Scientists find new way to fight treatment-resistant cancers

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Cancer, in its many forms, is a formidable enemy to medical scientists worldwide.

However, recent findings from the Van Andel Institute have shed light on a critical gene mutation that could pave the way for more effective treatments for certain treatment-resistant cancers.

The culprit: STK11 gene mutation

In a study published in Molecular Cell, the scientists detailed how the mutation in the STK11 gene triggers an uncontrollable inflammatory response.

This inflammation is like a chemical firestorm that damages healthy cells and fuels cancer growth.

Tumors that lose the STK11 gene are particularly difficult to treat, as they are resistant to conventional chemotherapy and many of the latest immunotherapies.

The domino effect: loss of the LKB1 protein

The mutation in the STK11 gene disrupts the gene’s encoded instructions, resulting in lower levels of the LKB1 protein. LKB1 is a tumor suppressor protein that helps regulate cell growth.

Without enough LKB1, cells can get out of control and lead to the development of cancerous cells.

This mutation is among the most common genetic changes in several types of treatment-resistant cancers, including lung, pancreatic and cervical cancer.

In addition, it plays an important role in the rare disease Peutz-Jehgers syndrome, which causes polyps in the digestive tract and an increased risk of cancer.

The inflammatory storm and epigenetic changes

The role of the LKB1 protein extends to managing inflammation, a crucial part of the body’s defense mechanism against injury and infection.

When there is not enough LKB1 due to the STK11 mutation, there is an epigenetic change in the cells that affects how the DNA instructions are interpreted.

This triggers excess inflammation that could push cells toward malignancy.

Outlook: Possible solutions and therapies

Shelby Compton, a Ph.D. Student at the Van Andel Institute Graduate School and first author of the study, describes the situation as a “perfect storm of problems”.

However, there are possible solutions to these problems. Compton hopes that this work will guide new therapeutic strategies not only for cancer but also for Peutz-Jehgers syndrome.

Russell Jones, Ph.D., the study’s corresponding author, highlights the next steps.

These include developing strategies to combat inflammation in LKB1-associated cancers and further investigating the role of LKB1 in Peutz-Jehgers syndrome.

The ultimate goal is to develop new, effective therapies for people suffering from these diseases.

Taken together, this research represents an important step towards understanding how specific gene mutations contribute to cancer development.

The findings could offer hope to those fighting treatment-resistant cancers and rare diseases

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The study was published in molecular cell.

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