The researchers suspected that some of the cancer cells may secrete a drug-busting molecule. So they tried filtering the cell cultures to see if they could catch it. Instead, they found that the cell cultures lost their resistance after their liquid broth passed through a pretty large filter—0.45 micrometers. This would catch large particles—like bacteria—but not small molecules, as the researchers were expecting. Looking closer, the researchers noticed that some of their cancer cells were contaminated with Mycoplasma hyorhinis. And these bacteria could metabolize gemcitabine, rendering the drug useless. When the researchers transplanted treatable cancer cells into the flanks of mice—some with and some without M. hyorhinis—the bacteria-toting tumors were resistant to gemcitabine treatment.
And it’s not just M. hyorhinis that can turn tumors resistant. When the researchers pinpointed the gene that encodes the molecular machinery for disarming gemcitabine in M. hyorhinis—a gene called CDDL—they found that it’s quite common in other bacteria. In initial testing of 27 bacterial species, 13 could knock out gemcitabine. When the researchers searched through the genetics of nearly 2,700 bacteria, they found that hundreds also had the gene for defeating gemcitabine. Most of those bacteria were in the Gammaproteobacteria class, a giant group of bacteria that includes E. coli and Salmonella.
An exhaustive 2016 study from the National Toxicology Program found increased incidence of cancer (over a control population) in rats exposed to nonionizing, radio-frequency radiation (RFR)—like the kind constantly bouncing from your phone to the closest cell tower. We’re well aware of the dangers presented by high-energy radiation, such as X-rays, which rip apart bonds at a molecular level. RFR might not be as destructive, but it emits enough energy to disrupt DNA—and that might lead to cancer. “We may not yet understand why these things are happening at the molecular level,” says Jerry Phillips, a biochemist at the University of Colorado Colorado Springs, who has studied this issue for years, “but there’s sufficient evidence to indicate there are numerous biological changes caused by exposure to cell phones.”
Dr Lea Weber, writing in the journal Breast Cancer - Targets and Therapy, said: "Capsaicin is capable of inducing apoptosis (cell death) and inhibiting cancer cell growth in many different types of cancer, for example, osteosarcoma, colon, and pancreatic cancer cells, while normal cells remained unharmed."
Other cancers including colon, bone and pancreatic could also be killed off by the compound. However, capsaicin isn't effective if it's eaten, inhaled or injected, and researchers think it will only be effective as a pill attached to another drug that targets cancer cells. When capsaicin reaches a cancer cell, the spicy ingredient attaches itself to the edge of the cell known as the cell membrane and switches on a cell receptor called TRPV1. The receptor TRPV1 is a channel that controls what substances such as calcium and sodium go in and out of the cancer cell. When TRPV1 is switched on by capsaicin, the cancer cell is sent into overdrive and starts to self-destruct.
"A research team led by scientists from Los Alamos National Laboratory compared tissue samples from 1,063 non-smokers and 2,490 smokers, examining each individual's DNA to look for mutations. They found that for every 50 cigarettes smoked, there is one extra DNA mutation for each cell in the lungs. Over the course of a year, this means that someone who smokes a pack a day (20 cigarettes) has 150 extra mutations per cell in the lung, 97 per larynx cell, 23 per mouth cell, 18 per bladder cell, and six per liver cell."
The scientists, who unveiled the test at the British Science Festival in Swansea, compared the new test to a smoke detector, because it does not actually find cancer but changes to red blood cells that occur when cancer is present.
The test detects mutations in proteins on the surface of red blood cells. In healthy people, the number of mutations of this type averages about five per million, but in cancer patients there can be 50 to 100 mutants per million. These mutations do not have a role in the development of cancer, with the researchers describing the effect as “collateral damage” caused by the disease. The test takes a few hours with standard laboratory equipment.
“The benefit of the blood cell mutation is that it can be monitored in a simple, efficient, and non-invasive way,” the statement said. Professor Jenkins said one of the reasons why oesophageal cancer was so deadly was that it was often diagnosed late. The average patient lives for about a year after diagnosis and just 15 per cent live for five years.
Melanoma is generally caused when ultraviolet rays -- from the sun, or from artificial sources, such as tanning beds -- damage the DNA of melanocytes, according to the cancer society. But a review of medical data between January 1990 and December 2014 revealed 123 patients at Shinshu University Hospital who had been diagnosed with melanoma on the soles of their feet. The average age of people diagnosed with melanoma on their feet was 73.5 years, the study reported.
"Chronic damage or pressure or chronic inflammation has not been linked to other areas of the body and melanoma, but it is linked to squamous cell skin cancer," said Schuchter, who also serves as an expert for the American Society of Clinical Oncology.
Lichtenfeld concurred. "The authors have provided us with useful and thought-provoking information, but whether stress is the cause of melanoma in these locations is unknown," he said. "It's unlikely this is the complete story about why these melanomas happened in the first place. There may well be other factors involved."
"An eight-year study led by Dr. Glen Boyle, from the QIMR Berghofer medical research institute in Brisbane, found a compound in a berry could kill head and neck tumours as well as melanomas. An experimental drug derived from the berry, EBC-46, has so far been used on 300 animals, including cats, dogs and horses. Dr. Boyle said in 75 per cent of cases, the tumour disappeared and had not come back.
The berry grows on the blushwood tree, which only grows in pockets of Far North Queensland. 'The tree is very, very picky on where it will grow,' Dr. Boyle said. 'It's only on the Atherton Tablelands at the moment and they're trying to expand that to different places of course because it'd be nice to be able to grow it on a farm somewhere.'"
