Human Immune-Boosting Cancer Drugs Seen Extending Lives

Bloomberg

Merck & Co. (MRK), Bristol-Myers Squibb Co. (BMY) and Roche Holding AG (ROG) have opened a new front against cancer with the next generation of experimental drugs that use the human immune system to seek and destroy tumor cells.

The new therapies have the potential to reap billions of dollars in sales while lengthening patient remissions, said doctors and analysts awaiting study results to be released this week as part of the American Society of Clinical Oncology meeting that starts May 31.

Building on the success of Bristol-Myers’ Yervoy drug for melanoma that reached the market in 2011, drugmakers are devising more potent immune therapies or combining treatments for maximum effectiveness. They are also testing the new medicines in more types of cancers, including lung and breast.

If the new generation of immune therapies lives up to its promise, “this is going to be a paradigm shift for treating cancer,” said Merck senior vice president Gary Gilliland in an interview. “We are pretty good at shrinking tumors, but not good at getting rid of them. Immune therapy is a way to begin to approach that.”

Genetically engineered virus kills liver cancer

MedicalExpress

Sixteen patients given a high dose of the therapy survived for 14.1 months on average, compared to 6.7 months for the 14 who got the low dose. “For the first time in medical history we have shown that a genetically-engineered virus can improve survival of cancer patients,” study co-author David Kirn told AFP. The four-week trial with the vaccine Pexa-Vec or JX-594, reported in the journal Nature Medicine, may hold promise for the treatment of advanced solid tumours. “Despite advances in cancer treatment over the past 30 years with chemotherapy and biologics, the majority of solid tumours remain incurable once they are metastatic (have spread to other organs),” the authors wrote. There was a need for the development of “more potent active immunotherapies”, they noted. Pexa-Vec “is designed to multiply in and subsequently destroy cancer cells, while at the same time making the patients’ own immune defence system attack cancer cells also,” said Kirn from California-based biotherapy company Jennerex.

Hope for cancer victims as scientists develop drug that sends cells to sleep to stop them spreading

It still is rather amazing that they’ve yet to cure cancer, but only able to find things such as this.

A new drug called Aflibercept tricks tumours into becoming dormant by flipping molecular switches in the structure of the cancer so it cannot spread.

Positive results are being seen already in the UK, where trials have seen patients enjoy a ‘significant’ extension of life.

Man jokingly takes pregnancy test, finds out he has testicular cancer

Whoa

Everyone knows what pregnancy tests are used for, but you may not know that they can also detect another delicate condition – testicular cancer in men.

The science of testicular cancer and pregnancy hormones is making the national news this week thanks to a Reddit post in which a man makes fun of his buddy for using an ex-girlfriend’s leftover pregnancy test. The test came back positive.

The post received thousands of comments, many of them urging the poster to get tested for testicular cancer. It turns out that beta human chorionic gonadotropin, the hormone detected by pregnancy tests in pregnant women, can also signal some types of testicular cancer, oncologist Dr. Mark Pomerantz told Good Morning America.

A second Reddit post by the same user claims that the man who took the pregnancy test, who is never named, did have a small testicular tumor. “Since it was caught early, it can be treated immediately,” the post states.

Dr. Christopher Wood of the M.D. Anderson Cancer Center in Houston told Good Morning America that he recommends all men conduct monthly self-exams to detect testicular cancer by feeling for lumps, as the cancer has a high survival rate and normally first presents itself as a painless lump. Click here to get more info on self-exams from the American Cancer Society.

FDA Approves Ingestible Sensor That Tracks Health From The Inside

MedicalNewsToday

The US Food and Drug Administration has approved an ingestible digital sensor that can be swallowed in a pill to track health data from inside the body. The idea is that the data can be used not only by patients themselves, but also by caregivers and doctors to individualize their care.

The ingestible sensor, formerly known as the Ingestion Event Marker or IEM, is already approved for use in Europe.

It is the first “digital pill” to receive FDA approval, in a move that its maker Proteus Digital Health, whose headquarters are in Redwood City, California, sees as the start of a era where digital medicine “shifts the care paradigm”.

On Monday, George Savage, co-founder and chief medical officer at Proteus Digital Health, told the press:

“We are thrilled to have achieved this important milestone to market our ingestible sensor in the United States now, as well as in Europe.”

