cell adhesion molecules, and the chromosomal changes in gastric differentiated-type carcinomas were examined. The phenotypic marker expression of the tumour was determined by the combination of the expression of the human gastric mucin (HGM), MUC6, MUC2 and CD10, and was evaluated in comparison with the expression of cell adhesion molecules, such as E-cadherin and beta-catenin, and chromosomal changes by comparative genomic hybridization (CGH) in 34 gastric differentiated-type carcinomas. Tumours were classified into the gastric- (G-), gastric and intestinal mixed- (GI-), intestinal- (I-), or unclassified- (UC-) phenotype according to the immunopositivity of staining for HGM, MUC6, MUC2, and CD10. G-phenotype tumours were significantly associated with a higher incidence of differentiated-type tumours mixed with undifferentiated-type component, compared with GI- and I-phenotype tumours (88.9 vs 33.3%, P=0.0498 and 88.9 vs 42.9%, P=0.0397; respectively). HGM-positive tumours were significantly associated with a higher incidence of tumours with abnormal expression of E-cadherin, compared with HGM-negative tumours (66.7 vs 21.1%, P=0.0135). GI-phenotype tumours were significantly associated with a higher incidence of tumours with abnormal expression of E-cadherin, compared with I-phenotype tumours (77.8 vs 21.4%, P=0.0131). HGM-negative tumours were significantly associated with higher frequencies of the gains of 19q13.2 and 19q13.3, compared with HGM-positive tumours (57.9 vs 20.0%, P=0.0382 and 63.2 vs 13.3%, P=0.0051; respectively). MUC6-positive tumours were significantly associated with higher frequencies of the gains of 20q13.2, compared with MUC6-negative tumours (71.4 vs 30.0%, P=0.0349). MUC2-positive tumours were significantly associated with the gain of 19p13.3, compared with MUC2-negative tumours (41.2 vs 5.9%, P=0.0391). I-phenotype tumours were significantly associated with higher frequencies of gains of 5p15.2 and 13q33-34, compared with G-phenotype tumours (66.7 vs 0%, P=0.0481, each) and also associated with higher frequencies of gain of 7p21, compared with GI-phenotype tumours (66.7 vs 0%, P=0.0481). Our present results show that gastric differentiated-type carcinomas have different characteristics according to the phenotypic marker expression of the tumour in terms of histological findings, E-cadherin expression and pattern of chromosomal changes.

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“…Of multiple locus of gene amplification and deletion, amplification of 2p24, 3q26, 5p13, 5p15, 6p21, 7q21, 8p23, 8q22, 8q24, 10q26, 11p11, 11p13, 11q13, 16p13, 17q12, 19q12-13, 20q13 and loss of 4q34, 9p21, 10q23, 19p13, 19q13 were consistent with the previous report in gastric cancer tissue or gastric cancer cell lines. [10][11][12][13][14][15][16][17][18][19][20][21] Most amplification loci were unique to single patients. The results thus suggest genetic alternations are less frequent in poorly differentiated gastric cancers and vary among individuals.…”

Section: Genomic Alternations In Poorly Differentiated Gastric Cancersmentioning

confidence: 99%

“…[4][5][6][7][8][9] Many chromosomal alternations have also been identified in primary gastric cancers and gastric cancer cell lines. [10][11][12][13][14][15][16][17][18][19][20][21] Gastric cancers are divided into 2 major subtypes, the intestinal type and the diffuse type (so called poorly differentiated), according to pathological classifications, originally proposed by Lauren. 22,23 These 2 subtypes correspond to tumor differentiation based on the degree of glandular formation.…”

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confidence: 99%

Krüppel‐like factor 12 plays a significant role in poorly differentiated gastric cancer progression

Nakamura

Migita

Hosoda³

et al. 2009

Intl Journal of Cancer

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Gastric cancer is the second common malignant neoplasia in Japan, and its poorly differentiated form is a deadly disease. To identify novel candidate oncogenes contributing to its genesis, we examined copy-number alterations in 50 primary poorly differentiated gastric cancers using an array-based comparative genomic hybridization (array-CGH). Many genetic changes were identified, including a novel amplification of the 13q22 locus. Several genes are located in this locus, and selective knockdown of one for the Kr€ uppel-like factor 12 (KLF12) induced significant growtharrest in the HGC27 gastric cancer cell line. Microarray analysis also demonstrated that genes associated with cell proliferation were mostly changed by KLF12 knockdown. To explore the oncogenic function of KLF12, we introduced a full length of human KLF12 cDNA into NIH3T3 and AZ-521 cell lines and found that overexpression significantly enhanced their invasive potential. In clinical samples, KLF12 mRNA in cancer tissue was increased in 11 of 28 cases (39%) when compared with normal gastric epithelium. Clinicopathological analysis further demonstrated a significant correlation between KLF12mRNA levels and tumor size (p 5 0.038). These data suggest that the KLF12 gene plays an important role in poorly differentiated gastric cancer progression and is a potential target of therapeutic measures. ' 2009 UICC

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Analysis by comparative genomic hybridization of gastric cancer with peritoneal dissemination and/or positive peritoneal cytology

Cited by 18 publications

References 21 publications

Marked Genomic Differences Characterize Primary and Secondary Glioblastoma Subtypes and Identify Two Distinct Molecular and Clinical Secondary Glioblastoma Entities

Marked Genomic Differences Characterize Primary and Secondary Glioblastoma Subtypes and Identify Two Distinct Molecular and Clinical Secondary Glioblastoma Entities

Gastric and intestinal phenotypic cell marker expressions in gastric differentiated-type carcinomas: association with E-cadherin expression and chromosomal changes

Krüppel‐like factor 12 plays a significant role in poorly differentiated gastric cancer progression

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