The husband and wife team of Seluanov and Gorbunova at the University of Rochester may be one step closer to discovering a practical cancer treatment. They have isolated a specific chemical in the naked mole rat which seems to gird the rodent Lothario’s cells against tumors. And as it turns out, curing wrinkles may have been better for your health than previously thought:

Seluanov and Gorbunova then showed that when HMW-HA was removed, the cells became susceptible to tumors, confirming that the chemical did play a role in making naked mole rats cancer-proof. The Rochester team also identified the gene, named HAS2, responsible for making HMW-HA in the naked mole rat. Surprisingly, the naked mole rat gene was different from HAS2 in all other animals. In addition naked mole rats were very slow at recycling HMW-HA, which contributed to the accumulation of the chemical in the animals’ tissues.

The next step will be to test the effectiveness of HMW-HA in mice. If that test goes well, Seluanov and Gorbunova hope to try the chemical on human cells. “There’s indirect evidence that HMW-HA would work in people,” said Seluanov. “It’s used in anti-wrinkle injections and to relieve pain from arthritis in knee joints, without any adverse effects. Our hope is that it can also induce an anti-cancer response.”

It was this same husband and wife team that, in November of last year, announced that they’d discovered a protein which may prevent run-away cell growth in NMR. Unchecked cell growth is the hallmark of cancer.

HMW-HA is known to help vascular health by maintaining the integrity of Endothelial cells, which line the inside of veins and arteries. It is this property that makes it desirable in wrinkle therapy. Seluanov and Gorbunova discovered the same chemical in a “goop” that seemed to clog up testing equipment while the scientists tested other properties of the NMR.

Certain types of cancers seem to show resistance to treatments that in earlier stages are very effective. An example of this is the breast cancer fighting drug known as Tamoxifan. In early stages, it is a standard drug to prescribe because of its effectiveness. But in later stages, it appears to have no effect whatsoever.

University of Rochester researchers believe they have isolated the difference between the two stages that causes this stymie. They have isolated a specific protein. that seems to make the difference. And with it, they may have discovered a way to extend the treatment of breast and other forms of cancer well beyond the early stages:

Led by doctoral student Hsing-Yu Chen and Mark Noble, Ph.D., professor of Biomedical Genetics at URMC, the team studied the molecular mechanism that allows basal-like breast cancer cells to escape the secondary effects of tamoxifen, and discovered that two proteins are critical in this escape. One protein, called c-Cbl, controls the levels of multiple receptors that are critical for cancer cell function. A second protein, Cdc42, can inhibit c-Cbl and is responsible for the tumor’s underlying resistance.

The team also discovered that targeting Cdc42 – and thus inhibiting the inhibitor – with an experimental drug compound known as ML141 restored c-Cbl’s normal function. Through additional work in animal models and in human cell cultures, the team demonstrated that when ML141 is paired with tamoxifen, it enhances the ability of tamoxifen to induce cancer cell death and suppress the growth of new cancer cells. Neither drug alone had the same effect on basal-like breast cells.

So in the future, a one / two punch of Tamoxifan and ML141 may be the program of choice when dealing with this difficult cancer.

Every type of tissue in the human body is capable of regeneration. This process of regeneration is started in adult stem cells, which are stem cells with a limited number of tissue types they can convert to. Adult liver stem cells, for example, can only become liver tissue types.

Now research from Cornell University is hinting that studying the adult stem cells of various cancer-prone organs might reveal clues to the tendency of one person’s organs to eventually become cancerous:

… the researchers microdissected ovary and hilum cells, inactivated two tumor suppressor genes p53 and Rb1, whose pathways are commonly altered in human aggressive ovarian carcinoma, and injected cells into the abdominal cavity of mice. Very few tumors developed in the mice injected with ovary cells, but almost all of the mice injected with hilum cells died after developing aggressive, metastasizing cancers that were similar to human ovarian carcinomas.

