New evidence in support of Warburg theory of cancer
A new study provides a novel theory for how delusions arise and why they persist. NYU Langone Medical Center researcher Orrin Devinsky, MD, performed an in-depth analysis of patients with certain delusions and brain disorders revealing a consistent pattern of injury to the frontal lobe and right hemisphere of the human brain. The cognitive deficits
Full Post: Delusions associated with consistent pattern of brain injury
German scientist Otto H. Warburg’s theory on the origin of cancer earned him the Nobel Prize in 1931, but the biochemical basis for his theory remained elusive.
His theory that cancer starts from irreversible injury to cellular respiration eventually fell out of favor amid research pointing to genomic mutations as the cause of uncontrolled cell growth.
Seventy-eight years after Warburg received science’s highest honor, researchers from Boston College and Washington University School of Medicine report new evidence in support of the original Warburg Theory of Cancer.
A descendant of German aristocrats, World War I cavalry officer and pioneering biochemist, Warburg first proposed in 1924 that the prime cause of cancer was injury to a cell caused by impairment to a cell’s power plant - or energy metabolism - found in its mitochondria.
In contrast to healthy cells, which generate energy by the oxidative breakdown of a simple acid within the mitochondria, tumors and cancer cells generate energy through the non-oxidative breakdown of glucose, a process called glycolysis. Indeed, glycolysis is the biochemical hallmark of most, if not all, types of cancers. Because of this difference between healthy cells and cancer cells, Warburg argued, cancer should be interpreted as a type of mitochondrial disease.
In the years that followed, Warburg’s theory inspired controversy and debate as researchers instead found that genetic mutations within cells caused malignant transformation and uncontrolled cell growth. Many researchers argued Warburg’s findings really identified the effects, and not the causes, of cancer since no mitochondrial defects could be found that were consistently associated with malignant transformation in cancers.
Boston College biologists and colleagues at Washington University School of Medicine found new evidence to support Warburg’s theory by examining mitochondrial lipids in a diverse group of mouse brain tumors, specifically a complex lipid known as cardiolipin (CL). They reported their findings in the December edition of the Journal of Lipid Research .
Abnormalities in cardiolipin can impair mitochondrial function and energy production. Boston College doctoral student Michael Kiebish and Professors Thomas N. Seyfried and Jeffrey Chuang compared the cardiolipin content in normal mouse brain mitochondria with CL content in several types of brain tumors taken from mice. Bioinformatic models were used to compare the lipid characteristics of the normal and the tumor mitochondria samples. Major abnormalities in cardiolipin content or composition were present in all types of tumors and closely associated with significant reductions in energy-generating activities.
The findings were consistent with the pivotal role of cardiolipin in maintaining the structural integrity of a cell’s inner mitochondrial membrane, responsible for energy production. The results suggest that cardiolipin abnormalities “can underlie the irreversible respiratory injury in tumors and link mitochondrial lipid defects to the Warburg theory of cancer,” according to the co-authors.
These findings can provide insight into new cancer therapies that could exploit the bioenergetic defects of tumor cells without harming normal body cells.
A new study by Narendra et al. suggests that Parkin, the product of the Parkinson’s disease-related gene Park2, prompts neuronal survival by clearing the cell of its damaged mitochondria. “[This is] an exciting new discovery that links the fields of mitochondrial quality control and the genetics of Parkinson’s disease (PD),” writes Heidi McBride of the
Full Post: Researchers shed new light on genetics of Parkinson’s
One of the most reliable indicators to predict that a person will develop type 2 diabetes is the presence of insulin resistance. Insulin is produced in the pancreas and is the hormone responsible for ensuring that glucose reaches several tissues and organs in the body, such as muscles. Insulin resistance is characterized by the lack
Full Post: More data released on key diabetes genes
Maas Biolab researchers CSO Eskil Elmer, M.D., Ph.D. and neuroscientist Magnus Hansson, M.D., Ph.D., and colleagues have for the first time ever demonstrated the mitochondrial permeability transition (mPT) or “megapore” occurs in viable adult human neuron mitochondria and the ability of cyclosporin-A to block its formation. These effects had previously been well characterized in animal
Full Post: Maas Biolab scientists validate cyclosporin human neuroprotection
If you’re a cancer cell, you want a protein called Bcl-2 on your side because it decides if you live or die. It’s usually a trusted bodyguard, protecting cancer cells from programmed death and allowing them to grow and form tumors. But sometimes it turns into their assassin. Scientists knew it happened, but they didn’t
Full Post: Scientists develop peptide that converts Bcl-2 protein from a cancer cell’s friend to a foe
Aging yeast cells accumulate damage over time, but they do so by following a pattern laid down earlier in their life by diet as well as the genes that control metabolism and the dynamics of cell structures such as mitochondria, the power plants of cells. These research findings, presented at the American Society for Cell
Full Post: Both theories about human cellular aging supported by new research