“We are very much looking forward to bringing the benefits of our ingestible sensor to the American public in the form of innovative product offerings,” he added.

The ingestible sensor, which is about the size of a grain of sand and made mostly of silicon, is part of an integrated system designed to give patients and their doctors “end-to-end personal health management”.

Embedded in a pill or tablet, the device can help keep an eye on whether patients are taking their medications at the prescribed time and rate.

This is important, because although the effectiveness and safety of drugs are established in clinical trials, those tend to follow well-controlled conditions, with patients taking their drugs at the prescribed rates in the right quantitities.

But at home, adherence to prescribed regimens may not be so easy to monitor, and without information about precisely when patients are taking their medication, doctors can’t see if that is the problem, should the drug not work as it should.

The sensor does not contain a battery, it works like a “potato battery” that children make in science lessons at school. It has two conductive materials, one on either side. When these get wet in the stomach, they power the sensor for a short amount of time.

So once it comes into contact with stomach fluid, the sensor powers up, and “communicates a unique signal that determines identity and timing of ingestion”, says Proteus.

The ingestible sensor passes through the body in much the same way as high-fiber food, according to information on the company’s website.

The signal that it sends from the stomach travels through the patient’s body to a patch worn on the skin. The patch contains technology that senses the signal and records the exact time the ingestible sensor was swallowed.

The patch can then send this information to a mobile phone application, and with the consent of the patient, be passed on to doctors and caregivers, so they can provide better quality care.

Proteus says its integrated “feedback” system is also designed to collect a range of other measurements, such as for heart rate, body position and activity.

Eric Topol, geneticist and cardiologist, is a professor of genomics at The Scripps Research Institute and wrote a book called “The Creative Destruction of Medicine: How the Digital Revolution Will Create Better Healthcare” where, among other things, he says technology that gives doctors a continuously updated picture of what is happening with each patient, will help them provide better, individualized care.

Topol told the press:

“The FDA validation represents a major milestone in digital medicine. Directly digitizing pills, for the first time, in conjunction with our wireless infrastructure, may prove to be the new standard for influencing medication adherence and significantly aid chronic disease management.”

Written by Catharine Paddock PhD

500 Mutations Per Blood Stem Cell By Age 50

Was Countess Elizabeth Báthory de Ecsed on to something?? Let’s not go there…

You collect about 10 mutations per blood stem cell per year. The accumulation of these mutations leads to a rising incidence of blood cancers (leukemias) as we age. We need youthful replacement stem cells that have very few harmful mutations

AML is a blood cancer that develops when too many immature blood cells crowd out the healthy cells. In recent years, Washington University researchers at the Siteman Cancer Center at Barnes-Jewish Hospital and Washington University School of Medicine have sequenced the genomes of 200 patients with AML to try to understand the mutations at the root of the disease.

Without fail, each patient’s leukemia cells held hundreds of mutations, posing a conundrum for scientists, who have long believed that all the mutations in a cancer cell are likely to be important for the disease to progress.

“But we knew all of these mutations couldn’t be important,” says co-first author Daniel Link, MD, professor of medicine. “It didn’t make any sense to us that so many mutations were present in all the cells in the tumor.”

To investigate the origin of these mutations, the researchers isolated blood stem cells from healthy people of different ages. The youngest were newborns, and the oldest was in his 70s.

Every person has about 10,000 blood stem cells in their bone marrow, and the researchers found that each stem cell acquires about 10 mutations over the course of a year. By age 50, a person has accumulated nearly 500 mutations in every blood stem cell.

Future stem cell therapies will likely involve first filtering thru many individual cells from around the body to find cells that have no harmful accumulated mutations. Individual cells will be grown into several cells so a cell can be taken and sequenced without loosing a good original cell. The best cell discovered this way will be used to grow cell lines in vitro that will be manipulated for eventual return to the body in large numbers.

If we can replace aged stem cells in the bone marrow and other locations with far less mutated cells then our risk of cancer will decline substantially and the youthful stem cells will divide to produce adult cells that replace lost cells in various organs.

Demystifying the immortality of cancer cells

MedicalPress

In cancer cells, normal mechanisms governing the cellular life cycle have gone haywire. Cancer cells continue to divide indefinitely, without ever dying off, thus creating rapidly growing tumors. Swiss scientists have discovered a protein complex involved this deregulated process, and hope to be able to exploit it to stop tumor formation in its tracks.