In other words, by injecting mice with cancer-prone ovarian adult stem cells, they were able to create mice who predictably grew aggressive cancers. Working backwards from that, it might be possible to look for the existence of the two “tumor suppressor genes” in living human patients and predict the likelihood of ovarian cancer.

Researchers think it may be possible to find identical markers in other tissue-generating cells and treat cancer in much earlier phases of the disease. The article notes that, particularly where epithelial ovarian cancer is concerned, patients often don’t know they have a problem until it is already very late in the process. Thus identifying a person’s likelihood of developing certain types of cancers may provide a huge head start for successful treatment.

The cure for cancer may be closer than we know.

At least that is what University of Rochester Professor Vera Gorbunova and Assistant Professor Andrei Seluanov think.

The blind mole rat was known to be one of two mammals that never develop cancer. It was only until recently that University of Rochester scientists found out how the blind mole rat had developed such an immunity.

For their test, the two professors isolated blind mole rat cells and forced them to grow at an accelerated rate. During this process, the scientists witnessed the rapidly growing cells rearrange themselves and secrete a “suicide protein” that halted the abnormal growth. They also found that the adjacent cells that were at at risk for developing cancer were also killed off, stopping any potential for cancer.

Gorbunova said that the next step in their research is to find out why the protein is released in the first place. Once this final secret is discovered, it could be the final piece of the puzzle that will allow scientists to prompt human cells to release a similar “suicide protein” that would allow people to be able to fight off some cancers.

Despite the excitement among the University of Rochester scientists, Jerry Shay, who studies cellular aging at University Texas, does not hold the same optimistic opinion. Shay says that the protein may not actually be what prevents cancer in blind mole rats. He suggests that researchers have simply not found a way to keep the test cells alive for a long enough time.

Even if scientists have not figured out how blind mole rats have managed to prevent cancer to grow, it still does not take away from the fact that they are mammals and that they are immune to it. This means that humans still have a future of becoming resistant to cancer for good as well.

The fall season is upon us Rochesterians, and you know what that means! A crisp “Red Delicious”, the crunch of fallen leaves on your morning commute (you go walkers!) and the steamy pool of cheese dripping, meat loaded, tasty chili.

But for Rochester and abroad, the University of Rochester Medical Center may have just put a damper on the New York fall fiesta. Out with a new study linking high cholesterol levels with a higher risk of cancer, members of the Rochester community may begin to take a second look at their dietary choices.

So come on, eat a handful of almonds, for your own good! Yeah it sounds a bit morbid, but hey, so is dieting.

From early on in the 20th century, scientists have been searching for a link between cancer and high cholesterol. It was not until very recently that they finally found what they were looking for – evidence proving their theory.

The data, published in the online journal Cell Reports, support several recent population-based studies that suggest individuals who take cholesterol-lowering drugs may have a reduced risk of cancer, and, conversely that individuals with the highest levels of cholesterol seem to have an elevated risk of cancer.

This new data is a stepping-stone for researchers, but most importantly, the human population as a whole.  Although not all scientists agree with the university’s conclusions, thanks to the U of R Medical Researchers, the combative fight against cancer may be forever changed.

Chiefly found in saturated fats, cholesterol is a compound produced in the body’s cells after intake. Animal based food products, such as eggs and cheese, have higher amounts of cholesterol and thus hold a greater risk factor for clogging arteries.

According to Hartmut (Hucky) Land (PH.D), head author of the groundbreaking study, and his partner Bradley Smith (PH.D), a gene found in cells called ABCA1 can be a preventative agent against cancer. A “cooperation response gene”, ABCA1 is essential in identifying cell strain and deterring cancerous tumor growth in cellular structures.

Without functioning ABCA1, fatty cholesterol is able to form excessively in mitochondria – the energy-producing organelle within a cell – creating structural rigidness on the outside of the cell. Simply put, ABCA1 can no longer control cholesterol levels and detect cell stress, thus unable to act as a barrier to cancerous abnormalities in cells.

