Chromosomal Instability in Oral Cancer Cells

Reshmi, Shalini C.; Gollin, Susanne M.

doi:10.1177/154405910508400203

Cited by 49 publications

(42 citation statements)

References 140 publications

(178 reference statements)

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“…For some samples scraped from the oral mucosa, stratified (keratinized) epithelial cells are observed (5). These cells most always There are several sources of chromosomal instability; the primary causes seem to be defects in chromosome segregation, telomere stability, cell cycle checkpoint regulation, and repair of DNA damage (98).…”

Section: Resultsmentioning

confidence: 99%

Smoking and Smokeless Tobacco-Associated Human Buccal Cell Mutations and Their Association with Oral Cancer—A Review

Proia

Paszkiewicz

Nasca³

et al. 2006

Cancer Epidemiology, Biomarkers &Amp; Prevention

142

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Reported herein are the results of a structured literature review that was undertaken to (a) determine if human buccal (mouth) cell changes are associated with smoking and smokeless (''chewing'') tobacco, (b) tabulate different buccal cell alterations that have been reported, (c) delineate buccal cell assays that have been used successfully, (d) determine whether buccal cell changes correlate with oral cancer as defined in clinicopathologic investigations, and (e) assess the feasibility of developing a high-throughput buccal cell assay for screening smokers for the early detection of oral cancer. The results of the studies reported herein have established that diverse buccal cell changes are associated with smoking and smokeless tobacco. This review documents also that buccal cells have been collected in a noninvasive manner, and repetitively for serial studies, from different sites of the mouth (e.g., cheek, gum, and tongue) and from normal tissue, preneoplastic lesions (leukoplakia), and malignant tumors. Tobacco-associated genetic mutations and nongenetic changes have been reported; a partial listing includes (a) micronuclei, (b) bacterial adherence, (c) genetic mutations, (d) DNA polymorphisms, (d) carcinogen-DNA adducts, and (e) chromosomal abnormalities. Clinical studies have correlated buccal cell changes with malignant tumors, and some oral oncologists have reported that the buccal cell changes are practical biomarkers. Summarily, the literature has established that buccal cells are useful not only for characterizing the molecular mechanisms underlying tobacco-associated oral cancers but also as exfoliative cells that express diverse changes that offer promise as candidate biomarkers for the early detection of oral cancer. (Cancer Epidemiol Biomarkers Prev 2006;15(6):1061 -77)

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Section: Resultsmentioning

confidence: 99%

Smoking and Smokeless Tobacco-Associated Human Buccal Cell Mutations and Their Association with Oral Cancer—A Review

Proia

Paszkiewicz

Nasca³

et al. 2006

Cancer Epidemiology, Biomarkers &Amp; Prevention

142

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“…CIN may then promote the survival of subpopulations within a given tumor. Various ways in which CIN may arise in tumor cells include (1) faulty mitotic apparatus machinery, (2) centrosome amplification, (3) telomere dysfunction, (4) defects in the DNA damage response, and (5) gene amplification (Reshmi and Gollin, 2005). In OSCC, amplification of chromosome band 11q13 occurs in the form of a homogeneously staining region (hsr) in approximately 45% of OSCC (Gollin, 2001).…”

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confidence: 99%

Inverted duplication pattern in anaphase bridges confirms the breakage-fusion-bridge (BFB) cycle model for 11q13 amplification

Roychoudhury

Feingold

et al. 2007

Cytogenet Genome Res

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The homogeneously staining region (hsr) involving chromosome band 11q13 includes amplified genes from this chromosome segment and carries a relatively poor prognosis in oral squamous cell carcinomas (OSCC), with shorter time to recurrence and reduced overall survival. We previously identified an inverted duplication pattern of genes within the 11q13 hsr in OSCC cells, supporting a breakage-fusion-bridge (BFB) cycle model for gene amplification. To validate our hypothesis that 11q13 gene amplification in OSCC occurs via BFB cycles, we carried out fluorescence in situ hybridization (FISH) using probes for band 11q13 on 29 OSCC cell lines. We demonstrate that all OSCC cell lines with 11q13 amplification express a significantly higher frequency of anaphase bridges containing 11q13 sequences compared to cell lines without amplification, providing further experimental evidence that 11q13 gene amplification in OSCC cells occurs via BFB cycles. Elucidation of mechanisms responsible for initiating and promoting gene amplification provides opportunities to identify new biomarkers to aid in the diagnosis and prognosis of oral cancer, and may be useful for developing novel therapeutic strategies for patients with OSCC.

