Sometimes stepping back and looking at the big picture can lend new clarity to an ongoing debate. In this case, it took the distant perspective of astrobiologists to reckon the origins of cancer.
The astrobiologists, working with oncologists in the US, have suggested that cancer resembles ancient forms of life that flourished between 600 million and 1 billion years ago.
The genes that controlled the behaviour of these early multicellular organisms still reside within our own cells, managed by more recent genes that keep them in check.
It’s when these newer controlling genes fail that the older mechanisms take over, and the cell reverts to its earlier behaviours and grows out of control.
Scientists from Maryland’s Johns Hopkins University, in conjunction with Danish researchers, have developed a drug using a Mediterranean weed that can target tumor cells and destroy them.
The extraordinary drug travels undetected through the bloodstream until it encounters a tumor cell, where it is activated by specific proteins. It destroys the tumor cells, neighboring cancer cells, and the blood vessels that act as their supply, but spares healthy cells and blood vessels.
The drug, called G202, was tested on mice and the study was led by Samuel Denmeade, MD, professor of oncology, urology, pharmacology and molecular sciences at Johns Hopkins University. Over the course of 30 days, the human prostate tumors grown in mice were reduced by an average of 50 percent. In comparison tests with the chemotherapy drug docetaxel, G202 reduced eight of nine tumors by more than 50 percent over the course of 21 days. Docetaxel reduced only one of the nine tumors in the same amount of time.
G202 also provided the same results for human models of bladder, kidney, and breast cancers.
An artificial “brain” built by a 17-year-old whiz kid from Florida is able to accurately assess tissue samples for signs of breast cancer, providing more confidence to a minimally invasive procedure.
The cloud-based neural network took top prize in this year’s Google Science Fair.
“I taught the computer how to diagnose breast cancer,” Brittany Wenger, the Lakewood Ranch resident, told me today.
“And this is really important because currently the least invasive form of biopsy is actually the least conclusive, so a lot of doctors can’t use them.”
Wenger wanted to create a way for more doctors to use the minimally invasive procedure, called Fine Needle Aspirate, in order to ease the process of having lumps examined.
Breast cancer affects one in eight women worldwide, she noted, including members of her family.
“Early detection is really important,” Wenger said. “And that is what I’m trying to do with my neural network.”
Researchers at Case Western Reserve University School of Medicine have discovered a mutant form of the gene, Chk1, that when expressed in cancer cells, permanently stopped their proliferation and caused cell death without the addition of any chemotherapeutic drugs. This study illustrates an unprecedented finding, that artificially activating Chk1 alone is sufficient to kill cancer cells.
Researchers have revealed how a molecule called telomerase contributes to the control of the integrity of our genetic code, and when it is involved in the deregulation of the code, its important role in the development of cancer. The University of Montreal scientists involved explain how they were able to achieve their discovery by using cutting edge microscopy techniques to visualize telomerase molecules in real time in living cells inMolecular Cell on December 9, 2011.
“Each time our cells divide, they need to completely copy the genomic DNA that encodes our genes, but the genome gets shorter each time until the cell stops dividing,” said Dr. Pascal Chartrand, a biochemistry professor at the University of Montreal and a senior author of the study. “However, the telomerase molecules can add bits of DNA called telomeres to the ends of our genome. Telomeres prevent the genome from deteriorating or joining up with other pieces of DNA, allowing cells to divide indefinitely and become cancerous. Normally, the telomerase gene is not active, but how it is controlled is poorly understood. One difficulty has been that we need to see exactly what individual telomerase molecules are doing on our genome and when.” Franck Gallardo, the study’s lead author, added that the team was able to apply techniques from other work that the team was doing in their lab. “We could in fact visualize what individual telomerases were doing in cells,” he said.