Refined mapping of loss of heterozygosity on 1q31.1-32.1 in sporadic colorectal carcinoma

Zhou, Chongzhi; Qiu, Guoqiang; Fan, Junwei; Wang, Xiaoliang; Tang, Huamei; Huang, Li Xi; Sun, Yuhao; Peng, Zhihai

doi:10.3748/wjg.14.1582

Cited by 4 publications

(2 citation statements)

References 36 publications

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“…At loci showing LOH, two alleles are observed in normal cells, while only one allele is detected in tumor cells because the other has been lost. When this occurs at a TSG locus where one of the alleles is already abnormal, it can result in neoplastic transformation [50][51][52][53][54].…”

Section: Tumor Suppressor Genes and Loss Of Heterozygositymentioning

confidence: 99%

Loss of heterozygosity in oral cancer

Kasamatsu

Uzawa

Usukura

et al. 2011

Oral Science International

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a b s t r a c tThe development and progression of oral squamous cell carcinoma (OSCC) is a multistep process, which involves many genetic factors. Among them, loss of heterozygosity (LOH) studies have been used to identify regions on chromosomes that may contain putative tumor suppressor genes (TSGs). Here, we searched PubMed for relevant publications including our previous studies and compared results of LOH in OSCCs from the articles. LOHs in OSCCs were observed at various loci on almost all chromosomes, except X and Y. In this review, the LOH in patients with OSCC and the interrelationship between TSGs and OSCC initiation and progression are discussed.

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Section: Tumor Suppressor Genes and Loss Of Heterozygositymentioning

confidence: 99%

Loss of heterozygosity in oral cancer

Kasamatsu

Uzawa

Usukura

et al. 2011

Oral Science International

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“…It can be considered that the tumor suppressor gene is localized on the 1q chromosome. Studies have shown that allelic losses on 1q are frequently associated with many cancers such as breast cancer, medulloblastoma, thyroid cancer, sporadic insulinoma, colorectal carcinomas, and esophageal cancers (Yang et al, 2005;Fromont et al, 2007;Zhou et al, 2008). In cases with 1q duplication, some cases with ambiguous genitalia and genital hypoplasia have been reported as well (Van Haelst et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

Trisomy of 1q31.3q42.12 Chromosome: Case Report

Solgun

Durmaz

Özbağ

et al. 2021

Black Sea Journal of Health Science

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Chromosome 1q duplication is one of the rare congenital anomalies accompanied by numerous visceral organ anomalies, dysmorphism, and psychomotor retardation. Our case is an 8-year-old male patient with 1q31.3q42.12 trisomy. The patient was brought to our rehabilitation center because he couldn't able to go up and down stairs and slopes without support also he couldn't run and jump. The patient receives physical therapy service for kyphotic posture, speech therapy for speech and drooling problems, and special education support for mild cognitive impairment. Our aim is to describe the dysmorphic features and posture examination of an 8-year-old male patient with chromosome 1q31.3q42.12 trisomy. In lateral, anterior and posterior posture examination, various anatomic and dysmorphic problems were observed on the patient. To improve the life quality and comfort of the patient, it should be prepared necessary treatment plans for this patients.

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Overexpression of maelstrom promotes bladder urothelial carcinoma cell aggressiveness by epigenetically downregulating MTSS1 through DNMT3B

Zhang

Jiang

et al. 2016

Oncogene

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We have recently identified and characterized a novel oncogene, maelstrom (MAEL) from 1q24, in the pathogenesis of hepatocellular carcinoma. In this study, MAEL was investigated for its oncogenic role in urothelial carcinoma of the bladder (UCB) tumorigenesis/aggressiveness and underlying molecular mechanisms. Here, we report that overexpression of MAEL in UCB is important in the acquisition of an aggressive and/or poor prognostic phenotype. In UCB cell lines, knockdown of MAEL by short hairpin RNA is sufficient to inhibit cell growth, invasiveness/metastasis and suppressed epithelial-mesenchymal transition (EMT), whereas ectopic overexpression of MAEL promoted cell growth, invasive and/or metastatic capacity and enhanced EMT both in vitro and in vivo. We further demonstrate that MAEL could induce UCB cell EMT by downregulating a critical downstream target, the metastasis suppressor 1 (MTSS1) gene, ultimately leading to an increased invasiveness of cancer cells. Notably, overexpression of MAEL in UCB cells substantially enhanced the enrichment of DNA methyltrans-ferase (DNMT)3B and histone deacetylase (HDAC)1/2 on the promoter of the MTSS1, and thereby epigenetically suppressing the MTSS1 transcription. Downregulation of MTSS1 by MAEL in UCB cells is partially dependent on DNMT3B. Furthermore, we identify that beside the gene amplification of MAEL, miR-186 is a key negative regulator of MAEL and downregulation of miR-186 is another important mechanism for MAEL overexpression in UCBs. These data suggest that overexpression of MAEL, caused by gene amplification and/or decreased miR-186, has a critical oncogenic role in UCB pathogenesis by downregulation of MTSS1, and MAEL could be used as a novel prognostic marker and/or effective therapeutic target for human UCB.

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Refined mapping of loss of heterozygosity on 1q31.1-32.1 in sporadic colorectal carcinoma

Cited by 4 publications

References 36 publications

Loss of heterozygosity in oral cancer

Loss of heterozygosity in oral cancer

Trisomy of 1q31.3q42.12 Chromosome: Case Report

Overexpression of maelstrom promotes bladder urothelial carcinoma cell aggressiveness by epigenetically downregulating MTSS1 through DNMT3B

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