Category Archives: Cancer

Clinical_Test

Prostate Cancer Clinical Trials

clinical trialBy involving yourself in a clinical trial, it could mean a really big change in the type of care you are now getting for your prostate cancer.  Cutting-edge treatment is involved and few people have had it before, but make sure you learn how it works and what it will be like for you.

A clinical trial is a study that gives the researchers a chance to show that a treatment works and is safe. The procedure nor medical device will not be approved by the FDA until the clinical trial is completed. FDA already approves some of these procedures and test drugs for other conditions, but the researchers want to see if they might work for prostate cancer as well. Another reason for the clinical trials is to see if there is a benefit to taking two treatments together that are usually done alone.

Some trials provide the patient with typical medication used to treat cancer and a placebo, or the experimental drug.  Other patients may get the typical medication used or the experimental drug. A patient can also get a placebo or the experimental therapy in some of the trials.

When you accept a clinical trial you are assigned at random an experimental or a control group. Regular care and the treatment being tested are in the experimental group. The control group gives you regular care and a placebo or “dummy pill.”

In cross-over studies the researchers give regular care and the experimental treatment to one group and the other group their regular care and the placebo.  The groups then switch, but everyone eventually gets the experimental treatment.

In the double-blinded studies you’ll get assigned to either of the groups, but while the trial is going on, neither you nor the doctor will know which group is getting the experimental treatment or the placebo.

Care during a clinical trial is closely checked by the doctors, because they need to see how the treatment is working.  They need to be sure they aren’t missing any important signals for good or bad. You will receive a lot of attention and care that might mean many trips to the research center.  

Sponsors usually pay for the trial experimental drugs and everything else related to it, such as tests and lab work.  Bills for any regular treatment are sent on to your insurance company and the insurance company cannot drop you for enrolling in an approved study.

Things to know before beginning a trial are what the experimental treatment is, the known and possible risks, if you might be getting a placebo, any treatments you might consider instead of experimental treatment, everything you need to do during the study and any money you will have to pay.  Get the answer to these questions before you agree to take part in the trial.

Usually your doctor will know and suggest a specific clinical trial as one of your treatment options.  If not, you might check these groups to find out about where to join a trial:

  • National Cancer Institute
  • The U.S. National Institutes of Health
  • World Health Organization
  • Prostate Cancer Clinical Trials Consortium
  • Online clinical trial listing services, such as eCancerTrials, CenterWatch and ClinicalTrialsSearch.

There is an online checklist of the information you need to search for a trial at the National Cancer Institute site.  Once you have found a trial that you or your doctor thinks might be right for you, either one of you can contact the research team so that you can apply.  But before subjecting yourself to the unknown, wouldn’t it make more sense to give nature a try and treat yourself with holistic, alternative care?  No unknowns and only proven all natural methods of care.

Dr Fredda Branyon

High carbs

Poor Carb Diets & Cancer Risk

High carbsAn article by EJ Mundell reported that even those people who’ve never smoked could get lung cancer.  A new study suggests their risk for the disease may rise if they eat a diet rich in certain carbohydrates.  These are high glycemic index diets that trigger higher levels of insulin in the blood and tend to be heavy in refined poor quality carbs, according to one expert.

Dr. Rishi Jain, a medical oncologist at Fox Chase Cancer Center in Philadelphia, says that the glycemic load and index are methods to estimate the quality and quantity of dietary carbohydrates.  A couple of examples of these high glycemic index foods would be white bread and white potatoes.

As the rates of obesity and heart risk factors rise in the U.S., so does the number of Americans with insulin resistance, which is a precursor to diabetes.  Insulin-linked disorders are often tied to high-glycemic diets and have been implicated as potential contributors to a variety of chronic conditions that include certain cancers.  Dr. Xifeng Wu, chair of cancer prevention at the university of Texas MD Anderson Cancer Center in Houston, conducted a new study to help answer the question “if lung cancer could be one of those malignancies.”

Dr. Xifeng Wu and her team looked at the health and dietary histories of more than 1,900 people with lung cancer and more than 2,400 people without the disease.  The intake of foods with a high glycemic index, such as the white bread and potatoes, were specifically looked at by the investigators. Those people who registered in the top 5th in terms of a high-glycemic diet had a 49% greater risk of developing lung cancer versus those in the bottom 5th.  The trend was stronger when the study focused on people who had never smoked.  Those who scored highest in terms of a high-glycemic diet had more than double the odds of lung cancer compared to never-smokers who had the lowest glycemic index scores.  The findings of this study was reported in the journal Cancer Epidemiology, Biomarkers & Prevention.  

