کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9890036 | 1539998 | 2005 | 20 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Chromosome instability in neoplasia: chaotic roots to continuous growth
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کلمات کلیدی
Telomerase RNA componentISCNSCEBFBPMLCGHTERCALTAPCTRAPataxia telangiectasia mutated - Ataxia telangiectasia جهش یافته استSKY - آسمانAneuploidy - آنیوپلوئیدی Microsatellite instability - بی ثباتی ریزماهواره ایChromosome instability - بی ثباتی کروموزومsister chromatid exchanges - تبادل کروماتید خواهرTERT - تترcomparative genomic hybridization - ترکیب هیبریداسیون ژنومی مقایسه شدهTelomerase reverse transcriptase - ترکیبریت معکوس تلومرازTelomeres - تلومرهاPopulation doubling - جمعیت دو برابر می شودCin - جینMin - حداقلATM - خودپردازCancer - سرطانfluorescent in situ hybridization - فلورسنت در محل hybridizationPromyelocytic leukemia - لوسمی PromyelocyticFish - ماهیTelomeric repeat amplification protocol - پروتکل تقویت تکرار تلومرanaphase-promoting complex - پیچیده ترویج آنافاز
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Chromosome instability in neoplasia: chaotic roots to continuous growth Chromosome instability in neoplasia: chaotic roots to continuous growth](/preview/png/9890036.png)
چکیده انگلیسی
Multiple rearrangements of chromosome number and structure are common manifestations of genomic instability encountered in mammalian tumors. In neoplasia, in continuous immortalized growth in vitro, and in animal models, the accumulation of various defects on DNA repair and telomere maintenance machineries, mitotic spindle abnormalities, and breakage-fusion-bridge cycles, deteriorate the precise mitotic distribution of the genomic content, thus producing various types of chromosomal anomalies. These lesions generate tremendous genomic imbalances, which are evolutionary selected, since they force the function of the whole genome towards continuous growth. For more than a century chromosomal rearrangements and aneuploidy in neoplasia have been discussed and a vast number of genes and pathways, directly or indirectly implicated, have been described. In this review, we focus on the biological mechanisms that generate numerical or structural deviations of the normal diploid chromosomal constitution in epithelial neoplasia. There is growing evidence that chromosomal instability is both an epiphenomenon and a leading cause of cancer. We will discuss the roles of genes, chromosome structure, and telomere dysfunction in the initiation of chromosomal instability. We will explore research strategies that can be applied to identify rates of chromosomal instability in a specimen, and the putative biological consequences of karyotypic heterogeneity. Finally, we will re-examine the longstanding hypothesis of the generation of aneuploidy in the context of telomere dysfunction and restoration.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: The International Journal of Biochemistry & Cell Biology - Volume 37, Issue 5, May 2005, Pages 1014-1033
Journal: The International Journal of Biochemistry & Cell Biology - Volume 37, Issue 5, May 2005, Pages 1014-1033
نویسندگان
Sarantis Gagos, Irmgard Irminger-Finger,