By Igor B. Roninson, J. Martin Brown, Dale E. Bredesen
Addressing a tremendous box of curiosity for oncologists, mobilephone biologists, and different biomedical researchers, Beyond Apoptosis presents an outline of ways various organic mechanisms of telephone demise, senescence and mitotic disaster cease the expansion of tumor cells taken care of with anticancer agents.
Written via across the world well known participants, this article includes:
- morphological illustrations, in addition to a DVD containing records and movies from numerous time-lapse microscopic reports of mobilephone loss of life and mitotic catastrophe
- the function and boundaries of apoptosis as a determinant of the toxicity of anticancer agents
- alternative mechanisms of the antiproliferative activities of anticancer medications and radiation, comparable to non-apoptotic phone loss of life, mobile senescence, and mitotic catastrophe
- non-apoptotic types of telephone loss of life, reminiscent of necrosis, paraptosis, autophagic cellphone loss of life, and others
- morphological and kinetic ameliorations of some of the different types of phone death
Read Online or Download Beyond Apoptosis: Cellular Outcomes of Cancer Therapy PDF
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Extra info for Beyond Apoptosis: Cellular Outcomes of Cancer Therapy
The apoptotic index (AI) is typically reported as apoptotic cells per 100 nonapoptotic tumor cells, per unit area, per grid, per field, or as a grade. The AI is often a small number and thus a significant number of cells need to be counted to minimize errors and take into account heterogeneity; most reports count 10 high-power fields. Several studies had undertaken a more quantitative approach and counted up to 2000 cells. To overcome the difficulties of the morphological method, many studies have used the in situ end labeling or the terminal deoxynucleotidyl transferase (TdT)–mediated dUTP biotin nick end-labeling (TUNEL) techniques.
Garrity MM, Burgart LJ, Mahoney MR, et al. Prognostic value of proliferation, apoptosis, defective DNA mismatch repair, and p53 overexpression in patients with resected Dukes’ B2 or C colon cancer: a North Central Cancer Treatment Group Study. J Clin Oncol 2004; 22(9):1572–1582. 57. Marijnen CA, Nagtegaal ID, Mulder-Stapel AA, et al. High intrinsic apoptosis, but not radiation-induced apoptosis, predicts better survival in rectal carcinoma patients. Int J Radiat Oncol Biol Phys 2003; 57(2):434–443.
Wolf HK, Stober C, Hohenfellner R, et al. Prognostic value of p53, p21/WAF1, Bcl-2, Bax, Bak and Ki-67 immunoreactivity in pT1 G3 urothelial bladder carcinomas. Tumour Biol 2001; 22(5):328–336. 109. Hussain SA, Ganesan R, Hiller L, et al. Proapoptotic genes BAX and CD40L are predictors of survival in transitional cell carcinoma of the bladder. Br J Cancer 2003; 88(4):586–592. 110. Lipponen PK, Aaltomaa S, Eskelinen M. Expression of the apoptosis suppressing bcl-2 protein in transitional cell bladder tumours.