Sunday December 8, 2019

Combination of Drugs for Diabetes and Hypertension may offer an effective new way to combat Cancer

the researchers found that the combination of the diabetes drug metformin and the antihypertensive drug syrosingopine drives cancer cells to programmed "suicide".

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Suicide for cancer cells via a combination drug
A combination drug of diabeties and hypertension to cure cancer,pixabay

London, December 28, 2016: A combination of drugs for diabetes and hypertension may offer an effective new way to combat cancer, suggests a new research.

In their experiments, the researchers found that the combination of the diabetes drug metformin and the antihypertensive drug syrosingopine drives cancer cells to programmed “suicide”.

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 “We have been able to show that the two known drugs lead to more profound effects on cancer cell proliferation than each drug alone,” said study first author Don Benjamin from the University of Basel in Switzerland.

“The data from this study support the development of combination approaches for the treatment of cancer patients,” Benjamin noted.

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Metformin is a widely prescribed drug for the treatment of Type-2 diabetes.

Besides its blood sugar lowering effect, it also displays anti-cancer properties. The usual therapeutic dose, however, is too low to effectively fight cancer.

At higher doses, the antidiabetic drug inhibits the growth of cancer cells but could also induce unwanted side effects.

The new research published in the journal Science Advances showed that the antihypertensive drug syrosingopine enhances the anti-cancer efficacy of metformin.

The study showed the cocktail of these two drugs is effective in a wide range of cancers.

“For example, in samples from leukemia patients, we demonstrated that almost all tumour cells were killed by this cocktail and at doses that are actually not toxic to normal cells”, Benjamin said.

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“And the effect was exclusively confined to cancer cells, as the blood cells from healthy donors were insensitive to the treatment,” Benjamin noted.

In mice with malignant liver cancer, enlargement of the liver was reduced after the therapy. Also the number of tumor nodules was less — in some animals the tumours disappeared completely.

The researchers found that the drugs interrupt the vital processes which provide energy for the cancer cell. (IANS)

  • Ruth

    I don’t like drink cocktail.

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Genetic Variations Influence Risk of Developing Cancer: Study

Study found that variations in the regions that regulate the expression of oncogenes and tumour suppressor genes affect cancer risk

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Cancer
While minor genetic changes only have a small impact on Cancer risk, the variations analysed in this study are numerous and common in the population. Pixabay

Shedding new light on why some people develop cancer while others do not, a new study has found that a person’s risk of developing cancer is affected by Genetic variations in regions of DNA that do not code for proteins, previously dismissed as “junk DNA”.

This study, published in the British Journal of Cancer, shows that inherited cancer risk is not only affected by mutations in key cancer genes, but that variations in the DNA that controls the expression of these genes can also drive the disease.

The researchers believe that understanding how non-coding DNA affects the development of this disease could one day improve genetic screening for cancer risk.

And in the future, this could lead to new prevention strategies, or help doctors diagnose the disease earlier, when it is more likely to be treated successfully.

“What we found surprised us as it had never been reported before — our results show that small genetic variations work collectively to subtly shift the activity of genes that drive cancer,” said lead researcher of the study John Quackenbush, Professor at Harvard T.H. Chan School of Public Health in the US.

Genetic
Shedding new light on why some people develop Cancer while others do not, a new study has found that a person’s risk of developing cancer is affected by genetic variations in regions of DNA that do not code for proteins, previously dismissed as “junk DNA”. Pixabay

“We hope that this approach could one day save lives by helping to identify people at risk of cancer, as well as other complex diseases,” Quackenbush said.

The researchers investigated 846 genetic changes within non-coding stretches of DNA, identified by previous studies as affecting cancer risk.

These Single Nucleotide Polymorphisms (SNPs) are particular positions in the human genome where a single letter of the genetic code varies between people.

Unlike mutations in coding DNA, such as BRCA, that are rare but significantly raise a person’s risk of developing cancer, non-coding SNPs are relatively common in the population but only slightly increase cancer risk.

The team analysed whether there was a correlation between the presence of a particular SNP and the expression of particular genes.

In total, they looked at over six million genetic variants across 13 different body tissues.

Genetic
The researchers believe that understanding how non-coding DNA affects the development of this disease could one day improve genetic screening for cancer risk. Pixabay

They found that variations in the regions that regulate the expression of oncogenes and tumour suppressor genes affect cancer risk.

The study also revealed that these cancer-risk SNPs tend to be specifically located in regions that regulate the immune system and tissue-specific processes — highlighting the importance of these cellular processes to the development of cancer.

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“While minor genetic changes only have a small impact on cancer risk, the variations analysed in this study are numerous and common in the population,” said Emily Farthing, senior research information manager at British charity Cancer Research UK. (IANS)