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“…Many previous studies have demonstrated that karyotypes of HNSCC and oral Squamous cell carcinoma consist of neartriploid chromosome numbers and contain various patterns of cytogenetic abnormality, including structural and numerical aberrations [15,16,17]. Chemotherapeutic drugs currently being used which may activate specific intracellular pathway(s) and induce apoptosis in target cells.…”

Section: Discussionmentioning

confidence: 99%

Chromosomal Rearrangements In Lymphocytes Of Head and Neck Squamous Cell Carcinoma Treated With Chemotherapeutic Agents

Desai¹,

Gadhia²

2012

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Squamous cell carcinoma especially of oral cavity is one of the most prevalent diseases in the world. Chromosomal rearrangements are known to play important role in the pathogenesis of many diseases including cancer. In case of Head and Neck Squamous Cell Carcinoma, chromosomal changes are detectable at all stages of tumor development providing excellent opportunity for chromosomal prognosis and therapy. The present work aimed to study the frequency and pattern of chromosomal aberrations in human peripheral blood lymphocyte culture of freshly diagnosed Head and Neck squamous cell carcinoma patients. Further In vitro anticancer drugs (5-Fluorouracil {5-FU } and Cisplatin) effects were studied for clastogenicity. Results indicated significant impact of chemotherapeutic agents on the frequency of different types of chromosomal rearrangements. Key words: chromosomal aberrations, head and neck squamous cell carcinoma (HNSCC), invitro chemotherapy, peripheral blood lymphocyte culture (PBLC)Oral squamous cell carcinoma (OSCC) is a major cause of morbidity and mortality worldwide, accounting for more than 275,000 new cases and over 120,000 deaths every year [1]. It is already known that non-random chromosomal aberrations occur in all human cancer types including squamous cell carcinoma (SCC) of the head and neck (HNSCC) [2]. Further many reports suggested that chromosomal aberrations and accumulation of mutations in many genes encoding crucial proteins or oncoproteins that control cell growth and apoptosis may also induce neoplastic formation [3,4,5]. However in case of Head and Neck SCC, chromosomal aberrations are found to be a dominant genetic event in carcinogenesis and may play an important role in cancer progression [6].In the present study, chromosomal rearrangements were observed in freshly diagnosed HNSCC patients who had not undergone any chemotherapeutic and/or radiation treatment. Further, peripheral blood lymphocytes of patients were exposed to anticancer drugs namely 5-Fluorouracil {5-FU} and Cisplatin commonly used for oral cancer treatment.5-FU is considered to be purely an S phase active chemotherapeutic agent [7] and also causes DNA damage, specifically double strand (and single-strand) breaks, during synthetic phase of cell cycle due to the misincorporation of FdUTP into DNA [8,9]. On the other hand, Cisplatin is a potent anti-tumor agent being cytotoxic to tumor cells via DNA-protein and DNA-DNA interstrand and intrastrand crosslinks [10]. The drug may also induce programmed cell death or apoptosis [11].Therefore, it is important to improve the patient survival rate in HNSCC and it is essential to find more accurate prognostic markers, if any, such as chromosomal rearrangements with different end points. Materials and MethodsLymphocyte Culture.Lymphocyte cultures were set by method of Hungerford [12] with slight modifications [13]. Heparinized whole blood (0.5 ml) was added to a mixture containing 5 ml of culture medium RPMI 1640 and 0.1 ml phytohemagglutinin (Lectin). Then the culture vials were ke...

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Chromosomal Instability in Oral Cancer Cells

Cited by 49 publications

References 140 publications

Smoking and Smokeless Tobacco-Associated Human Buccal Cell Mutations and Their Association with Oral Cancer—A Review

Smoking and Smokeless Tobacco-Associated Human Buccal Cell Mutations and Their Association with Oral Cancer—A Review

Inverted duplication pattern in anaphase bridges confirms the breakage-fusion-bridge (BFB) cycle model for 11q13 amplification

Chromosomal Rearrangements In Lymphocytes Of Head and Neck Squamous Cell Carcinoma Treated With Chemotherapeutic Agents

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