Thanks to the recent discovery by the University of Rochester Medical Center, people across the world will learn the importance that low cholesterol has on their health. With more research, cholesterol-controlling medicines may soon take on a new role in treating and preventing cancer.

So with a sip of our herbal tea, and a pair of bean shoots in our hands, we can toast to science. But if we must, (and sometimes we must) let’s stick to one slice of Granny’s Pumpkin Pie. Or better yet, just eat an apple.

According to the American Cancer Society, about 28,000 people will be diagnosed with liver cancer this year and at the same time, about 20,000 other patients will die of that same cancer. Both of those numbers have been increasing at a steady rate for decades now, and scientists aren’t entirely sure why.

But the researchers at the @UofR Wilmot Cancer Research Center have recently discovered an entirely new way to analyze the formation of liver cancer, which typically happens in an area of the liver known as the bile ducts. Bile is a substance produced by the liver that is essential to the digestion of food, and obviously, the ducts carry that bile out of the liver.

Researchers working in conjunction with researchers at Massachusetts General Hospital have found a way to genetically engineer mice to produce what is thought to be the most common vector for developing cancer of the liver, known by the charmingly-accessible name Intrahepatic Cholangiocarcinoma (IHCC). This allows the researchers to reproduce the same results over and over again to observe how it functions, and also to apply therapies to it to see what can be prevented.

Wilmot Researchers Create New Way to Study Liver Cancer – News Room – University of Rochester Medical Center.

Blood clots happen when blood, platelets and clotting proteins mass together in a single point. Most of the time, clots are the body’s way of defending itself against blood loss, however, in cancer patients it is common for these clots to happen in the lungs, abdomen or legs where they can become life threatening.

A new University of Rochester, Medical Center study – considered to be the largest population study of cancer patients of its kind – is revealing that outpatient treatment seems to coincide with a higher risk of these types of clots. As many as 78% of patients treated for blood clotting were treated out of hospital.

Outpatient treatment is generally considered healthier than inpatient where possible. The study does not seem to dispute that point. But identifying what specific problems may be associated with outpatient treatment could lead to even better recovery rates.

No theory was put forth for why clotting seems more common on outpatient basis. For more information, see the below press release:

URMC Study: Most Cancer-related Blood Clots Occur in Outpatients – News Room – University of Rochester Medical Center.

Gentlemen, find yourself a nice comfy chair and try not to squirm. We’re gonna talk about your butthole.

Prostate cancer affects 1 in 6 men and like all such diseases, especially cancers, we’re always looking for a way to avoid it. I mean, really: the only thing that makes cancer worse is if you put it in your butthole, right? Especially, like, you know: waaaay up in there.

But the U.S. Preventative Services Task Force (sort of the A-Team of butthole diagnosis) recently recommended that men over 50 not be tested quite so much. The reason is a combination of false-positives and also the belief – according to the below-linked article – that men over the age of 50 will probably die of something else entirely before the prostate cancer ever becomes a problem.

A University of Rochester study finds, though, that prostate cancer tends to be a lot more agressive in older men. So maybe that theory isn’t as sound as the recommendation seemed at the time. Either way, this is definitely one of those “talk to your doctor” kind of things.

Mind Wilferd. Check with your doctor. There's no reason not to,.. 'cept because you don't want a finger up yer butthole.

via Rochester Study: Age a Big Factor in Prostate Cancer Deaths – News Room – University of Rochester Medical Center.

Well, how about that? Scientists are discovering that the Human Pamplona Virus – linked in other studies to cervical cancer in women – is found in half of all adult males as well. Now mind you, I think there’s reason to doubt that this will raise any real hairs on the Christian Conservatives that currently hold the purse strings in Congress just yet: after all, its just cervical cancer in women.

But what other things is HPV complicating or causing for men? Dare I say: infertility? Maybe diminished sexual performance (also known as Floppy Dick)? Once we make that link, just watch Glaxo Smith-Kline suck up the research money to find a cure.

Half Of Adult Males Carry HPV – Science News.