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loss of heterozygosity: An independent prognostic factor of colorectal cancer

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World Journal of Gastroenterology 2005年第6期11卷 778-784页

作者： Shih-Ching Chang Jen-Kou Lin Tzu-Chen Lin Wen-Yih Liang Division of Colon and Rectal Surgery Department of Pathology

AIM: Colorectal cancers result from the accumulation of several distinct genetic alterations. This study was to investigate the frequency and prognostic value of loss of heterozygosity (LOH) and microsatellite instability (MSI) at 14 genetic loci located near or within regions containing important genes implicated in colorectal tumorigenesis. METHODS: We studied colorectal cancers with corresponding normal mucosae in 207 patients (139 males and 68 females, mean age at the time of tumor resection 66.2±12.4 years, range 22-88 years). There were 37 right-sided colonic tumors, 85 left-sided colonic tumors and 85 rectal tumors. The distribution of tumor staging was stage Ⅰ in 25, stage Ⅱ in 73, stage Ⅲ in 68, and stage Ⅳ in 41. We analyzed the LOH and MSI of HPC1, hMSH2, hMLH1, APC, MET, P53, NH23-H1, DCC, BAT25, BAT26, D17S250, MYCL1 and D8S254 with fluorescent polymerase chain reaction and denatured gel electrophoresis. High-frequency LOH was determined to be greater than three, or more than 50% of the informative marker with LOH. High-frequency MSI (MSI-H) was determined as more than four markers with instability (>30%). Correlations of LOH and MSI with clinical outcomes and pathological features were analyzed and compared. RESULTS: The occurrence of MSI-H was 7.25%, located predominantly in the right colons (7/15) and had a higher frequency of poor differentiation (6/15) and mucin production (7/15). LOH in at least one genetic locus occurred in 78.7% of the tumors and was significantly associated with disease progression. Of the 166 potentially cured patients, 45 developed tumor recurrence within 36 mo of follow-up. Clinicopathological factors affecting 3-year disease-free survival (DFS) were TNM staging, grade of differentiation, preoperative CEA level, and high LOH status. Patients with high LOH tumors had a significantly lower DFS (50%) compared with patients with low LOH tumors (84%). Of the patients developing subsequent tumor recurrence, the number and percenta

关键词： Colorectal Cancer loss of heterozygosity Prognosis

loss of heterozygosity OF ER GENE IN BREAST CANCER AND ITS CLINICAL SIGNIFICANCE

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Chinese Journal of Cancer Research 2002年第2期14卷 122-125页

作者：郑唯强郑建明卢建胡凤仙 Department of Pathology Changhai Hospital Second Military Medical University Shanghai 200433 Department of Pathophysiology Faculty of Basic Medicine Second Military Medical University Shanghai 200433

Objective: Clinically, the reason of resistance for breast cancer to endocrine therapy has not been well known. The current study attempted to examine loss of heterozygosity (LOH) on the estrogen receptor (ER) gene in breast cancer and its relationship to clinicopathologic findings. Methods: DNAs of tumor tissues and blood lymphocytes were collected from 40 cases of primary breast cancer patients and LOH were detected using the microsatellite repeat assay and combined with other ER immunohistochemical assays. Results: ER-positive staining was observed in 65% of breast cancer. Heterogeneity of ER expression was found. Seven of the patients (17.5%) showed LOH. In three of the seven cases, there was total loss, and there was a marked reduction in the intensity of signal in the other four cases. LOH was associated with histologic grade, occurring more frequently in ER-negative and lymph node metastasis group, but not with tumor size and patient ages. Conclusion: This result implied that LOH of the ER gene may have an important role in the progression of breast cancer. It was postulated that the lack of ER function induced by LOH may contributed to endocrine therapy resistance of breast cancer since the tumor clone would escape from the ER regulation, obtain growth predisposition and finally lost response to therapy.

关键词： Breast cancer Estrogen receptor loss of heterozygosity Endocrine therapy

loss of heterozygosity AT 17p13 IN GASTRIC CANCER AND COLORECTAL CANCER

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Chinese Journal of Cancer Research 1997年第1期9卷 24-27页

作者：李明发单祥年吴国俊余龙赵寿元

Southern hybridization was done on DNA samples of22 gastric tumors and corresponding normal tissues, 14colorectal tumors and corresponding normal tissues by probe phs53B mapping at 17P13.1 and probe PYNZ22mapping at 17pl3.3 which were purchased from the American Type Culture Collection. RFLP heterozygosity was observed in 12 normal tissues of gastric cancers and 10 normal tissues of colorectal cancers. Among these informative tumors, 6(50%) cases of gastric cancers and 6(60%) cases of colorectal cancers showed the loss of beterozygosity at 17p13. Our results demonstrated that the inactivation of wild type p53 might be involved in the carcinogenesis of gastric cancers and colorectal ***, the mode of inactivation of p53 was in accord with the 'two hits' hypothesis by Anudson. The signincance was discussed regarding the presence of LOH detected by probe PYNZ22 mapping at 17pl3.3.