Focusing on never-smokers is important as it eliminates smoking as a confounding risk factor showing the potential role of diet in lung cancer risk.  Smoking is a major factor for lung cancer but does not account for all the variations in lung cancer risk.

Stephanie Melkonian, a study co-author says that high-glycemic diets are linked to insulin resistance, which may encourage the activity of certain cellular growth factor chemicals that are known to play a role in cancer.  Their study can’t prove the cause-and-effect and also fails to take into account the potential role of other illnesses, such as diabetes, high blood pressure or heart disease. The downstream effect of a high-glycemic diet on cellular growth factors explaining the link to lung cancer risk was agreed on by Jain.  He further stated that this association was more pronounced in nonsmokers, suggesting that increased intake of poorer quality carbs might be more detrimental in this group.

The study contributes to the growing evidence that poor dietary habits and obesity do play a critical role in cancer development.

Dr Fredda Branyon

Personalized Drugs

Personalized Medicine

Personalized DrugsThose who have cancer, along with their family and friends, have been searching anything that’s available to find the best possible way to beat the disease.  Things like “personalized medicine,” “precision medicine,” or “targeted drugs” are things you have likely seen. But are these things that can help you, and exactly what are they?  Precision medicine is also called pharmacogenetics and a new way of fighting cancer by taking information about you and your tumor to decide what’s driving the disease and then strives to create a plan specifically for you.

Cancer treatment has been a cookie-cutter process for years where surgery would be chosen to remove a tumor, then chemo or radiation was used to kill the cancer cells.  Blasting the cancers with chemotherapy or radiation kills the healthy cells as well and can most likely lead to a host of really nasty side effects. The researchers now have the ability to examine your cancer cells and learn the order of the genes in their DNA.  Most of the cells in the body have identical genes. Those in cancer cells have mutation or changes and this allows them to grow into tumors.

Someone else’s cancer may have different genetic changes than yours and the scientists know that genetically, one person’s breast cancer may be more similar to another person’s stomach tumor than to other breast cancers.  This makes having personalized medicine an even greater need.

More than a dozen drugs that target one of these mutations has been approved by the FDA. Imatinib (Gleevec), a drug used on chronic myelogenous leukemia, and the breast cancer drugs trastuzumab (Herceptin), are included. Doctors learn which drugs won’t work from the tumor genetics.  As an example you won’t be given two colon drugs if your cancer has a genetic mutation called KRAS, as they know they won’t work. Tumor profiling is also performed in many clinical centers where the doctor takes a look at your tumor’s genes.  If your cancer might have specific mutations, your doctor might start you on a specific drug that’s approved for your type of cancer. Otherwise, a genetic test would tell him in a certain drug might work for you. This genetic profiling can help if other treatment options haven’t worked for you.  The genetic mutation could point the medical team toward an unexpected drug like one that was originally designed for another type of cancer.

This is not a magic bullet but the personalized approach works better to shrink tumors and save lives than the traditional treatment, but is not always a cure.  Cells with different gene mutations can appear in tumors, so a targeted therapy designed to pick off cells with one mutation may work on only part of a tumor while the other cells may keep growing.

There are some trials available to test cancer treatments using people whose tumors are similar in size or location.  Only those with stage IV lung cancer might be chosen, but now that there is personalized medicine, the researchers now need ways to study how targeted treatments work on a variety of cancers.  Creating new treatments require a constant effort between doctors and scientists. After new drugs are made to combat the new gene changes, they are tested in the clinic. More drugs will become available as tumors change in new ways.  

Dr Fredda Branyon

Low-Dose Aspirin & Cancer

AspirinAna Sandolu has written another article explaining the use of low-dose aspirin and the prevention of cancer.  As well known, cancer is a leading cause of morbidity and death worldwide and is predicted to increase in the following years.  Making healthy lifestyle choices and getting tested if at risk are some prevention strategies. I have always been aware of taking a “baby” aspirin for heart maintenance but never as a possible prevention of cancer.  The new research is suggesting that a small dose of aspirin may help prevent the formation of cancer cells and explains how.

The World Health Organization (WHO) reveals that cancer is one of the leading causes of death accounting for 8.2 million deaths in 2012 alone.  They recommend making healthy lifestyle and dietary choices as well as avoiding tobacco, alcohol and staying physically active with a diet of plenty of fruits and vegetables.