All our cells come equipped with an automatic self-destruct mechanism; they are programmed to die after a certain number of divisions. This internal clock is of great interest to cancer researchers, because most forms of cancer exhibit a defect in this innate timing mechanism. Cancer cells continue to divide indefinitely, long past the moment at which a normal cell would self-destruct. A team of researchers from professor Joachim Lingner’s laboratory at EPFL has learned how this defect is regulated in a tumor. Post-doctoral researcher Liuh-Yow Chen led the team in publishing an article appearing in the journal Nature on the 4th of July 2012. Their hope is that the discovery will provide new targets for drug therapies to combat the deadly disease.

Cellular immortality, which is responsible for cancer formation, hearkens back to a critical function of the cells of the developing embryo. At the ends of every chromosome there is a special sequence of DNA known as a telomere, whose length is governed by the telomerase enzyme. This sequence represents the lifespan of the cell. Every time the cell divides, it is shortened, and when the telomere finally runs out, the cell dies. This reserve allows most cells to divide about 60 times – sufficient for the cell to play its given role in the organism, without succumbing to inevitable genetic mutation.

Cellular immortality, cancer’s common denominator

Normally, once the embryonic stage is completed, our cells stop producing telomerase – with the notable exception of somatic stem cells. But occasionally, a cell will mutate and reactivate production of the enzyme, so that when the cell divides, the telomere gets longer instead of shorter. This is what gives cancer cells their immortality.

“This mutation, on its own, is not enough to cause cancer,” explains Joachim Lingner, co-author and head of the lab. “But cellular immortality is a critical element in tumor formation in 90% of known cancers.” Researchers the world over hope to be able to stop the runaway growth of cancer cells by targeting this mechanism with drug therapy.

But interestingly enough, even in a cancer cell the telomere doesn’t grow indefinitely long. With each cell division it loses some 60 nucleotides, like most cells, but then the activated telomerase causes it to gain just as many back. The internal clock is reset to zero, and the cell becomes immortal. But there’s one interesting question here: What is stopping the telomere from getting indefinitely long?

Stopping the clock with three proteins

The EPFL team was able to provide an answer to this question; they identified three proteins that join together and then attach themselves to the telomere. A bit like a lid on a pot, this protein complex prevents telomerase from acting on the telomere. But in the cancer cell, their timing is off – their involvement takes place too late.

“If we could cause these proteins to act earlier, or if we could recreate a similar mechanism, the cancer cell would no longer be immortal,” explains Ligner. The cancer cells would die a normal death. Clinical applications are still a long way off, however, he insists. “Our discovery may allow us to identify potential targets – for example, a secondary protein to which these three proteins also attach. But right now our work is still in the basic research stages.”

Why Chronic Infections Cause Cancer

FuturePundit

Infection leads to cancer.

CAMBRIDGE, Mass. — One of the biggest risk factors for liver, colon or stomach cancer is chronic inflammation of those organs, often caused by viral or bacterial infections. A new study from MIT offers the most comprehensive look yet at how such infections provoke tissues into becoming cancerous.

The study, which is appearing in the online edition of Proceedings of the National Academy of Sciences the week of June 11, tracked a variety of genetic and chemical changes in the livers and colons of mice infected with Helicobacter hepaticus, a bacterium similar to Helicobacter pylori, which causes stomach ulcers and cancer in humans.

What I wonder: How much cancer could be prevented if we all got tested for chronic infections and got treated for any infections found? Or could a round of antibiotics without even first testing for a bacterial infection cut cancer risks?

The immune system generates toxic chemicals to kill bacteria. But those toxic chemicals also damage tissue in ways that can lead to cancer.

In the colon, but not the liver, neutrophils secreted hypochlorous acid (also found in household bleach), which significantly damages proteins, DNA and RNA by adding a chlorine atom to them. The hypochlorous acid is meant to kill bacteria, but it also leaks into surrounding tissue and damages the epithelial cells of the colon. The researchers found that levels of one of the chlorine-damage products in DNA and RNA, chlorocytosine, correlated well with the severity of the inflammation, which could allow them to predict the risk of chronic inflammation in patients with infections of the colon, liver or stomach. Tannenbaum recently identified another chlorine-damage product in proteins: chlorotyrosine, which correlates with inflammation. While these results point to an important role for neutrophils in inflammation and cancer, “we don’t know yet if we can predict the risk for cancer from these damaged molecules,” Dedon says.

