anti-cancer drug Archives - Amazing Health Advances

Chemotherapy May Fuel Cancer Regrowth: New Research Reveals Disturbing Findings

The AHA! Team — Fri, 18 Jul 2025 05:27:38 +0000

Lori Alton via NaturalHealth365 – According to current statistics, about one million people a year (in the U.S. alone) undergo chemotherapy in an attempt to beat cancer. Yet this toxic treatment has a poor success rate in treating most kinds of cancer, and its benefits can be short-lived. Making the picture even grimmer is the fact that cancer recurrence after chemotherapy is frequently deadly. Now, from the front lines of cancer research comes the disturbing news that one particular type of chemotherapy can actually lead to cancer regrowth and recurrence. One approach to treating cancer creates a breeding ground for cancer stem cells Chemotherapy-induced senescence, often touted as a new weapon in cancer therapy, involves “putting cancer cells to sleep.” The protocol is intended to place cancer cells in a state of arrested growth, where they are alive but not dividing. While senescence is supposed to prevent further cancerous growth, new research shows that it can serve as a sort of “nursery” and safe harbor for cancer stem cells – the most dangerous and treatment-resistant type of cancer cells. A pair of recent studies reveal the consequences of therapy-induced senescence. In an explosive article published in Frontiers in Oncology, Markus Schosserer, Ph.D., wrote that there is ample evidence that senescent cancer cells can produce inflammatory molecules that promote a rich environment for cancer regrowth. In a breakthrough German study published in Nature, the team presented startling conclusions: senescence not only helps cancer cells avoid death but actually transforms them into cancer stem cells. This is very bad news, as stem cells – which can break from a tumor and metastasize throughout the body – are also the most resistant to treatment. Cancer cells can “outmaneuver” induced senescence In the German study, researchers examined human lymphoma cells treated with drugs to induce senescence and discovered they were developing “stemness.” In other words, the lymphoma cells started to express genes vital for maintaining stem cell function. When the team “released” the cancer cells from senescence, they discovered an alarming outcome. The cells began to multiply again – and more rapidly than those that had not become senescent. Although senescence is supposed to be irreversible, the team found evidence that cancer cells can escape it on their own – without the help of the genetic manipulation they used. Testament to this unfortunate possibility is that the scientists found more previously senescent stem cells in tumor patients after lymphoma recurred than had existed in the same individuals when they received their initial treatment. This demonstrated to the scientists that at least some cells had “figured out” how to outwit senescence. Noted professor of experimental oncology Dr. Jan Paul Medema commented, ‘There is compelling evidence … that … when cancer cells escape from senescence, they have an enhanced ability to drive tumor growth.’ Study leader Dr. Clemens A. Schmitt reported that switching off a specific cell signaling pathway could work to neutralize stemness in the previously senescent cells. However, there is no doubt that the study findings pose a definite setback for a formerly promising protocol. In addition, other studies have emerged showing that chemotherapy can do more harm than good. Chemotherapy for breast cancer can spread cancer cells A common protocol for breast cancer patients is to surgically remove tumors after chemo has been administered. The theory is that the chemo will help shrink the tumor while preventing the spread of cancer throughout the body. However, the treatment may accomplish the opposite effect. The toxic chemo drugs may actually switch on a repair mechanism – creating more blood vessel pathways and permitting tumors to grow back even stronger. In a study at the Albert Einstein College of Medicine, researchers found that chemotherapy triggered the circulation of more cancer cells throughout the lungs and the body. Chemotherapy features toxic side effects The American Cancer Society acknowledges that chemotherapy damages healthy cells – and reports that chemotherapy side effects include vomiting, diarrhea, anemia, hair loss, fertility problems, chronic fatigue, and infections. Neutropenia, the most serious side effect, involves the depletion of white blood cells needed to fight diseases and infections. Weight changes and mood changes – with depression, memory loss, and inability to concentrate – may also occur. Normal cells damaged by chemotherapy Normal cells most likely to be damaged by chemotherapy are cells in hair follicles, blood-forming cells in the bone marrow, cells in the mouth and digestive tract, and cells in the reproductive system. Experts report that in some situations – for example, the early stages of colorectal cancer – chemotherapy has been shown to provide some benefit, granting extra years of life. But on the whole, chemotherapy yields disappointing results and may even exacerbate cancer cell growth – as shown in this pair of startling studies. Editor’s note: Discover the many natural ways to stop cancer cell growth, own the Stop Cancer Docu-Class created by NaturalHealth365 Programs. Sources for this article include: NIH.gov Medicalnewstoday.com Sciencedaily.com Cancer.org To read the original article click here.