The idea that low-dose aspirin intake may also help to prevent cancer and inhibit the proliferation of cancer cell reinforces the idea through new research.  The United States Preventive Services Task Force recommended in September of 2015, the daily use of a small dose of aspirin to help with cardiovascular disease as well as colorectal cancer.

This low dose of aspirin may very well inhibit cancer cell proliferation and metastasis.  The scientists from Oregon Health and Science University in collaboration with Oregon State University published their research results in the journal AJF-Cell Physiology.  They reported that the benefit of aspirin might be due to its effect on blood cells called platelets, rather than acting directly on tumor cells.  Our blood platelets also increase the levels of a certain protein that may support cancer cells and help them to spread. This oncoprotein is called c-MYC.  Its function is to regulate the expression over 15% of all the genes of the human body. The c-MYC regulator controls the life-and-death cycle of cells, the synthesis of proteins and the cells’ metabolism. Research has shown that in human cancers, this oncogene is overexpressed.

This work suggests that the anti-cancer action of aspirin might be in part during their transit in the blood; circulating tumor cells interact with platelets, which spur tumor cell survival by activating oncoproteins such as c-MYC.  This inhibition of platelets with aspirin therapy reduces the signaling between platelets and tumor cells, thus reducing tumor cell growth.

Blood platelets can play a protective role for the early cancer cells and aid metastasis.  Aspirin appears to interfere with that process and c-MYC may explain part of that mechanism.

It is also noted by the researchers that almost 1/3 of colon cancer patients and 42% of patients with pancreatic cancer had overexpression of the c-MYC oncoprotein.  The impact that aspirin has on blood platelets is just as effective in high doses as it is at low ones. The clinicians can weigh the risks and benefits of aspirin intake as well as reduce the risk of bleeding, which is a common side effect of ingesting too much aspirin.  It is emphasized the crucial role of physicians and healthcare professionals when considering even a low-dose aspirin intake.

The interaction between platelets and cancer cells is believed to occur early and the use of anti-platelet doses of aspirin might serve as a safe and efficacious preventive measure for patients at risk for cancer.

Dr Fredda Branyon

Jet_Lag

Jet Lag, Obesity & Pathways to Liver Cancer

Jet LagHepatocellular carcinoma, the most common type of liver cancer, has nearly tripled since 1980, and obesity related liver disease is one of the driving forces behind the increasing number of cases.  Baylor College of Medicine researchers are now examining other lifestyle factors that may affect your health. By using mice, the scientists have shown that repeated jet lag increases both obesity related liver disease and the risk of liver cancer.  The Cancer Cell has published the study.

Liver cancer is rising worldwide and through human studies, we’ve seen that patients can progress from fatty liver disease to liver cancer without any middle steps such as cirrhosis, according to David Moore, a professor of molecular and cellular biology who led the study with Associate Professor Loning Fu, both at Baylor.  Studies in the Fu Lab found that chronically jet-lagged mice developed liver cancer in a very similar way as that described for obese humans.

Our bodies’ central circadian clock in the brain resets when we are exposed to light.  Traveling constantly through different time zones, working night shifts or pushing us to stay awake at the regular sleep time causes our central clock to be chronically disrupted.  This also extends to clocks in other tissues that are controlled by the central clock.

The researchers modeled the effects of chronic jet lag in normal mice who were fed a healthy diet by changing the times the lights went on and off during the night each week.  The mice gained weight and fat and developed fatty liver disease. This progressed to chronic inflammation and eventually to liver cancer in some of the cases.

Normal control of liver metabolism was lost on the jetlagged mice.  This included the buildup of fat and also increased production of bile acids, which are produced by the liver to help us digest our food.  Some studies linking high bile acid levels to liver cancer, in mice and humans, were done in earlier studies. Circadian clock disruption activated two nuclear receptors that help regulate liver bile acid metabolism.  A receptor called FXR, which keeps bile acid level in the liver within a normal physiological range in the jetlagged mice lacking the receptor, had higher bile acid levels and much more liver cancer. Those lacking a receptor called CAR, which regulates bile acid breakdown and known to promote liver cancer, did not get any liver tumors.

These receptors work in a similar manner in humans. The scientists did not directly study jetlag in humans, but there is evidence that sleep disruption increases both fatty liver disease and liver cancer risk in humans.