Unfortunately, we live in a time when drug resistant strains of tuberculosis, gonorrhoea, and other bacteria are spreading globally. Be careful. Bacteria should be taken as a serious threat to health once again.

Childhood Cancer Survivors Face Cancer Risk Even after Treatment

MedicalDaily

Girls who undergo radiation to treat childhood cancer are at increased risk of developing breast cancer in later life, researchers say.

Researchers analyzed data from more than 1,200 women who were treated with radiation for childhood breast cancers.

By age 50, almost 24 percent were diagnosed with breast cancer. People who were treated with higher doses of radiation had higher chances (30 percent) of having another cancer.

“We find that by age 50, approximately 30 percent of women treated with radiation for Hodgkin lymphoma” as girls have developed breast cancer,” said Chaya Moskowitz, a biostatistician at Memorial Sloan-Kettering Cancer Center, New York. Moskowitz is the lead researcher in the present study.

“We need to know how to take care of survivors and change childhood cancer therapies, so this doesn’t happen to the next group of survivors. Children treated for Hodgkin lymphoma today are treated with therapies that try to maintain the excellent cure rates but use as little radiation as possible,” said Lisa Diller of Boston’s Dana-Farber Cancer Institute, to USA Today.

“These are rather striking data. We have an obligation to those many thousands and thousands of young women we treated years ago. Hopefully this will increase our awareness of [the] need for mammogram screening of this population,” said Dr. Nicholas Vogelzang of the Comprehensive Cancer Centers of Nevada in Las Vegas and US Oncology, to WebMD. Vogelzang was not part of the study.

Another study published in the journal Annals of Internal Medicine said that childhood cancer survivors who were exposed to abdominal radiation have increased risk of developing gastrointestinal cancers later in life.

Scientists Discover How Curry Spice Strengthens Immune Response in Fighting New Infections

YUMMM!

Eating curry may help prevent new infections by strengthening the immune system, scientists say.

A new study found that a compound found in turmeric, an orangy-yellowish spice that is commonly found in South Asian and Middle Eastern cuisine and has been used for 2,500 years in India’s traditional Ayurvedic remedies, increases levels of the cathelicidin antimicrobial peptide or CAMP protein that helps the immune system fight off various bacteria, viruses or fungi that the body has never been exposed to.

Previous research has also found that vitamin D can also increase levels of CAMP proteins, the only known antimicrobial peptide of its type in humans that can kill a wide variety of bacteria, including ones that cause tuberculosis and sepsis, a severe condition in which the bloodstream is saturated by bacteria.

However, high amounts of vitamin D in the body can be toxic, and can cause more calcium to be released in the blood leading to hypercalcemia, which can cause symptoms such as poor appetite, nausea and vomiting.

Researchers reporting Friday in the Journal of Nutritional Biochemistry say that the latest discovery could pen new research avenues in nutrition and pharmacology.

“This research points to a new avenue for regulating CAMP gene expression,” said Adrian Gombart, an associate professor of biochemistry and biophysics in the Linus Pauling Institute in Cornvallis, Oregon said in a news release.

“It’s interesting and somewhat surprising that curcumin can do that, and could provide another tool to develop medical therapies,” he added.

Gombart and his team compared the effectiveness of curcumin and omega-3 fatty acids in increasing the expression of the CAMP gene. While omega-3 fatty acids appeared to be useless in increasing the protein, laboratory experiments showed that curcumin nearly tripled levels of CAMP in human cells.

“Curcumin, as part of turmeric, is generally consumed in the diet at fairly low levels,” Gombart said. “However, it’s possible that sustained consumption over time may be healthy and help protect against infection, especially in the stomach and intestinal tract.”

Curcumin, which is known for its anti-inflammatory and antioxidant properties, is also being studied by British scientists as being an effective compound to fight cancer.

Earlier this month, researcher in the cancer trial said that they hope curcumin will increase the success of chemotherapy while reducing side-effects.

“We’ve shown that [curcumin] has well over 100 mechanisms of damaging cancer cells, particularly colon cancer cells,” Professor Will Stewart of England’s University in Leicester told the Australian Broadcasting Corporation.

“One of the major mechanisms is affecting the way that they grow blood vessels into themselves,” Stewart added.