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Updated: Aug 29, 2026

Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis
Published on: February 16, 2015
Getting back on track, or what to do when apoptosis is de-railed: recoupling oncogenes to the apoptotic machinery
1Apoptosis Section, Regulation of Cell Growth Laboratory, NCI-Frederick, Maryland 21702, USA. hfearnhead@ncifcrf.gov
Abstract:
Programmed cell death or apoptosis is of fundamental importance to cancer as it both limits tumorigenesis and is also triggered by many cancer chemotherapeutics. Many oncogenes that deregulate the cell cycle also trigger apoptosis, so eliminating cells that are proliferating inappropriately. To acquire a complete neoplastic phenotype, cancer cells often acquire mutations that compromise the apoptotic process, allowing these cells to escape both normal growth constraints but to also become resistant to many anti-cancer drugs and leading to the emergence of drug-resistant malignancies. Thus discovering how oncogenes are coupled to apoptosis and how these links are compromised in cancer is central to both understanding cancer progression and developing new therapies to counter chemo-resistant cancers. This review will consider how oncogenes activate apoptosis and how this response is subverted in cancer cells with a focus on the proposed therapeutic strategies that exploit these changes.
Insights
Cancer cells evade programmed cell death (apoptosis) through oncogene mutations, leading to drug resistance. Understanding these links is key to developing new cancer therapies targeting apoptosis.
Area of Science:
- Oncology
- Molecular Biology
- Cell Death Research
Background:
- Programmed cell death (apoptosis) is crucial in limiting cancer development and is a target for chemotherapy.
- Oncogenes that disrupt cell cycle control often induce apoptosis, eliminating abnormal cells.
- Cancer cells acquire mutations to evade apoptosis, promoting uncontrolled growth and drug resistance.
Purpose of the Study:
- To review how oncogenes activate apoptosis.
- To examine the mechanisms by which cancer cells subvert apoptotic pathways.
- To discuss therapeutic strategies targeting these apoptosis-related changes in cancer.
Main Methods:
- Literature review of oncogene function in apoptosis.
- Analysis of genetic mutations compromising apoptotic pathways in cancer.
- Synthesis of current and proposed therapeutic approaches.
Main Results:
- Oncogenes are intrinsically linked to apoptosis activation.
- Cancer cells develop resistance by disabling apoptotic signaling.
- Therapeutic strategies aim to restore or exploit apoptotic pathways.
Conclusions:
- Understanding the oncogene-apoptosis axis is vital for cancer progression insights.
- Targeting apoptosis offers a promising avenue for overcoming chemo-resistance in malignancies.
- Developing novel therapies that re-engage apoptosis is central to effective cancer treatment.
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