Loss of heterozygosity at chromosomes 1p35-pter, 4q, and 18q and protein expression differences between adenocarcinomas of the distal stomach and gastric cardia

Xu, Yan; Mao, Xiaohui; Lv, Zhi; Liu, Deming; Sun, Zhe; Chen, Hong; Wang, Zhenning; Luo, Yang; Xu, Hui

doi:10.1016/j.humpath.2012.01.024

Cited by 9 publications

(3 citation statements)

References 24 publications

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“…Multiple studies have demonstrated TGFBR2 inactivating mutations in GC [16,[48][49][50][51]. Similar observations have been made regarding SMAD 4 mutations, resulting in diminished signal transduction following TGF receptor-ligand interaction [16,51,52].…”

Section: Tgf-β Pathwaymentioning

confidence: 53%

Molecular Mechanisms in Gastric Carcinogenesis

2015

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Section: Tgf-β Pathwaymentioning

confidence: 53%

Molecular Mechanisms in Gastric Carcinogenesis

2015

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“…Moreover, the prognostic effect of annexin expression in malignancy has been differentially demonstrated according to cancer subtypes and locations . Several previous studies have reported that ANXA10 is a tumor suppressor, diagnostic marker, potential therapeutic target, or prognostic factor in various malignancies, including hepatocellular carcinoma, acute myeloid leukemia, gastric carcinoma, oral squamous cell carcinoma, pancreatobiliary adenocarcinoma, and urothelial carcinoma . However, to our knowledge, ANXA10 expression in CRC and benign colorectal tumors had not been explored prior to the recent study by Gonzalo et al.…”

Section: Discussionmentioning

confidence: 99%

Annexin A10 expression correlates with serrated pathway features in colorectal carcinoma with microsatellite instability

Kim

Rhee

Kim

et al. 2014

APMIS

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Annexin A10 (ANXA10) has recently been identified as a marker of sessile serrated adenomas/polyps of the colorectum. Although the serrated neoplasia pathway is thought to be involved in the majority of microsatellite instability-high (MSI-H) sporadic colorectal carcinomas (CRCs), the clinicopathological implications of ANXA10 expression in CRC are unknown. Here, we evaluated ANXA10 expression status in 168 MSI-H CRCs by immunohistochemistry. Among 168 MSI-H CRCs, nuclear staining for ANXA10 in tumor cells revealed 28 cases (17%) with ANXA10-positive (ANXA10+) tumors. Most of the ANXA10+ tumors were located in the proximal colon (96%, p< 0.001). The ANXA10+ phenotype in MSI-H CRC was significantly associated with female gender (68%, p = 0.016), CpG island methylator phenotype-high (CIMP-H) (68%, p < 0.001), MLH1 promoter hypermethylation (61%, p < 0.001), loss of MLH1 expression (82%, p = 0.019), and wild-type KRAS status (96%, p = 0.023). Survival analysis revealed no prognostic significance of ANXA10 expression in MSI-H CRC. In conclusion, ANXA10+ MSI-H colon carcinomas are characterized by serrated pathway features, including proximal location, female predominance, and high frequencies of CIMP-H status and MLH1 methylation.

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“…This is mainly caused by the lack of knowledge about the cancer driver genes of MPNSTs. Chromosome fragment 4q22‐23 is frequently deleted in MPNSTs and many other types of human cancers 13‐21 . However, the critical cancer driver genes on this CNA remain largely unknown.…”

Section: Introductionmentioning

confidence: 99%

Loss of smarcad1a accelerates tumorigenesis of malignant peripheral nerve sheath tumors in zebrafish

Han

Jiang

Kumari

et al. 2021

Genes Chromosomes & Cancer

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Malignant peripheral nerve sheath tumors (MPNSTs) are a type of sarcoma that generally originates from Schwann cells. The prognosis for this type of malignancy is relatively poor due to complicated genetic alterations and the lack of specific targeted therapy. Chromosome fragment 4q22‐23 is frequently deleted in MPNSTs and other human tumors, suggesting tumor suppressor genes may reside in this region. Here, we provide evidence that SMARCAD1, a known chromatin remodeler, is a novel tumor suppressor gene located in 4q22‐23. We identified two human homologous smarcad1 genes (smarcad1a and smarcad1b) in zebrafish, and both genes share overlapping expression patterns during embryonic development. We demonstrated that two smarcad1a loss‐of‐function mutants, sa1299 and p403, can accelerate MPNST tumorigenesis in the tp53 mutant background, suggesting smarcad1a is a bona fide tumor suppressor gene for MPNSTs. Moreover, we found that DNA double‐strand break (DSB) repair might be compromised in both mutants compared to wildtype zebrafish, as indicated by pH2AX, a DNA DSB marker. In addition, both SMARCAD1 gene knockdown and overexpression in human cells were able to inhibit tumor growth and displayed similar DSB repair responses, suggesting proper SMARCAD1 gene expression level or gene dosage is critical for cell growth. Given that mutations of SMARCAD1 sensitize cells to poly ADP ribose polymerase inhibitors in yeast and the human U2OS osteosarcoma cell line, the identification of SMARCAD1 as a novel tumor suppressor gene might contribute to the development of new cancer therapies for MPNSTs.

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Loss of heterozygosity at chromosomes 1p35-pter, 4q, and 18q and protein expression differences between adenocarcinomas of the distal stomach and gastric cardia

Cited by 9 publications

References 24 publications

Molecular Mechanisms in Gastric Carcinogenesis

Molecular Mechanisms in Gastric Carcinogenesis

Annexin A10 expression correlates with serrated pathway features in colorectal carcinoma with microsatellite instability

Loss of smarcad1a accelerates tumorigenesis of malignant peripheral nerve sheath tumors in zebrafish

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