Cancer cell death

Standley SM, Toft DJ, Cheng H et al (2010) Induction of cancer cell death by selfassembling nanostructures incorporating a cytotoxic peptide. Cancer Res 70 3020-3026... 

Fig. 3. Mechanism of synthetic lethality between PARP inhibition and BRCA deficiency. PARP inhibition blocks the activity of BER and leads to DNA SSB accumulation inside cells. When cells enter the next round of DNA replication, these DNA SSBs are converted to DNA DSBs which can be efficiently repaired through the HR pathway in normal cells. BRCA deficient cancer cells are unable to repair the DNA DSBs that accumulate following PARP inhibition. This eventually causes toxicity and cancer cell death.

Royer C, Lu X (2011) Epithelial cell polarity a major gatekeeper against cancer Cell Death Differ 18 1470-1477... 

Ghosh J. 2003. Inhibition of arachidonate 5-lipoxygenase triggers prostate cancer cell death through rapid activation of c-Jun N-terminal kinase. Biochem Biophys Res Commun 307 342-349. 

Periwinkle has been shown to lower blood sugar and to act as a diuretic. The main alkaloids, vinblastine and vincristine, appear to bind to proteins in some microtubules, facilitating cancer-cell death (see Chapter 62). 

Cytokine-provided survival signals are known to suppress apoptosis through inhibition of mitochondrial pathways that involve Bci-2 family members. It was also discovered that IFNy-TNFa synergism, rather than the Fas ligand as currently believed, is responsible for the apoptosis in cancer cell deaths. ... 

Fournie GJ, Courtin JP, Laval F, Chale JJ, Pourrat JP, Pujazon MC> et al. Plasma DNA as a marker of cancerous cell death. Investigations in patients suffering from lung cancer and in nude mice bearing human tumours. Cancer Lett 1995 91 221-7. 

The globo H vaccine is being tested in clinical trials to determine whether it will block the reappearance or progression of cancer. Thus far, in a group of 27 women with metastatic breast cancer, globo H raised blood levels of IgM antibodies. In 16 of these patients, IgM antibodies bound to the cancer cells, and some patients showed evidence of cancer cell death (52). 

McCarty, in the article cited earlier, first explains his finding in terms of cyclic AMP levels, which others have found to make cancer cells liable to contact inhibition, and thus more benign. A possible scenario is that glucagon inhibits a growth factor supporting cancer proliferation, and also induces cancer cell death by apoptosis. The cancers especially noted to be inhibited by a vegan diet are of the breast, prostate, and colon. 

In addition to cell cycle arrest, all FASN inhibitors induce cell death in tumor cells (Pizer et al., 1996a, 1998a Kridel et al., 2004 Zhou et al., 2007). Cerulenin induces breast and prostate cancer cell death that correlates with DNA fragmentation and morphology characteristic of apoptosis (Pizer, et al., 1996a, 2000 Furuya, et al., 1997). The mitochondria have also been linked to facilitation of cell death induced by cerulenin. For instance, the pro-apoptotic mitochondrial factor Bax is induced in cells treated with cerulenin. (Heiligtag et al.,... 

We will consider here this problem in the context of cancer chemotherapy. Since antineoplastic drugs by necessity are quite toxic, it would seem that meaningful mathematical models could be important guides in the optimization of various types of experimental and clinical trials. The mode of action of many of these drugs, at least semiempirically, is qualitatively and sometimes quantitatively known, and the pharmacokinetics of several types have been studied. More specific information seems to be available concerning the action on tumor cells than toxicity in critical normal cells such as bone marrow and gastrointestinal tract. However, to be useful in a clinical sense, both effects must be predictable since successful therapy is based on the balance between the cancer cell death and the toxicity. 

Berry D, Lynn D M, Sasisekharan R (2004). Poly(b-amino ester)s promote cellular uptake of heparin and cancer cell death. Chem. Bio. 11 487-498. 

Chemotherapy was first used for the treatment of advanced lymphomas in the 1940s [1], Since then several classes of chemotherapeutic compounds such as alkylating agents, antimetabolites, anthracyclines, plant alkaloids, and later topoisomerase inhibitors and taxanes have been identified or synthesized to treat various forms of cancer [2, 3], Although numerous in vitro and animal studies have demonstrated their effectiveness in inducing cancer cell death (cytotoxic) or cell growth arrest (cytostatic), these promising anticancer activities seen in the controlled environment of the laboratory frequently do not translate well into the expected clinical outcomes [4-8]. 

Obeid M et al. Calreticulin exposure dictates the immunogenicity of cancer cell death. Nat Medimi-, 13 54-61. 

Photodynamic therapy (PDT) involves the administration of a photosensitizer and activation of the photosensitizer with light irradiation in the tumor tissue, resulting in cancer cell death. Photodynamic therapy causes cell death through... 

Oren, M. (2003). Decision making by p53 Life, death and cancer. Cell Death Differ. 10, 431-442. 

Makhov P, Golovine K, Teper E, Kutikov A, Mehrazin R, Corcoran A, et al. Piper-longumine promotes autophagy via inhibition of Akt/m TOR signaling and mediates cancer cell death. Br J Cancer 2014 110(4) 899-907. 

Srikanth S, Kraft AS. Inhibition of caspases by cytokine response modifier A blocks androgen ablation-mediated prostate cancer cell death in vivo. Cancer Res 1998 58 834-839. 

Another bisindolyhnaleimide, MKC-1 (142), induces cancer cell death (apoptosis) by targeting tubulin. This agent demonstrated activity in phase II trials against breast, ovarian, and non-small cell lung cancer and leukemia, but it was subsequently withdrawn from further smdy [150,160],... 

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