Gene expression profiles in squamous cell cervical carcinoma using array-based comparative genomic hybridization analysis

Choi, Young-Seok; Bae, Seog Nyeon; Kim, Y.‐W.; Lee, H.N.; Park, T.C.; Ro, Duck Yeong; Shin, Jung-Young; Shin, Sun; Seo, Jong-Soo; Ahn, Woong Shick

doi:10.1111/j.1525-1438.2007.00834.x

Cited by 101 publications

(72 citation statements)

References 31 publications

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“…The SIPL1 gene resides at 8q24.3 (http://www.ncbi.nlm.nih.gov/). Amplification of 8q24.3 occurs commonly in sporadic breast cancer (45) and squamous cell cervical carcinoma (46), two types of carcinomas that display a tendency toward SIPL1 expression with PTEN positivity. Increases in the copy number at the 8q24.3 locus were also observed in astrocytoma (47), gastroesophageal junction cancer (48), prostate cancer (49), chemoresistant ovarian cancer (50), larynx and pharynx squamous cell carcinoma (51), liver cancer (52,53), and colorectal cancer (54,55).…”

Section: Discussionmentioning

confidence: 99%

Shank-interacting protein–like 1 promotes tumorigenesis via PTEN inhibition in human tumor cells

He¹,

Ingram²,

Rybak³

et al. 2010

J. Clin. Invest.

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Inactivation of phosphatase and tensin homolog (PTEN) is IntroductionWhile PTEN displays phosphatase activity for both protein and lipid substrates (1), accumulating evidence reveals that its lipid phosphatase activity, which dephosphorylates the 3ʹ-position phosphate from the inositol ring of phosphatidylinositol 3,4,5-triphosphate (PIP 3 ) (2, 3), contributes to PTEN's tumor suppression activities. Thus, PTEN directly antagonizes a critical oncogenic activity mediated by PI3K (4, 5).Consistent with its biochemical functions, inactivation of PTEN is a critical step during tumorigenesis. Typical mechanisms responsible for PTEN inactivation in human cancers include genetic and epigenetic events. The PTEN gene is frequently mutated in human cancers (6-8), including more than 50% of glioblastomas and melanomas, 30%-50% of endometrial carcinomas, and 10% of breast cancers (4, 9, 10). A missense mutation, PTEN/G129E, leading to loss of PTEN's PIP 3 phosphatase activity (4, 11), was detected in Cowden disease (12), a multiple hamartoma syndrome with predisposition to multisystemic malignant tumors (13). Hypermethylation of the PTEN promoter in sporadic colorectal cancers and reduction of PTEN protein without mutations in the PTEN gene in prostate and cervical cancers have also been observed (14-16).Inactivation of PTEN is known to contribute to cervical tumorigenesis. Low levels (2%-16%) of mutations in the PTEN gene as well as the loss of heterozygosity of PTEN have been reported in cervical cancer (17)(18)(19)(20). Consistent with the hypermethylation of PTEN in cervical cancer, reduction in the PTEN protein was observed in approximately 15% of cervical squamous cell carcinomas (21,22). Furthermore, essential pathways that promote cervical tumorigenesis have been shown to inhibit PTEN function. The E6 and E7

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Section: Discussionmentioning

confidence: 99%

Shank-interacting protein–like 1 promotes tumorigenesis via PTEN inhibition in human tumor cells

He¹,

Ingram²,

Rybak³

et al. 2010

J. Clin. Invest.

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“…HDAC9, which is a unique gene located in the 7p21.1 amplified region, encodes a member of the class IIa histone deacetylase (HDAC) enzyme family, which is involved in chromatin condensation and transcriptional repression (46). HDAC9 gain has been described in squamous cell cervical carcinomas (47), and higher HDAC9 expression has been associated with poor prognosis in childhood acute lymphatic leukemias (48). DOCK5, which maps to 8p21.2-p21.3, encodes the dedicator of cytokinesis 5 protein and is recurrently deleted and underexpressed in osteosarcoma (49,50).…”

Section: Discussionmentioning

confidence: 99%

Recurrent Mutations of MYD88 and TBL1XR1 in Primary Central Nervous System Lymphomas

González-Aguilar

Idbaïh

Boisselier

et al. 2012

Clinical Cancer Research

223

171

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Purpose: Our objective was to identify the genetic changes involved in primary central nervous system lymphoma (PCNSL) oncogenesis and evaluate their clinical relevance.Experimental Design: We investigated a series of 29 newly diagnosed, HIV-negative, PCNSL patients using high-resolution single-nucleotide polymorphism (SNP) arrays (n ¼ 29) and whole-exome sequencing (n ¼ 4) approaches. Recurrent homozygous deletions and somatic gene mutations found were validated by quantitative real-time PCR and Sanger sequencing, respectively. Molecular results were correlated with prognosis.Results: All PCNSLs were diffuse large B-cell lymphomas, and the patients received chemotherapy without radiotherapy as initial treatment. The SNP analysis revealed recurrent large and focal chromosome imbalances that target candidate genes in PCNSL oncogenesis. The most frequent genomic abnormalities were (i) 6p21.32 loss (HLA locus), (ii) 6q loss, (iii) CDKN2A homozygous deletions, (iv) 12q12-q22, and (v) chromosome 7q21 and 7q31 gains. Homozygous deletions of PRMD1, TOX, and DOCK5 and the amplification of HDAC9 were also detected. Sequencing of matched tumor and blood DNA samples identified novel somatic mutations in MYD88 and TBL1XR1 in 38% and 14% of the cases, respectively. The correlation of genetic abnormalities with clinical outcomes using multivariate analysis showed that 6q22 loss (P ¼ 0.006 and P ¼ 0.01) and CDKN2A homozygous deletion (P ¼ 0.02 and P ¼ 0.01) were significantly associated with shorter progression-free survival and overall survival.Conclusions: Our study provides new insights into the molecular tumorigenesis of PCNSL and identifies novel genetic alterations in this disease, especially MYD88 and TBL1XR1 mutations activating the NF-kB signaling pathway, which may be promising targets for future therapeutic strategies.

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“…Of these, 7 have already been described as tumour suppression genes showing decreased expression in high-grade neoplasms. Expression of LRP1B, which belongs to the low density lipoprotein receptor gene family, is inactivated by genetic and transcript alterations in non-small cell lung cancer (31) or altered by deletion in high-grade urothelial cancer (32) and the region of the chromosome containing the gene is frequently deleted in squamous cell cervical carcinoma (33). Loss of DDR1, originally named TU3A, is also frequently seen in other high-grade tumours, such as renal cell carcinoma (34), and downregulation of its expression may also contribute to glioma progression (35).…”

Section: ------------------------------------------------------------mentioning

confidence: 99%

Microarray gene expression profiling in meningiomas: Differential expression according to grade or histopathological subtype

Fèvre-Montange¹

2009

Int J Oncol

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Gene expression profiles in squamous cell cervical carcinoma using array-based comparative genomic hybridization analysis

Cited by 101 publications

References 31 publications

Shank-interacting protein–like 1 promotes tumorigenesis via PTEN inhibition in human tumor cells

Shank-interacting protein–like 1 promotes tumorigenesis via PTEN inhibition in human tumor cells

Recurrent Mutations of MYD88 and TBL1XR1 in Primary Central Nervous System Lymphomas

Microarray gene expression profiling in meningiomas: Differential expression according to grade or histopathological subtype

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