shot-button
Subscribe Now Subscribe Now
Home > Lifestyle News > Health And Fitness News > Article > Study shows how cancer cells evade drug treatments

Study shows how cancer cells evade drug treatments

Updated on: 20 July,2024 09:09 PM IST  |  Mumbai
IANS |

Cancer cells exploit cell cycles to multiply rapidly, a process known as proliferation. Cancer drugs aim to halt this growth by initiating a complex sequence of genetic and cellular events. However, these treatments often yield mixed results

Study shows how cancer cells evade drug treatments

Image for representational purposes only. Photo Courtesy: iStock

US researchers have found during a study how cancer cells manage to evade despite treatment. Published in the Proceedings of the National Academy of Sciences, the study delves into the cellular processes that allow cancer cells to proliferate even when targeted by anticancer drugs. 


Cancer cells exploit cell cycles to multiply rapidly, a process known as proliferation. Cancer drugs aim to halt this growth by initiating a complex sequence of genetic and cellular events. However, these treatments often yield mixed results.


The team led by Jean Cook of the Department of Biochemistry and Biophysics at University of North Carolina, Chapel Hill, identified a crucial enzyme that plays a key role in stopping cancer cell proliferation, particularly during treatment with anti-cancer drugs.


This enzyme's function varies among individuals. The researchers also discovered mechanisms through which cancer cells evade therapies designed to inhibit them.

Cells regulate protein expression by turning genes "on" and "off".

Some proteins ensure precise and effective cell division, akin to musicians in an orchestra guided by a conductor.

Cells can deactivate these regulatory proteins, allowing uncontrolled division and DNA replication.

To explore protein degradation's role in halting cell growth, Cook and graduate student Brandon Mouery treated cultured human cells with palbociclib, a metastatic breast cancer drug.

Using microscopy, flow cytometry, and proteomics, they found that the enzyme APC/C, which targets proteins for degradation to regulate the cell cycle, enhances the effectiveness of palbociclib.

This finding suggests that APC/C levels in tumours could help predict patient responses to palbociclib and similar drugs.

Reduced APC/C activity might indicate poor treatment response or a higher relapse risk.

The researchers also observed that both cancerous and non-cancerous cells can bypass drug-induced proliferation arrest.

These escapee cells struggle to replicate DNA independently, likely delegating DNA replication to proteins that initiate cell division later in the cell cycle.

This indicates that cells can use alternate pathways for uncontrolled growth.

"Cell proliferation has been intensively studied for decades, yet we can still be surprised," Cook noted. "Sometimes our textbook understanding is still quite incomplete, so we need to keep an open mind and continually challenge paradigms."

These findings could lead to new interventions that induce long-lasting proliferation arrest by exploiting this escape mechanism and cancer-associated DNA replication errors, potentially forcing cancer cells into a "self-destructive" growth mode.

This story has been sourced from a third party syndicated feed, agencies. Mid-day accepts no responsibility or liability for its dependability, trustworthiness, reliability and data of the text. Mid-day management/mid-day.com reserves the sole right to alter, delete or remove (without notice) the content in its absolute discretion for any reason whatsoever

"Exciting news! Mid-day is now on WhatsApp Channels Subscribe today by clicking the link and stay updated with the latest news!" Click here!

Register for FREE
to continue reading !

This is not a paywall.
However, your registration helps us understand your preferences better and enables us to provide insightful and credible journalism for all our readers.

Mid-Day Web Stories

Mid-Day Web Stories

This website uses cookie or similar technologies, to enhance your browsing experience and provide personalised recommendations. By continuing to use our website, you agree to our Privacy Policy and Cookie Policy. OK