“Is everything we eat associated with cancer?” asked a much noted 2012 paper in the American Journal of Clinical Nutrition. That paper reviewed the academic studies conducted on common cookbook ingredients. Of the 50 ingredients considered, 40 had been studied for their relation to cancer. Individually, most of those studies found that consumption of the food was correlated with cancer. But when the research on any given ingredient was considered collectively, those effects typically shrank or disappeared.
“Many single studies highlight implausibly large effects, even though evidence is weak,” the authors concluded.
"The researchers found when they restored normal miRNA signals in cancer cells, they could reverse the process so growth did not get out of control. The team became interested in the problem when they tried to reconcile conflicting results that were coming to light about two adhesion proteins: E-cadherin and p120 catenin. The researchers say that when PLEKHA7 is lost, the E-cadherin/p120 adhesion complex is disrupted, the miRNAs become misregulated, and E-cadherin/p120 become tumor-promoting.
Meanwhile, Medical News Today recently learned how researchers at the University of Freiburg in Germany discovered that migrating cancer cells alter bone tissue to form tumors. The researchers found that migrating cancer cells produce a protein called cathepsin K that appears to help them survive, and possibly even thrive, in bone tissue. The second protein is called matrixmetalloprotease-9 (MMP-9) - a key regulator of tumor development. This protein digests the bone matrix and allows the arriving cancer cells to establish themselves in their new environment. MMP-9 also helps form new blood vessels to feed the growing tumor."
The researchers found that the more servings of oranges, grapefruits or juices from these fruits that the participants consumed overall, the higher their risk of melanoma. Subjects who consumed a serving of these fruits or their juices at least 1.6 times a day, for example, were found to be at 36% higher melanoma risk.
"These substances are potential carcinogens, as found in both mice and humans. Psoralens and furocoumarins interact with UV light to stimulate melanoma cells to proliferate," explains Dr. Marianne Berwick, of the University of New Mexico in Albuquerque, in an editorial linked to the study.
However, the team notes no association was found between consumption of other foods rich in furocoumarins - such as celery and carrots - and increased risk of melanoma. But Dr. Wu says this is likely because people often cook these vegetables, and the heat reduces furocoumarin levels.
"This device could help us identify the best chemotherapy agents and combinations for every tumor prior to starting systemic administration of chemotherapy, as opposed to making choices based on population-based statistics. This has been a longstanding pursuit of the oncology community and an important step toward our goal of developing precision-based cancer therapy," says Jose Baselga, chief medical officer at Memorial Sloan Kettering Cancer Center and an author of the paper."
"Research published in the British Journal of Nutrition discovered that the risk of breast cancer decreases with increased consumption of specific dietary carotenoids, the pigments in some vegetables and fruits. The women that consumed more beta-carotene in their diet showed a 46 percent lower risk of breast cancer, while those that consumed more alpha-carotene had a 39 percent reduced incidence. The scientists found the protective element of increased carotenoid consumption more evident among pre-menopausal women and those exposed to second-hand smoke.
Dark green leafy vegetables such as kale, spinach and dandelion greens top the list of sources rich in luteins and zeaxanthins, which also includes watercress, basil, parsley, arugula and peas. The highest levels of beta-carotene are found in sweet potatoes, grape leaves, carrots, kale, spinach, collard and other leafy greens. Carrots, red peppers, pumpkin, winter squash, green beans and leafy greens contain alpha-carotene. Red peppers, butternut squash, pumpkin persimmons and tangerines are high in beta-cryptoxanthin."
"A diet rich in complex carbohydrates and lower in protein and fat is associated with a 60 percent to 70 percent reduced risk of prostate cancer, said Adriana Vidal, a co-author of two of the studies and an assistant professor at Duke University School of Medicine in Durham, N.C. In addition, a fiber-filled diet reduced the risk of aggressive prostate cancer by 70 percent to 80 percent, according to Vidal.
Researchers also found that men with multiple metabolic syndrome risk factors had a progressively increased risk of prostate cancer (increased blood pressure, a high blood sugar level, excess body fat around the waist and abnormal cholesterol levels)."
"So how can companies overcome these challenges? Developing a treatment that’s unequivocally transformational, in dramatically changing disease outcomes – a Gleevec, for instance – is one solution. But although most companies strive to create drugs whose value to patients and payers is unambiguous relative to competitors, the reality is that most won’t. The majority of advances are incremental.
In this world of grey, 'substantially more rigor around payer analytics would be helpful,' says Baynes. 'We need a very transparent, rules-based approach to how we look at evidence and value. It should be pegged in some way to the magnitude of the benefit.'"
"In the last fifty years many plant-derived agents (vinblastine, vincristine, vindesine, paclitaxel, docetaxel, topotecan, irinotecan, elliptinium) played a major role in cancer treatment. Other very promising plant-derived anticancer agents (combrestatins, betulinic acid, roscovitine, purvalanols, indirubins) are in clinical or preclinical trials."
"Recent evidence suggests as many as 60% of men who have initial treatment for low-risk prostate cancer might not have required any therapy in their lifetimes, the authors noted in their introduction. Most of these men will have at least one long-term adverse effect of treatment."
"A molecular signature predictive of indolent prostate cancer."
They then used a decision-tree learning model, a type of computer algorithm, to identify three genes — FGFR1, PMP22, and CDKN1A — that together can accurately predict the outcome of seemingly low-risk tumors. Tumors that test negative for the biomarker are deemed aggressive. Of the 43 patients, 14 ultimately developed advanced prostate cancer. All 14 were correctly identified by the test.