Overcoming resistance to anti-cancer drugs by targeting cell 'powerhouses'

Public release date: 22-May-2013
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Contact: Michael Bernstein
m_bernstein@acs.org
202-872-6042
American Chemical Society

Re-routing anti-cancer drugs to the "power plants" that make energy to keep cells alive is a promising but long-neglected approach to preventing emergence of the drug-resistant forms of cancer source of a serious medical problem, scientists are reporting. That's the conclusion of a new study published in the journal ACS Chemical Biology.

Shana Kelley and colleagues explain that doxorubicin and other common forms of chemotherapy work by damaging the genes inside the nucleus of cancer cells. Cancer cells divide and multiply faster than surrounding normal cells, making copies of their genes. The drugs disrupt that process. But cancer cells eventually adapt, developing structures that pump out nucleus-attacking drugs before they can work. Kelley's team explored the effects of targeting doxorubicin to the mitochondria, the energy-producing structures in cells that also contain genes.

They describe a re-targeting approach that involved mating doxorubicin with a small piece of protein that made the drug travel to mitochondria instead of the nucleus. The combo killed cancer cells, even those that had developed pumps. Such an approach could work with a whole family of anti-cancer drugs that target the nucleus, the scientists indicate.

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The authors acknowledge funding from the Canadian Institutes of Health Research.

The American Chemical Society is a nonprofit organization chartered by the U.S. Congress. With more than 163,000 members, ACS is the world's largest scientific society and a global leader in providing access to chemistry-related research through its multiple databases, peer-reviewed journals and scientific conferences. Its main offices are in Washington, D.C., and Columbus, Ohio.

To automatically receive news releases from the American Chemical Society, contact newsroom@acs.org.

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Public release date: 22-May-2013
[ | E-mail | Share ]

Contact: Michael Bernstein
m_bernstein@acs.org
202-872-6042
American Chemical Society

Re-routing anti-cancer drugs to the "power plants" that make energy to keep cells alive is a promising but long-neglected approach to preventing emergence of the drug-resistant forms of cancer source of a serious medical problem, scientists are reporting. That's the conclusion of a new study published in the journal ACS Chemical Biology.

Shana Kelley and colleagues explain that doxorubicin and other common forms of chemotherapy work by damaging the genes inside the nucleus of cancer cells. Cancer cells divide and multiply faster than surrounding normal cells, making copies of their genes. The drugs disrupt that process. But cancer cells eventually adapt, developing structures that pump out nucleus-attacking drugs before they can work. Kelley's team explored the effects of targeting doxorubicin to the mitochondria, the energy-producing structures in cells that also contain genes.

They describe a re-targeting approach that involved mating doxorubicin with a small piece of protein that made the drug travel to mitochondria instead of the nucleus. The combo killed cancer cells, even those that had developed pumps. Such an approach could work with a whole family of anti-cancer drugs that target the nucleus, the scientists indicate.

###

The authors acknowledge funding from the Canadian Institutes of Health Research.

The American Chemical Society is a nonprofit organization chartered by the U.S. Congress. With more than 163,000 members, ACS is the world's largest scientific society and a global leader in providing access to chemistry-related research through its multiple databases, peer-reviewed journals and scientific conferences. Its main offices are in Washington, D.C., and Columbus, Ohio.

To automatically receive news releases from the American Chemical Society, contact newsroom@acs.org.

Follow us: Twitter Facebook

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AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.

Source: http://www.eurekalert.org/pub_releases/2013-05/acs-ort052213.php

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