Cytological studies on onion root-tip cells treated with water-soluble extract of tobacco smoke condensate from commercial cigarettes

Sabharwal, P. S.; Gulati, Dushyant K.; Bhalla, P. R.

doi:10.1016/0165-1161(75)90003-5

Cited by 10 publications

(1 citation statement)

References 6 publications

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“…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. cronuclei (Balansky et al, 1988;Mohtashamipur et al, 1988;Stoichev et al, 1993;Saunders et al, 2000), lagging chromosomes (Sabharwal et al, 1975;Saunders et al, 2000), as well as chromosomal aneuploidy and various structural chromosome rearrangements, including gene amplification (Lafi and Parry, 1988;Luo et al, 2004). One ongoing problem with treating OSCC is that tumors from the same site within the oral cavity respond differently to identical treatment regimens.…”

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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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