Mapping of the candidate tumor suppressor genes’ loci on human chromosome 3 in head and neck squamous cell carcinoma of an Indian patient population

Dasgupta, Santanu; Mukherjee, Nupur; Roy, Sangita; A, Roy; Sengupta, Arunava; Roychowdhury, Susanta; Panda, Chinmay Kumar

doi:10.1016/s1368-8375(00)00131-7

Cited by 65 publications

(93 citation statements)

References 24 publications

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“…CGH studies indicate that these 2 regions are amplified in head-and-neck cancer. [51][52][53] Gain of 3q is one of the earliest genetic markers for invasion and metastasis and correlates with poor prognosis. 52 This region (3q26.…”

Section: Discussionmentioning

confidence: 99%

Molecular classification of oral cancer by cDNA microarrays identifies overexpressed genes correlated with nodal metastasis

Warner

Reis

Jurišica

et al. 2004

Intl Journal of Cancer

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Section: Discussionmentioning

confidence: 99%

Molecular classification of oral cancer by cDNA microarrays identifies overexpressed genes correlated with nodal metastasis

Warner

Reis

Jurišica

et al. 2004

Intl Journal of Cancer

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“…In contrast, transfection of chromosome 3 restores responses to both exogenous and autocrine TGF-␤, indicating that some genes other than TGF-␤ RII on chromosome 3 are required to cooperate with RII to restore full TGF-␤ sensitivity. Little is known about those genes; however, chromosome 3 has been postulated to bear potential tumor suppressor activities (67,68).…”

Section: Figmentioning

confidence: 99%

Autocrine and Exogenous Transforming Growth Factor β Control Cell Cycle Inhibition through Pathways with Different Sensitivity

Wang

Sergina

et al. 2004

Journal of Biological Chemistry

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NEO-transfected control cells (designated NEO pool) before entering exponential growth in tissue culture. The prolonged growth arrest of RII Cl 37 cells was associated with markedly reduced cyclindependent kinase (CDK)2 activity. Our results demonstrate that p21 induction by autocrine TGF-␤ is responsible for reduced CDK2 activity, which at least partially contributes to prolonged growth arrest and reduced cell proliferation in RII Cl 37 cells. In contrast to RII transfectants, HCT116 cells transfected with chromosome 3 (designated HCT116Ch3), which bears the RII gene, restored the response to exogenous TGF-␤ as well as autocrine TGF-␤ activity. Autocrine TGF-␤ activity in HCT116Ch3 cells induced p21 expression as seen in RII Cl 37 cells; however, in addition to autocrine activity, HCT116Ch3 cells responded to exogenous TGF-␤ as decreased CDK4 expression and reduced pRb phosphorylation mediated a TGF-␤ inhibitory response in these cells. These results indicate that autocrine TGF-␤ regulates the cell cycle through a pathway different from exogenous TGF-␤ in the sense that p21 is a more sensitive effector of the TGF-␤ signaling pathway, which can be induced and saturated by autocrine TGF-␤, whereas CDK4 inhibition is a less sensitive effector, which can only be activated by high levels of exogenous TGF-␤.

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“…The other 70 specimens, which included cancerous tissues and paired adjacent normal laryngeal tissues (PANLs) typically 4-15 mm in diameter, were frozen immediately after collection and stored at 80˚C for loss of heterozygosity (LOH) and microsatellite instability (MI). Normal cells presenting as contaminants in the primary laryngeal lesions were removed using a microdissection procedure (14). Samples containing <60% tumor cells were not taken for analysis.…”

Section: Methodsmentioning

confidence: 99%

“…High molecular weight genomic DNA was extracted from LSCC tissues and PANLs according to standard procedure (14). Three highly polymorphic microsatellite markers were used.…”

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

confidence: 99%

A combined strategy of conventional cytogenetics, fluorescent in situ hybridization and microsatellite polymerase chain reaction to analyze the deletion of chromosome 6 in laryngeal squamous cell carcinoma

Kang

Li²,

Fu³

et al. 2007

Oncol Rep

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Abstract. Laryngeal squamous cell carcinoma (LSCC) is a common cancer of the upper respiratory tract. The cytogenetic and molecular events involved in the pathogenesis of LSCC are not well understood. In this study, a combined strategy of conventional cytogenetics, fluorescent in situ hybridization (FISH) and microsatellite polymerase chain reaction was performed to analyze the deletion of chromosome 6 in LSCC. Karyotype analysis indicated that the deletions of 6q were marker chromosomes potentially specific to LSCC. To further characterize the loss of 6q, metaphase cells derived from both solid tumors and the Hep-2 cell line were investigated using FISH, with results consistent with those of conventional cytogenetics. Moreover, tumor-adjacent normal tissue DNA pairs from 70 LSCC in China were analyzed for loss of heterozygosity (LOH) and microsatellite instability (MI) on chromosome 6q in the region 6q25 by polymerase chain reaction (PCR) and three microsatellite markers. Overall, the highest frequency of microsatellite alteration (68.2%) was located at D6S980, which revealed that the region around D6S980 in 6q25 might harbor some important genes related to the pathogenesis of LSCC in Chinese patients. The pattern of chromosomal changes detected using the combined strategy suggests that it will become the most suitable way to find novel cancer-related genes and discover the relationship between the aberration of genetics and their tumorigenic mechanism.

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Mapping of the candidate tumor suppressor genes’ loci on human chromosome 3 in head and neck squamous cell carcinoma of an Indian patient population

Cited by 65 publications

References 24 publications

Molecular classification of oral cancer by cDNA microarrays identifies overexpressed genes correlated with nodal metastasis

Molecular classification of oral cancer by cDNA microarrays identifies overexpressed genes correlated with nodal metastasis

Autocrine and Exogenous Transforming Growth Factor β Control Cell Cycle Inhibition through Pathways with Different Sensitivity

A combined strategy of conventional cytogenetics, fluorescent in situ hybridization and microsatellite polymerase chain reaction to analyze the deletion of chromosome 6 in laryngeal squamous cell carcinoma

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