Marked for destruction: Newly developed compound triggers cancer cell death

May 24, 2012, Journal of Clinical Investigation

The BCL-2 protein family plays a large role in determining whether cancer cells survive in response to therapy or undergo a form of cell death known as apoptosis. Cells are pressured toward apoptosis by expression of pro-apoptotic BCL-2 proteins. However, cancer cells respond to therapy by increasing expression of anti-apoptotic proteins, which bind and neutralize pro-apoptotic family members and mediate therapeutic resistance. Therefore, development of therapeutic strategies to neutralize resistance to apoptosis will be critical to clinical improvements.

A research group from the Dana-Farber Cancer Institute, led by Dr. Loren Walensky, developed a compound modeled directly from the pro-apoptotic the death domain of BCL-2, the BIM BH3 domain. This compound, known as a stapled BIM BH3 peptide, was found to competitively bind with anti-apoptotic proteins and led to enhanced apoptosis in . They also showed that tumor growth in mice was suppressed by the stapled BIM BH3 compound and that the new compound worked synergistically with other with pharmaceutical agents that promote apoptosis. The potential therapeutic effects of stapled BIM BH3 were further shown by activation of cell death in an tumor model in mice with little side effects on surrounding tissue.

Their study presents a new formulation of a BH3 mimetic that has broad BCL-2 family targeting and may provide significant clinical benefit.

Explore further: Research predicts how cancers will respond to chemo, rewrites old theory of why chemo works

Related Stories

Research predicts how cancers will respond to chemo, rewrites old theory of why chemo works

October 27, 2011
Challenging a half-century-old theory about why chemotherapy agents target cancer, scientists at Dana-Farber Cancer Institute have devised a test that can predict how effective the drugs will be by determining whether a patient's ...

New strategy to attack tumor-feeding blood vessels

June 6, 2011
Scientists at the Walter and Eliza Hall Institute have discovered a key molecule needed to kill the blood vessels that supply tumours.

Recommended for you

'Hijacker' drives cancer in some patients with high-risk neuroblastoma

January 23, 2018
Researchers have identified mechanisms that drive about 10 percent of high-risk neuroblastoma cases and have used a new approach to show how the cancer genome "hijacks" DNA that regulates other genes. The resulting insights ...

Enzyme inhibitor combined with chemotherapy delays glioblastoma growth

January 23, 2018
In animal experiments, a human-derived glioblastoma significantly regressed when treated with the combination of an experimental enzyme inhibitor and the standard glioblastoma chemotherapy drug, temozolomide.

Scientists block the siren call of two aggressive cancers

January 23, 2018
Aggressive cancers like glioblastoma and metastatic breast cancer have in common a siren call that beckons the bone marrow to send along whatever the tumors need to survive and thrive.

Researchers identify a protein that keeps metastatic breast cancer cells dormant

January 23, 2018
A study headed by ICREA researcher Roger Gomis at the Institute for Research in Biomedicine (IRB Barcelona) has identified the genes involved in the latent asymptomatic state of breast cancer metastases. The work sheds light ...

Workouts may boost life span after breast cancer

January 22, 2018
(HealthDay)—Longer survival after breast cancer may be as simple as staying fit, new research shows.

Boosting cancer therapy with cross-dressed immune cells

January 22, 2018
Researchers at EPFL have created artificial molecules that can help the immune system to recognize and attack cancer tumors. The study is published in Nature Methods.

0 comments

Please sign in to add a comment. Registration is free, and takes less than a minute. Read more

Click here to reset your password.
Sign in to get notified via email when new comments are made.