Non-lethal outcomes of engaging regulated cell death pathways in cancer

Kalkavan, Halime; Rühl, Sebastian; Shaw, Jeremy J.P.; Green, Douglas R.

doi:10.1038/s43018-023-00571-6

Cited by 13 publications

(12 citation statements)

References 165 publications

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“…The processes of cell survival after engaging apoptosis and other modes of regulated cell death are well established and extensively reviewed (e.g., [80][81][82][83][84][85][86][87][88][89][90][91][92][93]). Some key discoveries are outlined below to illustrate the basis for the main purpose of the current review: a paradigm shift in oncology to focus on apoptosis-suppressing (rather than promoting) strategies.…”

Section: Rethinking Pro-apoptotic Strategies To Combat Solid Tumorsmentioning

confidence: 99%

“…Comprehensive review articles have been published by two members of the Nomenclature Committee on Cell Death (NCCD), Douglas Green and associates [92] and Boris Zhivotovsky and associates [85], as well as other authors (e.g., [93]), in which they have extensively discussed the mechanisms of cancer cell survival after engaging regulated cell death. These articles have concluded that ".…”

Section: Conflicting Reports On Cancer Cell Fate After Engaging Apopt...mentioning

confidence: 99%

“…. .the goal of most cancer therapies (to induce regulated cell death in cancer cells) directly brings about the cellular changes that we seek to avoid" [92], ". .…”

Section: Conflicting Reports On Cancer Cell Fate After Engaging Apopt...mentioning

confidence: 99%

“…This review was not intended to provide an in-depth discussion of all aspects of therapy resistance in different types of malignancies. For those who are interested in further reading, we suggest recent reviews by our group and others on related topics such as the dark side of regulated cell death in solid tumor therapy [20,33,84,85,92], cancer cell dormancy and disease recurrence post-therapy [20,59,62], the challenges and promises of cancer immunotherapy [120,121], the significance of wild-type p53 signaling in suppressing (treacherous) apoptosis [21,118,122], the impact of host immune response on the outcome of cancer therapy [24,123], the role of tumor microenvironment in therapy resistance and disease relapse [124], and tumor cell plasticity [125,126].…”

Section: Further Readingmentioning

confidence: 99%

“…dark side of regulated cell death in solid tumor therapy [20,33,84,85,92], cancer cell dormancy and disease recurrence post-therapy [20,59,62], the challenges and promises of cancer immunotherapy [120,121], the significance of wild-type p53 signaling in suppressing (treacherous) apoptosis [21,118,122], the impact of host immune response on the outcome of cancer therapy [24,123], the role of tumor microenvironment in therapy resistance and disease relapse [124], and tumor cell plasticity [125,126].…”

Section: Conflicts Of Interestmentioning

confidence: 99%

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Changing the Landscape of Solid Tumor Therapy from Apoptosis-Promoting to Apoptosis-Inhibiting Strategies

Mirzayans

2024

CIMB

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The many limitations of implementing anticancer strategies under the term “precision oncology” have been extensively discussed. While some authors propose promising future directions, others are less optimistic and use phrases such as illusion, hype, and false hypotheses. The reality is revealed by practicing clinicians and cancer patients in various online publications, one of which has stated that “in the quest for the next cancer cure, few researchers bother to look back at the graveyard of failed medicines to figure out what went wrong”. The message is clear: Novel therapeutic strategies with catchy names (e.g., synthetic “lethality”) have not fulfilled their promises despite decades of extensive research and clinical trials. The main purpose of this review is to discuss key challenges in solid tumor therapy that surprisingly continue to be overlooked by the Nomenclature Committee on Cell Death (NCCD) and numerous other authors. These challenges include: The impact of chemotherapy-induced genome chaos (e.g., multinucleation) on resistance and relapse, oncogenic function of caspase 3, cancer cell anastasis (recovery from late stages of apoptosis), and pitfalls of ubiquitously used preclinical chemosensitivity assays (e.g., cell “viability” and tumor growth delay studies in live animals) that score such pro-survival responses as “lethal” events. The studies outlined herein underscore the need for new directions in the management of solid tumors.

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Section: Rethinking Pro-apoptotic Strategies To Combat Solid Tumorsmentioning

confidence: 99%

Section: Conflicting Reports On Cancer Cell Fate After Engaging Apopt...mentioning

confidence: 99%

“…. .the goal of most cancer therapies (to induce regulated cell death in cancer cells) directly brings about the cellular changes that we seek to avoid" [92], ". .…”

Section: Conflicting Reports On Cancer Cell Fate After Engaging Apopt...mentioning

confidence: 99%