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Evaluating the Angiogenetic Properties of Ovarian Cancer Stem-Like Cells using the Three-Dimensional Co-Culture System, NICO-1
Published on: December 5, 2020
Overview of BH3 mimetics in ovarian cancer
Donatella Del Bufalo1, Giovanna Damia2
1Preclinical Models and New Therapeutic Agents Unit, IRCCS Regina Elena National Cancer Institute, Via E. Chianesi 53, 00144 Rome, Italy.
Abstract:
Ovarian carcinoma is the leading cause of gynecological cancer-related death, still with a dismal five-year prognosis, mainly due to late diagnosis and the emergence of resistance to cytotoxic and targeted agents. Bcl-2 family proteins have a key role in apoptosis and are associated with tumor development/progression and response to therapy in different cancer types, including ovarian carcinoma. In tumors, evasion of apoptosis is a possible mechanism of resistance to therapy. BH3 mimetics are small molecules that occupy the hydrophobic pocket on pro-survival proteins, allowing the induction of apoptosis, and are currently under study as single agents and/or in combination with cytotoxic and targeted agents in solid tumors. Here, we discuss recent advances in targeting anti-apoptotic proteins of the Bcl-2 family for the treatment of ovarian cancer, focusing on BH3 mimetics, and how these approaches could potentially offer an alternative/complementary way to treat patients and overcome or delay resistance to current treatments.
Insights
Targeting Bcl-2 family proteins with BH3 mimetics offers a promising strategy to overcome treatment resistance in ovarian cancer. This approach aims to restore apoptosis, improving patient outcomes for this deadly gynecological cancer.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Ovarian carcinoma is a leading cause of gynecological cancer death with poor prognosis, often due to late diagnosis and treatment resistance.
- Bcl-2 family proteins regulate apoptosis and are implicated in ovarian cancer development, progression, and therapeutic response.
- Evasion of apoptosis is a key mechanism driving resistance to current ovarian cancer therapies.
Purpose of the Study:
- To review recent advancements in targeting anti-apoptotic Bcl-2 family proteins for ovarian cancer treatment.
- To focus on the role and potential of BH3 mimetics in overcoming therapeutic resistance.
- To explore BH3 mimetics as a complementary or alternative strategy for ovarian cancer patients.
Main Methods:
- Discussion of recent scientific literature and clinical studies.
- Focus on the mechanism of action of BH3 mimetics.
- Analysis of BH3 mimetics in preclinical and clinical settings for ovarian cancer.
Main Results:
- BH3 mimetics are small molecules designed to inhibit pro-survival Bcl-2 proteins.
- These agents induce apoptosis by disrupting the function of anti-apoptotic proteins.
- BH3 mimetics show potential as single agents or in combination therapies.
Conclusions:
- Targeting Bcl-2 family proteins with BH3 mimetics represents a novel therapeutic avenue for ovarian cancer.
- This approach may help overcome or delay resistance to existing cytotoxic and targeted treatments.
- BH3 mimetics could offer a new treatment option to improve survival rates for ovarian cancer patients.
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