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Dozens of Potential Anti-Cancer Drugs Netted in Massive Screening Study

AHA Publisher — Sun, 02 Feb 2020 08:00:16 +0000

Dana-Farber Cancer Institute via Newswise – A variety of existing drugs for treating conditions such as diabetes, inflammation, alcohol abuse, and arthritis in dogs can also kill cancer cells in the lab, according to a study by scientists at Dana-Farber Cancer Institute and the Broad Institute of MIT and Harvard. Newswise — BOSTON – Nearly 50 existing non-cancer drugs were found to kill some cancer cell lines in the lab and researchers were surprised at the high yield of compounds active against cancer cells. Some of the compounds might in due course be tested in clinical trials, while others could help jump-start new drug development. Scientists reported their findings in the new journal Nature Cancer, saying they found an “unexpectedly high rate of anti-cancer activity” among 4,518 drugs that were tested against 578 laboratory cancer cell lines spanning 24 tumor types. Most of the drugs tested were not originally developed or used in oncology (cancer treatment). Using a massive search strategy designed to identify drugs that could be repurposed as cancer treatments or as candidates for cancer drug development, the scientists identified 49 non-cancer drugs that selectively killed cancer cells and whose activity against cancer could be predicted using molecular biomarkers. They reported that another 103 compounds with less selectivity against the cancer cell lines were also identified. “It is conceivable that some non-oncology drugs could be brought directly to clinical trials for testing in cancer patients,” said the authors, led by Steven Corsello, MD, of Dana-Farber, the study’s first author and the founder of the Broad’s Drug Repurposing Hub. However, they said, it is likely that the potential drug candidates will require further study and modification before being introduced into clinical studies. “We thought we’d be lucky if we found even a single compound with anti-cancer properties, but we were surprised to find so many,” said Todd Golub, MD, chief scientific officer and director of the Cancer Program at the Broad, Charles A. Dana Investigator in Human Cancer Genetics at Dana-Farber, and professor of pediatrics at Harvard Medical School. The new work is the largest study yet to employ the Broad’s Drug Repurposing Hub, a collection that currently comprises more than 6,000 existing drugs and compounds that are either FDA-approved or have been proven safe in clinical trials (at the time of the study, the Hub contained 4,518 drugs). The study also marks the first-time researchers screened the entire collection of mostly non-cancer drugs for their anti-cancer capabilities. Some of the compounds killed cancer cells in unexpected ways. “Most existing cancer drugs work by blocking proteins, but we’re finding that compounds can act through other mechanisms,” said Corsello. Some of the four-dozen drugs he and his colleagues identified appear to act not by inhibiting a protein but by activating a protein or stabilizing a protein-protein interaction. For example, the team found that nearly a dozen non-oncology drugs killed cancer cells that express a protein called PDE3A by stabilizing the interaction between PDE3A and another protein called SLFN12 — a previously unknown mechanism for some of these drugs. Most of the non-oncology drugs that killed cancer cells in the study did so by interacting with a previously unrecognized molecular target. For example, the anti-inflammatory drug tepoxalin, originally developed for use in people but approved for treating osteoarthritis in dogs, killed cancer cells by hitting an unknown target in cells that overexpress the protein MDR1, which commonly drives resistance to chemotherapy drugs. The researchers were also able to predict whether certain drugs could kill each cell line by looking at the cell line’s genomic features, such as mutations and methylation levels, which were included in the CCLE database. This suggests that these features could one day be used as biomarkers to identify patients who will most likely benefit from certain drugs. For example, the alcohol dependence drug disulfiram (Antabuse) killed cell lines carrying mutations that cause depletion of metallothionein proteins. Compounds containing vanadium, originally developed to treat diabetes, killed cancer cells that expressed the sulfate transporter SLC26A2. The observations in the study may represent starting points for new drug development. “The genomic features gave us some initial hypotheses about how the drugs could be acting, which we can then take back to study in the lab,” said Corsello. “Our understanding of how these drugs kill cancer cells gives us a starting point for developing new therapies.” This collaboration involved the Broad’s Center for the Development of Therapeutics, the PRISM team, the Cancer Data Sciences team, and the labs of Todd Golub and Matthew Meyerson, MD, PhD, of Dana-Farber and the Broad. The work was funded in part by SIGMA (Carlos Slim Foundation, Slim Initiative in Genomic Medicine for the Americas), the National Institutes of Health, the Conquer Cancer Foundation (Conquer Cancer Foundation of the American Society of Clinical Oncology), and the Next Generation Fund at the Broad Institute of MIT and Harvard. To read the original article click here.

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