关键词： Gastric cancer Colorectal cancer loss of heterozygosity p53

loss of heterozygosity on 10q23.3 and mutation of tumor suppressor gene PTEN in gastric cancer and precancerous lesions

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World Journal of Gastroenterology 2005年第2期11卷 285-288页

作者： Yi-LingLi ZhongTian Dong-YingWu Bao-YuFu YahXin DepartmentofGastroenterology FirstHospitalofChinaMedicalUniversitySh_enyang110001LiaoningProvinceofChina DepartmentofSurgery SecondHospitalofChinaMedicalUniversityShenyang110003LiaoningProvinceChina TheFourthLaboratory CancerInstituteFirstHospitalofChinaMedicalUniversityShenyang110001LiaoningProvinceChina

AIM: To investigate the loss of heterozygosity (LOH) and mutation of tumor suppressor gene PTEN in gastric cancer and precancerous lesions. METHODS: Thirty cases of normal gastric mucosa, advanced and early stage gastric cancer, intestinal metaplasia, atrophic gastritis, and atypical hyperplasia were analyzed for PTEN LOH and mutations within the entire coding region of PTEN gene by PCR-SSCP denaturing PAGE gel electrophoresis, and PTEN mutation was detected by PCR-SSCP sequencing followed by silver staining. RESULTS: LOH rate found in respectively atrophic gastritis was 10% (3/30), intestinal metaplasia 10% (3/30), atypical hyperplasia 13.3% (4/30), early stage gastric cancer 20% (6/30), and advanced stage gastric cancer 33.3% (9/30), None of the precancerous lesions and early stage gastric cancer showed PTEN mutations, but 10% (3/30) of the advanced stage gastric cancers, which were all positive for LOH, showed PTEN mutation. CONCLUSION: LOH of PTEN gene appears in precancerous lesions, and PTEN mutations are restricted to advanced gastric cancer, LOH and mutation of PTEN gene are closely related to the infiltration and metastasis of gastric cancer.

关键词： Gastric cancer Precancerous lesions PTEN gene loss of heterozygosity Mutation

loss of heterozygosity analyzed by single nucleotide polymorphism array in cancer

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World Journal of Gastroenterology 2005年第43期11卷 6740-6744页

作者： Hai-Tao Zheng Zhi-Hai Peng Sheng Li Lin He Department of General Surgery Shanghai First People's Hospital Shanghai Jiaotong University Shanghai 200080 China Shanghai Institutes for Nutrition Science Chinese Academy of Sciences Shanghai 200031 China

Neoplastic progression is generally characterized by the accumulation of multiple genetic alterations including loss of tumor suppression gene function. loss of heterozygosity （LOH） has been used to identify genomic regions that harbor tumor suppressor genes and to characterize different tumor types, pathological stages and progression. LOH pattern has been detected by allelotyping using restriction fragment length polymorphism, and later by simple sequence length polymorphisms （SSLPs or microsatellite） for 10 years. This paper reviews the detection of LOH by recently developed single nucleotide polymorphism （SNP） arrays （all analyzed by Affymetrix array）; furthermore, its advantage and disadvantage were analyzed in several kinds of cancer.

关键词： loss of heterozygosity Single nucleotidepolymorphism Array Cancer

loss of heterozygosity of Kras2 gene on 12p12-13 in Chinese colon carcinoma patients

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World Journal of Gastroenterology 2006年第7期12卷 1033-1037页

作者： Jun wan Hong Li Yuan Li Mei-Ling Zhu Po Zhao 不详 Department of Gastroenterology General Hospital of the Chinese PLA Beijing 100083 China In patient Department General Hospital of the Chinese PLA Beijing 100083 China Department of Pathology General Hospital of the Chinese PLA Beijing 100083 China

