Elsevier

Drug Resistance Updates

Volume 4, Issue 2, April 2001, Pages 132-134
Drug Resistance Updates

Debate
Apoptosis is critical for drug response in vivo

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    Salvage treatments for this patient population should address mechanisms of resistance to initial treatment. One mechanism-of-resistance is inactivation of the master regulators of apoptosis, p16/CDKN2A and TP53 [1-8], by mutation, deletion or epigenetics that confers resistance to multiple lines of therapy that share apoptosis (cytotoxicity) as a common final pathway of action (reviewed in [9-14]). Treatments that do not require the p53/p16-CDKN2A apoptosis-axis are hence needed.

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    Instead, results of long-term assays employing local tumor control as primary endpoint might provide a more reliable surrogate parameter predicting clinical efficacy. In addition, the analysis of long-term outcomes after increasing apoptosis induction by any means is of crucial importance in radiation oncology because it has been generally questioned in how far modulations of apoptosis rates would improve treatment outcomes (20–22). Thus, based on the results of the initial efficacy testing, we decided to complement the results from our growth delay data by long-term tumor control assays.

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    Defects in the physiological pathway for apoptosis contribute to carcinogenesis. Moreover, aberrant inhibition of apoptosis interferes with normal cell regulation and promotes tumorigenesis (Borst et al., 2001; Reed, 2001; Schmitt and Lowe, 2001). Several anti-apoptotic genes, such as inhibitor of apoptosis protein (IAP) family members, take part in pathogenesis, progression and chemo- or radio-resistance of cancers (Reed, 2001).

  • The protozoan toxin climacostol inhibits growth and induces apoptosis of human tumor cell lines

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    In order to explain the “anomalies” observed in PCD of A431 cells, it is useful to remark the increasing amount of evidence suggesting that some forms of drug-induced cell death cannot readily be classified as apoptosis, or necrosis, and are better associated with apoptosis-like, or necrosis-like PCD models [40]. Cell death can occur in an apoptosis-like programmed fashion, but in complete absence and/or independently of caspase activation [41–44]. Examples of apoptosis-like PCD are provided by ginkolic acids and sorbitol.

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