Identifying tumor suppressor genes in human colorectal cancer

Science ◽  
1990 ◽  
Vol 247 (4938) ◽  
pp. 12-13 ◽  
Author(s):  
E. Stanbridge
Keyword(s):  
Colorectal Cancer ◽  
Tumor Suppressor ◽  
Tumor Suppressor Genes ◽  
Human Colorectal Cancer ◽  
Suppressor Genes

scholarly journals Patterns of somatic uniparental disomy identify novel tumor suppressor genes in colorectal cancer

2015 ◽  
Vol 36 (10) ◽  
pp. 1103-1110 ◽  
Author(s):  
Keyvan Torabi ◽  
Rosa Miró ◽  
Nora Fernández-Jiménez ◽  
Isabel Quintanilla ◽  
Laia Ramos ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Tumor Suppressor ◽  
Tumor Suppressor Genes ◽  
Uniparental Disomy ◽  
Suppressor Genes

Progression of colorectal cancer is associated with multiple tumor suppressor gene defects but inhibition of tumorigenicity is accomplished by correction of any single defect via chromosome transfer

1992 ◽  
Vol 12 (3) ◽  
pp. 1387-1395
Author(s):  
M C Goyette ◽  
K Cho ◽  
C L Fasching ◽  
D B Levy ◽  
K W Kinzler ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Tumor Suppressor ◽  
Tumor Suppressor Genes ◽  
Loss Of Function ◽  
Chromosome 18 ◽  
Chromosome 5 ◽  
Suppressor Genes ◽  
Single Defect

Carcinogenesis is a multistage process that has been characterized both by the activation of cellular oncogenes and by the loss of function of tumor suppressor genes. Colorectal cancer has been associated with the activation of ras oncogenes and with the deletion of multiple chromosomal regions including chromosomes 5q, 17p, and 18q. Such chromosome loss is often suggestive of the deletion or loss of function of tumor suppressor genes. The candidate tumor suppressor genes from these regions are, respectively, MCC and/or APC, p53, and DCC. In order to further our understanding of the molecular and genetic mechanisms involved in tumor progression and, thereby, of normal cell growth, it is important to determine whether defects in one or more of these loci contribute functionally in the progression to malignancy in colorectal cancer and whether correction of any of these defects restores normal growth control in vitro and in vivo. To address this question, we have utilized the technique of microcell-mediated chromosome transfer to introduce normal human chromosomes 5, 17, and 18 individually into recipient colorectal cancer cells. Additionally, chromosome 15 was introduced into SW480 cells as an irrelevant control chromosome. While the introduction of chromosome 17 into the tumorigenic colorectal cell line SW480 yielded no viable clones, cell lines were established after the introduction of chromosomes 15, 5, and 18. Hybrids containing chromosome 18 are morphologically similar to the parental line, whereas those containing chromosome 5 are morphologically distinct from the parental cell line, being small, polygonal, and tightly packed. SW480-chromosome 5 hybrids are strongly suppressed for tumorigenicity, while SW480-chromosome 18 hybrids produce slowly growing tumors in some of the animals injected. Hybrids containing the introduced chromosome 18 but was significantly reduced in several of the tumor reconstitute cell lines. Introduction of chromosome 5 had little to no effect on responsiveness, whereas transfer ot chromosome 18 restored responsiveness to some degree. Our findings indicate that while multiple defects in tumor suppressor genes seem to be required for progression to the malignant state in colorectal cancer, correction of only a single defect can have significant effects in vivo and/or in vitro.

scholarly journals Screening of tumor suppressor genes on 1q31.1-32.1 in Chinese patients with sporadic colorectal cancer

2008 ◽  
Vol 121 (24) ◽  
pp. 2479-2486 ◽  
Author(s):  
Chong-zhi ZHOU ◽  
Guo-qiang QIU ◽  
Xiao-liang WANG ◽  
Jun-wei FAN ◽  
Hua-mei TANG ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Tumor Suppressor ◽  
Tumor Suppressor Genes ◽  
Chinese Patients ◽  
Sporadic Colorectal Cancer ◽  
Suppressor Genes

scholarly journals The co-regulatory networks of tumor suppressor genes, oncogenes, and miRNAs in colorectal cancer

2017 ◽  
Vol 56 (11) ◽  
pp. 769-787 ◽  
Author(s):  
Martha L. Slattery ◽  
Jennifer S. Herrick ◽  
Lila E. Mullany ◽  
Wade S. Samowitz ◽  
John R. Sevens ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Tumor Suppressor ◽  
Tumor Suppressor Genes ◽  
Regulatory Networks ◽  
Suppressor Genes

scholarly journals Screening of Tumor Suppressor Genes in Metastatic Colorectal Cancer