Studies show that more than 80% of the population in the U.S. adopts a lifestyle that leads to chronic disruption in their sleep schedules.  This has reached an epidemic level in other developed countries and coupled with the increase in obesity and liver cancer risk.

They hope to continue their research to further examine if drugs interacting with the nuclear receptors can help to prevent jet lag from affecting bile acid levels in the liver with a goal of using them as pharmaceutical strategies to prevent liver cancer in humans.

Bottom line results are that chronic jet lag was sufficient to induce liver cancer.  Results definitely show that chronic circadian disruption alone leads to malfunction of these receptors, so maintaining internal physiological homeostasis is very important for liver tumor suppression.

Dr Fredda Branyon

Graphene

Graphene to Detect Cancer Cells

 

Researchers at the University of Illinois at Chicago have shown that by interfacing brain cells onto graphene, they can differentiate a single hyperactive cancerous cell from a normal cell, pointing the way to developing a simple, noninvasive tool for early cancer diagnosis.  This system is able to detect the level of activity of an interfaced cell, according to Vikas Berry, associate professor and head of chemical engineering at UIC. Berry led the research along with Ankit Mehta, assistant professor of clinical neurosurgery in the UIC College of Medicine.

Graphene is very sensitive to whatever happens on its surface and is the thinnest known material.  The nanomaterial is composed of a single layer of carbon atoms that are linked in a hexagonal chicken-wire pattern.  All of the atoms share a cloud of electron that move freely about the surface. Berry also said that the cell’s interface with graphene then rearranges the charge distribution in the graphene and modifies the energy of atomic vibration as detected by Raman spectroscopy.  She refers this to a powerful workhorse technique that is routinely used to study graphene.

The atomic vibration energy in graphene’s crystal lattice does differ, depending on whether it’s in contact with a cancer cell or a normal cell.  This is because the cancer cell’s hyperactivity leads to a higher negative charge on its surface and the release of more protons.

The electrons in graphene’s electron cloud are pushed away by the electric field around the cell.  This changes the vibration energy of the carbon atoms. Raman mapping with a resolution of 300 nanometers, allowing characterization of the activity of a single cell, can pinpoint this change.

The journal ACS Applied Materials & Interfaces published the report that looked at cultured human brain cells, compared normal astrocytes to their cancerous counterpart and the highly malignant brain tumor glioblastoma multiforme.  They are now studying the technique in a mouse model of cancer with results that look very promising. Down the road the experiments would be with patient biopsies.

They could use this technique to see if the tumor relapses once a patient has brain tumor surgery.  They would need a cell sample that they could interface with graphene and look to see if cancer cells are still present.  This same technique might also work to differentiate between other types of cells or the activity of cells.

They may be able to use it with bacteria to see if the strain is Gram-positive or Gram-negative and might be able to use it to detect sickle cells.  Berry and other coworkers introduced nanoscale ripples in graphene earlier this year causing it to conduct differently in perpendicular directions, useful for electronics.  The graphene was wrinkled by draping it over a string of rod-shaped bacteria and vacuum-shrinking the germs.

The earlier work was essentially flipped over so that instead of laying graphene on cells, they laid cells on graphene and studied graphene’s atomic vibrations.

Co-authors on the study are Bijentimala Keisham and Phong Nguyen of UIC chemical engineering and Arron Cole of UIC neurosurgery.

Dr Fredda Branyon

E-cigarette

E-Cigarettes Harmful

E-Cigarettes Harmful

There was a surprising article written by Honor Whiteman that revealed the harm that e-cigarettes can have for our oral health.  They are marketed as a safer alternative to conventional cigarettes, but when it comes to our oral health, new research suggests that vaping may be just as harmful as smoking.

An article was published in the journal Oncotarget revealing that researchers had found the chemicals present in electronic cigarette vapor were just as damaging, and in some cases even more damaging to the mouth cells, as tobacco smoke.  This can lead to an array of oral health problems that include gum disease, tooth loss and even mouth cancer.

The battery-operated e-cigarette devices contain a heating device and a cartridge that holds a liquid solution. The device vaporizes the liquid when the user “puffs” on the device resulting in vapor being inhaled.  E-cigarettes do not contain the highly harmful tobacco, a highly harmful component of conventional cigarettes, but they do contain nicotine and other chemicals, including flavoring agents.

The Centers for Disease Control and Prevention (CDC) reports that the e-cigarette usage has increased in recent years, especially among the young people.  About 16% of high-school students in 2015 reported using the devices where only 1.5% used the devices in 2011. There is little known about the long term effects of vaping on the health, but e-cigarettes are considered to be safer than conventional smoking by many.