AIM： To study the loss of heterozygosity （LOH） on 12p12-13 in Chinese colon carcinoma patients.METHODS： DNA was extracted from 10 specimens of cancer tissue, 10 specimens of adjacent tissue and 10 specimens of normal tissue, respectively. LOH of Kras2 gene was analyzed by polymerase chain reaction （PCR） and denaturing polyacrylamide gel electrophoresis using 11 microsatellite markers on 12p-12-13.RESULTS： LOH of Kras gene was detected at least on one marker of 12p-12-13 in 30% （3/10） of adjacent tissue specimens. The highest frequency of LOH was identified on D12S1034 in 28.57% （2]7） of adjacent tissue specimens. LOH was detected at least on one marker of 12p12-13 in 60% （6/10） of carcinoma tissue specimens, the most frequent LOH was found on D12S1034 and D12S1591 in 42.86% （3/7） of carcinoma tissue specimens. LOH was detected in 30% （3/10） of carcinoma tissue specimens, 30% （3/10） of adjacent tissue specimens, and no signal in 1% （1/0） carcinoma tissue specimen. The occurrence of LOH did not correlate with sex, age, tumor size and lymph node metastasis.CONCLUSION： Genomic instability may occur on 12p-12-13 of Kras2 gene in the development and progression of colon carcinoma. The high LOH of Kras2 gene may directly influence the transcription and translation of wild type Kras2 gene.

关键词： Colon carcinoma loss of heterozygosity Kras2

loss of heterozygosity and microsatellite DNA instability on chromosomes 3 and 9 in esophageal cancer tissues

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Progress in Natural Science:Materials International 1996年第4期 76-82页

作者：李卫东王亮王秀琴吴旻张春林张涛毛学正 Beijing 100021 Cancer Institute Cancer Institute of Yangquan China Department of Cell Biology Peking Union Medical College. Chinese Academy of Medical Sciences State Key Laboratory of Molecular Oncology Yangquan 045000

loss of heterozygosity and microsatellite DNA instability in 36 pairs of sporadic esophageal cancer and their corresponding normal tissue were detected by microsatellite DNA polymorphism-PCR-silver stain method by using 10 pairs of primers on chromosomes 3 and 9. High frequency of loss of heterozygosity was found on loci of 9p22-23, 3p23, 3p14.2, 3p21.3 and 3q21-22. It is suggested that there may be clues of tumor suppressor genes. Simultaneously, high frequency of microsatellite DNA instability was also detected on some chromosome loci Widespread microsatellite instability not only exists in familial cancer, but also in sporadic tumors.

关键词： loss of heterozygosity microsatellite DNA instability esophageal cancer.

High frequency loss of heterozygosity in the region of the DBH locus in bladder cancer

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Chinese Medical Journal 2000年第2期113卷 21-23页

作者：杨晓峰申鹏飞姚开泰米振国刘尚莹张泓王东文刘春刘红耀 China 030001 China 410078 China 410078

Objective To determine the location of a putative tumor suppressor gene (TSG), and evaluate the frequency loss of heterozygosity (LOH) of the long arm of chromosome 9 (9q) in bladder cancer Methods We analyzed 25 patients with bladder cancer for LOH of 9q using 25 high density microsatellite markers Results Twenty three samples (92%) showed LOH at least at one locus on 9q We identified that the commonly deleted region were at 9q12 q21, 9q22, and 9q34 The rate of LOH was 44 0%, 22 7%, 22 7%, 16 0%, 12 0% on DBH, D9S15, D9S1815, D9S1831, D9S176 locus, respectively, and was not significantly related with grades and stages of tumor Conclusion These data suggest that alteration of a TSG at DBH of 9q may play an important role in the development of bladder cancer

关键词： bladder cancer loss of heterozygosity DBH

p53 mutation, EGFR gene amplification and loss of heterozygosity on chromosome 10, 17?p in human gliomas

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Chinese Medical Journal 2000年第7期 86-90页

作者：金卫新徐贤秀杨天明华子春

To further illustrate the roles of p53 gene, epidermal growth factor receptor (EGFR) gene and loss of heterozygosity (LOH) on chromosome 10 and 17?p in human glioma progression Methods p53 mutations were scanned in 50 gliomas with various malignant grades using the polymerase chain reaction single strand conformation polymorphism (PCR SSCP) assay, and were confirmed by direct sequencing LOH for chromosome 10, 17?p and amplification of the EGFR gene were also assessed using Southern blot analysis Results p53 mutations were found in 9 of 17 high grade astrocytomas (53%), 1 of 15 low grade astrocytomas (7%), and the only subject of eppendymoblastoma but in none of the 10 medulloblastomas and 7 eppendymomas The majority of gliomas (38/50) analyzed here retained both 17?p alleles The frequency of p53 mutations was 13% in this group of tumors and increased to 50% (6/12) in tumors with one 17?p allele ( P loss of alleles on chromosome 10 and the amplification of the EGFR gene appear to be restricted to high grade tumors, suggesting that these events may be related to tumor progression rather than initiation

关键词： glioma genetics loss of heterozygosity single strand conformation polymorphism p53 genetics EGFR gene