2017 ◽  
Vol 2017 ◽  
pp. 1-7 ◽  
Author(s):  
Lu Qi ◽  
Yanqing Ding
Keyword(s):  
Colorectal Cancer ◽  
Tumor Suppressor ◽  
Mrna Expression ◽  
Binding Site ◽  
Methylation Level ◽  
Tumor Suppressor Genes ◽  
Enrichment Analysis ◽  
Suppressor Genes ◽  
Genes Expression ◽  
Chromosome 17P13

Most tumor suppressor genes are commonly inactivated in the development of colorectal cancer (CRC). The activation of tumor suppressor genes may be beneficial to suppress the development and metastasis of CRC. This study analyzed genes expression and methylation levels in different stages of CRC. Genes with downregulated mRNA expression and upregulated methylation level in advanced CRC were screened as the potential tumor suppressor genes. After comparing the methylation level of screened genes, we found that MBD1 gene had downregulated mRNA expression and upregulated methylation levels in advanced CRC and continuously upregulated methylation level in the progression of CRC. Enrichment analysis revealed that genes expression in accordance with the elevated expression of MBD1 mainly located on chromosomes 17p13 and 17p12 and 8 tumor suppressor genes located on chromosome 17p13. Further enrichment analysis of transcription factor binding site identified that SP1 binding site had higher enrichment and could bind with MBD1. In conclusion, MBD1 may be a tumor suppressor gene in advanced CRC and affect the development and metastasis of CRC by regulating 8 tumor suppressor genes through binding with SP1.

Methylation Profiles of Tumor Suppressor Genes in Inflammatory Bowel Disease-Associated and Sporadic Colorectal Cancer: A Comparison

2011 ◽  
Vol 140 (5) ◽  
pp. S-349
Author(s):  
Marian M. Claessen ◽  
Frank P. Vleggaar ◽  
Marguerite E. Schipper ◽  
John W. Hinrichs ◽  
Remco D. Radersma ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Inflammatory Bowel Disease ◽  
Tumor Suppressor ◽  
Bowel Disease ◽  
Tumor Suppressor Genes ◽  
Sporadic Colorectal Cancer ◽  
Suppressor Genes ◽  
Inflammatory Bowel

Exome Resequencing Identifies Potential Tumor-Suppressor Genes that Predispose to Colorectal Cancer

2013 ◽  
Vol 34 (7) ◽  
pp. 1026-1034 ◽  
Author(s):  
Christopher G. Smith ◽  
Marc Naven ◽  
Rebecca Harris ◽  
James Colley ◽  
Hannah West ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Tumor Suppressor ◽  
Tumor Suppressor Genes ◽  
Suppressor Genes ◽  
Potential Tumor Suppressor

scholarly journals Alterations of Tumor Suppressor Genes Expression in Colorectal Cancer: Their Impact on Progression and Prediction of Patients Outcome

2018 ◽  
pp. 1-11
Author(s):  
Menha Swellam ◽  
Tamer E. Mosa ◽  
Mie Afify ◽  
Mohamed D. E. Abdelmaksoud ◽  
Lobna R. Ezz El Arab
Keyword(s):  
Gene Expression ◽  
Colorectal Cancer ◽  
Tumor Suppressor ◽  
Cancer Patients ◽  
Tumor Suppressor Genes ◽  
Clinicopathological Factors ◽  
Suppressor Genes ◽  
Formalin Fixed Paraffin ◽  
Patient’S Outcome ◽  
Colorectal Cancer Patients

Background: Deregulation of tumor suppressor genes as APC, DCC and SMAD2 are related to tumorgenesis thus we aimed to investigate their expression among colorectal cancer to validate their relation with clinicopathological factors and the clinical outcome for CRC patients. Materials and Methods: Formalin-fixed paraffin samples from 115 colorectal cancer were investigated for APC, DCC and SMAD2 gene expression using quantitative PCR (QPCR) and their levels were analyzed versus clinicopathological factors and the overall survival (OS) of colorectal cancer patients. Results: A significant relation was reported between DCC and SMAD2 gene expression with clinical stages as they reported decrease expression among those with stage III. The three investigated genes were decreased significantly with poor histological differentiation colorectal cancer patients. The correlations between the expressions of the investigated genes revealed a significant correlation between SMAD2 and APC as well as between SMAD2 and DCC. Moreover patients with mean levels below and equal their expression values showed a considerable difference with OS. Conclusion: Gene expression of tumor suppressor genes APC, DCC and SMAD2 were significantly related to differential grading and patient's outcome thus pointing out their potential role as predictive markers for prognosis of colorectal cancer.

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