Thursday March 21, 2019

Healthy lifestyle crucial for cancer prevention

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New York: Offering a new explanation for what drives cancer, recent research has shown that cells with cancerous mutations can suddenly find themselves most fit, allowing their population to expand when the tissue ecosystem changes due to ageing, smoking, or other stressors. mother-491952_640

Arguing against the commonly held “accumulation of mutations” model of cancer, the study favors a model that depends on evolutionary pressures acting on populations of cells. It, therefore, contends that the ecosystem of a healthy tissue landscape lets healthy cells out compete ones with cancerous mutations.

This new thinking about what drives cancer development may have profound implications for cancer therapy and drug design.

“We have been trying to make drugs that target mutations in cancer cells,” said study senior author James DeGregori, associate director for basic science at University of Colorado Cancer Center in the US.

“But if it is the ecosystem of the body, and not only cancer-causing mutations, that allows the growth of cancer, we should also be prioritizing interventions and lifestyle choices that promote the fitness of healthy cells in order to suppress the emergence of cancer,” said DeGregori.

The proposed model, presented in the journal PNAS, helps to answer a longstanding question in cancer science known as Peto’s Paradox — if cancer is due to random activating mutation, larger animals with more cells should be at greater risk of developing the disease earlier in their lives.

Well, then why do mammals of vastly different sizes and lifespans all seem to develop cancer mostly late in life? The answer to this proposed by researchers is that in addition to activating mutation, cancer may require age-associated changes to the tissue landscape in order for evolution to favor the survival and growth of cancer cells over the competition from healthy cells.

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Researchers Discover Balance of Two Enzymes That May Help Treat Pancreatic Cancer

While still in the earliest stages, Newton hoped this information might one day aid pancreatic diagnostics and treatment

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Cancer
Cancer Ribbon. Pixabay

A new research has set the stage for clinicians to potentially use levels of a pancreatic cancer patient’s PHLPP1 and PKC enzymes as a prognostic and for researchers to develop new therapeutic drugs that change the balance of the two enzymes as a means to treat the disease.

The study, published on Wednesday in Molecular Cell, was led by Alexandra Newton, professor in the Department of Pharmacology at the University of California, San Diego, School of Medicine, and Timothy Baffi, a graduate student in her lab, Xinhua news agency reported.

The new study built on the team’s work in 2015 that found the enzyme PKC, which was believed in previous studies to promote tumour growth, actually suppressed it.

The latest study took the investigation a step further by uncovering how cells regulate PKC activity and discovered that any time an over-active PKC is inadvertently produced, the PHLPP1 “proofreader” tags it for destruction.

Cancer patient
Cancer patient.

“That means the amount of PHLPP1 in your cells determines your amount of PKC,” Newton said. “And it turns out those enzyme levels are especially important in pancreatic cancer.”

The team observed 105 pancreatic cancer tumours to analyze the enzyme levels in each one. About 50 per cent of patients with low PHLPP1/high PKC lived longer than five-and-a-half years.

Also Read- A Brain Circuit Can Help Reverse Craving for Liquor, Says Study

While still in the earliest stages, Newton hoped this information might one day aid pancreatic diagnostics and treatment.

Pancreatic cancer is caused by the abnormal and uncontrolled growth of cells in the pancreas, a large gland in the digestive system. It typically doesn’t show symptoms in the early stages. Sufferers tend to develop signs, such as back pain and jaundice, when it has spread to other organs. (IANS)