The research team exposed gum tissue of nonsmokers to either tobacco or menthol-flavored e-cigarette vapor and found that tobacco-flavored vapor contained 16 milligrams of nicotine, while the menthol flavor contained 13-16 milligrams of nicotine or no nicotine.  All e-cigarette vapors caused damage to gum tissue cells comparable to that caused by exposure to tobacco smoke. When the vapors from an e-cigarette are burned, it causes cells to release inflammatory proteins, which is turn aggravate stress within cells and result in damage that could lead to various oral diseases.

Even though it is a fact that nicotine is a known contributor to gum disease, the e-cigarette flavoring appears to exacerbate the cell damage caused by e-cigarette vapor, with menthol-flavored vapor causing the most harm.  

Another study published in the Journal of Cellular Physiology revealed a high rate of mouth cell death with exposure to e-cigarette vapor over just 3 days and killed 53% of mouth cells.  E-cigarette vapor was pumped into the chamber at a rate of two 5-second puffs every 60 seconds for 15 minutes a day and performed over 1, 2 or 3 days.  Upon analyzing the vapor-exposed epithelial cells under a microscope, the researchers identified a significant increase in the rate of cell damage and death.  It was found that with exposure to e-cigarette vapor, the number of dead or dying cells rose to 18%, 40% and 53% over 1, 2 and 3 days, respectively. This leads researchers to believe that their findings are a cause for concern as over the longer term, it may also increase the risk of cancer.

Dr Fredda Branyon

Chilli_Pepper

Chili Pepper Compound & Cancer

 

chilli pepper

An article written by Ana Sandoiu reveals that research has identified different subtypes of breast cancer that respond to varying treatment types.  The so-called triple-negative breast cancer is especially aggressive and difficult to treat but new research may have uncovered a molecule that slows down this type of cancer.

The most prevalent form of cancer in women around the world is breast cancer, with almost 1.7 million new cases diagnosed in 2012.  This is also the most common form of cancer in women in the U.S., regardless of the race or ethnicity.

There is genetic research that has enabled scientists to classify breast cancer into subtypes that respond differently to different kinds of treatment and are categorized according to the presence or absence of three receptors known to promote breast cancer.  Estrogen, progesterone and the epidermal growth factor receptor 2 (HER2) are those receptors.

Those types of cancer that test negatively for HER2, estrogen and progesterone are called triple-negative breast cancer.  Triple-negative cancer is more difficult to treat according to some studies, so chemotherapy is the only option.

There is new research from the Ruhr University in Bochum, Germany that tested the effects of a spicy molecule on cultivated tumor cells of this aggressive type of cancer.  Dr. Hanns Hatt and Dr. Lea Weber were the researchers who collaborated with several institutions in Germany. The effect of an active ingredient commonly found in chili or pepper called capsaicin, was tested on SUM149PT cell culture, which is a model for triple-negative breast cancer.  It has been suggested that several transient receptor potential (TRP) channels influence cancer cell growth, which motivated the scientists. The TRP channels are membranous ion channels that conduct calcium and sodium ions and can be influenced by several stimuli including temperature or pH changes.  The olfactory receptor TRPV1 is one of the TRP channels that play a significant role in the development of several diseases and received a lot of attention from researchers. Researches aimed to investigate the expression of TRP channels in breast cancer tissue, as well as to analyze and understand how TRPV1 could be used in the breast cancer therapy.

Several typical olfactory receptors were found in the cultivated cells.  These are proteins that bind smell molecules together and are located on olfactory receptor cells lining the nose.  The TRPV1 receptor appeared very frequently. This receptor is normally found in the 5th cranial nerve called the trigeminal nerve.  The receptor is activated by the spicy molecule capsaicin as well as by helional, which is a chemical compound giving the scent of fresh sea breeze.

The team found TRPV1 in the tumor cells of 9 different samples from the breast cancer patients.  They then added capsaicin and helional to the culture for several hours or days, which activated the TRPV1 receptor in the cell culture.  This resulted in the cancer cells dying more slowly. Tumor cells died in larger numbers and those remaining were not able to move as quickly as before; suggesting their ability to metastasize was reduced.

Their conclusions were that an intake of capsaicin through food or inhalation would be insufficient to treat triple-negative cancer but specially designed drugs might help.  By switching on the TRPV1 reception with those drugs, it might constitute a new treatment approach for this type of cancer.

