Evidence in mice that bacteria in tumors help cancer cells metastasize

Bacteria promote cancer metastasis by bolstering the strength of host cells against mechanical stress in the bloodstream, promoting cell survival during tumor progression, researchers report.

Quelle: Sciencedaily

Cause of metastasis in prostate cancer discovered

Prostate cancers remain localized in the majority of cases, giving affected individuals a good chance of survival. However, about 20% of patients develop incurable metastatic prostate cancer, resulting in approximately 5,000 deaths each year in Austria alone. Medical research has not yet adequately explained why metastases occur in some people and not in others. A research team has now discovered specific changes in a protein that drive the growth and spread of prostate cancer.

Quelle: Sciencedaily

Cause of metastasis in prostate cancer discovered

Prostate cancers remain localized in the majority of cases, giving affected individuals a good chance of survival. However, about 20% of patients develop incurable metastatic prostate cancer, resulting in approximately 5,000 deaths each year in Austria alone. Medical research has not yet adequately explained why metastases occur in some people and not in others. A research team has now discovered specific changes in a protein that drive the growth and spread of prostate cancer.

Quelle: Sciencedaily

Getting fuel to an invading cell’s front line

Invading armies need a steady supply of fuel and armaments. That’s just as true when the invaders are cells, such as when tumor cells break away and spread to other parts of the body in a process called metastasis — the most deadly part of cancer. Now, a study in C. elegans worms provides new insight into how invading cells deploy fuel to the front lines of invasion to power their break-through machinery.

Quelle: Sciencedaily

Researchers reduce breast cancer metastasis in animal models by modifying tumor electrical properties

Researchers have found that manipulating voltage patterns of tumor cells — using ion channel blockers already FDA-approved as treatments for other diseases — can in fact significantly reduce metastasis in animal models of breast cancer.

Quelle: Sciencedaily

Reducing copper in the body alters cancer metabolism to reduce risk of aggressive breast cancer

Depleting copper levels may reduce the production of energy that cancer cells need to travel and establish themselves in other parts of the body by a process referred to as metastasis, according to a new study. The discovery of the underlying mechanisms of how copper depletion may help reduce metastasis in breast cancer will help inform the design of future clinical trials.

Quelle: Sciencedaily

Small molecule may prevent metastasis in colorectal cancer

The compound works by hindering a key pathway that cancer cells rely upon to hoard energy, and is already undergoing clinical trials.

Quelle: Sciencedaily

Mitochondria and the evolutionary roots of cancer

Cancer is a group of almost 200 diseases that involve variety of changes in cell structure, morphology, and physiology. Cancer phenotype is underlying several alterations in cellular dynamics with three most critical features, which includes self-sufficiency in growth signals and insensitivity to inhibitory signals, evasion of programmed cell death and limitless replicative potential with a potential for the invasion of other organs. Cancer disease is widespread among metazoans. Some properties of cancer cells such as uncontrolled cell proliferation, lack of apoptosis, hypoxia, fermentative metabolism and free cell motility, i.e. metastasis, resemble a prokaryotic lifestyle, which leads to the assumption of a reversal like evolution from eucariotic back to proteobacterial state. This phenotype matches the phenotype of the last universal common ancestor (LUCA) that resulted from the endosymbiosis between archaebacteria and α-proteobacteria, which later became the mitochondria.

 Davila AF and Zamorano P (2013) Mitochondria and the evolutionary roots of cancer. Phys. Biol. 10 (2013) 026008, doi:10.1088/1478-3975/10/2/026008