Is genetic instability the key to beating cancer?

April 24, 2014

Cancerous tumors may be poised at the edge of their own destruction, an insight that could help researchers find new, more effective treatments, suggest SFI External Professor Ricard Solé and colleagues in an April 9 paper in the journal Bioessays.

Despite decades of work, cancer researchers still aren't sure what makes the disease tick, but Solé says a key observation is that cancer thrives on . Mistakes are common when cells replicate, and they're usually corrected. But if errors arise in genes responsible for correcting those mistakes, the genome can become unstable. Then, increasing instability can drive the growth of a mass of , each with its own, slightly different DNA.

Still, there's a point where cancer starts choking on its largesse. "In a normal cell, instability is not good news, but in a cancer cell it's kind of the driving engine, except that you have a limit," says Solé. "You cannot be infinitely unstable."

That suggests a threshold beyond which start dying, having lost their most basic functions to rapid mutations. If so, researchers might be able to identify those functions and target them, or simply dial up the mutation rate – a strategy experiments show prevents RNA viruses from infecting people.

The time is right for a new approach, Solé says. Recent studies suggest that the usual treatments – surgery followed by chemotherapy – leave behind the strongest cells, which can grow into new, deadlier tumors.

"The strategy should probably shift in some direction, and that's why I think it's very important to figure out what the architecture is for these unstable cells, because we really don't understand that yet," Solé says.

Explore further: Double dose of genes can trigger poor cancer survival

More information: Solé, R. V., Valverde, S., Rodriguez-Caso, C. and Sardanyés, J. (2014), "Can a minimal replicating construct be identified as the embodiment of cancer?" Bioessays, 36: 503–512. doi: 10.1002/bies.201300098

Read a commentary about the paper by Bioessays Editor-In-Chief Andrew Moore (April 9, 2014): onlinelibrary.wiley.com/doi/10 … /bies.201400051/full

Related Stories

Double dose of genes can trigger poor cancer survival

January 23, 2014
(Medical Xpress)—Cancer Research UK scientists have shown that accidental DNA doubling in bowel cancer cells could predict which patients have potentially poor survival and help doctors plan their treatment, according to ...

New view of tumors' evolution

March 13, 2014
Cancer cells undergo extensive genetic alterations as they grow and spread through the body. Some of these mutations, known as "drivers," help spur cells to grow out of control, while others ("passengers") are merely along ...

Researchers develop new dichloroacetate formulation for cancer treatment

April 16, 2014
Health forums were abuzz in 2007 with news that a simple, inexpensive chemical may serve as a viable treatment to many forms of cancer. The drug dichloroacetate, or DCA, was touted as a cure-all, but after years of work, ...

Bowel cancers reshuffle their genetic pack to cheat treatment

February 27, 2013
Bowel cancer cells missing one of three genes can rapidly reshuffle their genetic 'pack of cards' – the chromosomes that hold the cell's genetic information. This reshuffling has been previously shown to render tumours ...

Recurrent but rare mutations might underlie cancer growth

February 26, 2014
A potential new gene mutation that might drive lung cancer development and growth has been identified by researchers at The Ohio State University Comprehensive Cancer Center – Arthur G. James Cancer Hospital and Richard ...

Recommended for you

Cancer-death button gets jammed by gut bacterium

July 27, 2017
Researchers at Michigan Medicine and in China showed that a type of bacterium is associated with the recurrence of colorectal cancer and poor outcomes. They found that Fusobacterium nucleatum in the gut can stop chemotherapy ...

Researchers release first draft of a genome-wide cancer 'dependency map'

July 27, 2017
In one of the largest efforts to build a comprehensive catalog of genetic vulnerabilities in cancer, researchers from the Broad Institute of MIT and Harvard and Dana-Farber Cancer Institute have identified more than 760 genes ...

Long-sought mechanism of metastasis is discovered in pancreatic cancer

July 27, 2017
Cells, just like people, have memories. They retain molecular markers that at the beginning of their existence helped guide their development. Cells that become cancerous may be making use of these early memories to power ...

Blocking the back-door that cancer cells use to escape death by radiotherapy

July 27, 2017
A natural healing mechanism of the body may be reducing the efficiency of radiotherapy in breast cancer patients, according to a new study.

Manmade peptides reduce breast cancer's spread

July 27, 2017
Manmade peptides that directly disrupt the inner workings of a gene known to support cancer's spread significantly reduce metastasis in a mouse model of breast cancer, scientists say.

Glowing tumor technology helps surgeons remove hidden cancer cells

July 27, 2017
Surgeons were able to identify and remove a greater number of cancerous nodules from lung cancer patients when combining intraoperative molecular imaging (IMI) - through the use of a contrast agent that makes tumor cells ...

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.