Dr Fredda Branyon

Patient

Cancer Patients & Online Forums

          When people are faced with a life-threatening disease like cancer, they often seek information about the disease and support from peers.  Hearing the personal stories from other cancer patients that post online in forums and scientific websites are the very best resources. These will provide comfort during these stressful times and help with the anxieties of being faced with a horrible disease, according to a new study recently published.

          Watching television entertainment shows and medical dramas can leave people feeling fearful and concerned though, because the storylines can be suspenseful in the hopes of holding the viewers’ attention.  Secondly, is the information found on the Internet reliable? People are looking for more than just information. They want comfort and support offered by the stories and reactions of those who are, or have gone through, the same ordeal.  Jan Van den Bulck, professor of communication studies at the University of Michigan was co-author of the study, published online in the Journal of Cancer Education.   She collaborated on the research with Sara Nelissen and Kathleen Bellens of the University of Leuven in Belgium.  Many other studies have focused on cancer patients using the Internet for peer support but the current research investigates how this group uses television and the Internet to access peer stories and what the emotional outcomes are.

          The study used data from the Leuven Cancer Information Survey and looked at 621 individuals diagnosed with cancer and living in Belgium.  The average age was 54 years old and mostly female. They provided personal background and indicated if they viewed television and the Internet to follow peer stories and how they felt.  Most preferred to use websites, forums and informative television programs to learn more about their disease. These forums can generate interaction between the individuals who are posting real-life stories and those who are reading the stories.  They also provide more factual and less visual information, which can be more comforting than the dramatic TV shows with emotional visual content.

          The differences between men and women diagnosed with cancer, was also looked at.  Women made significantly more use of all sources for following peer stories than the men.  If I were diagnosed with any type of cancer or life-threatening disease, I would certainly want my information from those who are either going through it or have gone through it, for more exact personal information.  I would want to know if they used any type of alternative medicine prior to any chemo treatment to build their health in giving them a better chance at survival. Perhaps some could completely avoid chemo, and that’s what I would want.  After watching my best friend die from her chemo poisoning, this would be my last resort. Gather your information personally from those who are facing the same trials you are.

Dr Fredda Branyon

DNA

Cancer Cells Hijack DNA Repair Networks

Cancer Cells Hijack DNA Repair Networks

The university of Pittsburgh Cancer Institute (UPCI) scientists have completed research that has revealed how cancer cells hijack DNA repair pathways to prevent telomeres, the end caps of chromosomes, from shortening and allowing the tumor to spread.  The findings of this research are published in the journal Cell Reports.

When a cell is formed, a countdown clock begins ticking that determines how long the cell can live.  This is the telomere, a series of repeating DNA letters at the ends of each chromosome in the cell.  But, the cancer cell cleverly hijack this telomere clock and reset it, thus lengthening the telomere every time it shortens.  The cell is then lead into thinking it is still young and can divide, spreading the tumor.

Most of the cancers do this by increasing the activity of an enzyme that lengthens telomeres, however, approximately 15% of cancers use a different mechanism for resetting the clock, called alternative lengthening of telomeres (ALT).  There is also evidence that suggests tumors that activate the ALT pathway are aggressive and more resistant to treatment.  ALT was identified close to two decades ago and identified how this mechanism works and has proven elusive.

By identifying the parts that the cancer cell tweaks to reset the countdown time might provide targets for developing new cancer drugs or making existing ones more effective, according to senior author Roderick O’Sullivan, Ph.D., assistant professor of pharmacology and chemical biology at Pitt’s School of Medicine and a member of UPCI.

The team used a recently developed technique called proximity dependent biotinylation (BioID), which allowed them to quickly identify proteins that were physically close to, and potentially associated with, telomere lengthening in cancer cells.  When they compared cancer cells in which either telomerase or ALT were active, the BioID technique identified 139 proteins that were unique to ALT-activated cells.  The team took a closer look and one enzyme, DNA polymerase, took them by surprise.

They expected to see DNA repair proteins but saw Poln was activated only in cells that were damaged by UV light that they did use in their experiments.  Knowing the molecular players in the ALT pathway opens a whole new area of research as well as potential drug targets.

The co-first authors of the study were Laura Garcia-Exposito, Ph.D., a postdoctoral fellow in O’Sullivan’s lab, and Elodie Bournique, a graduate student in the laboratory of Dr. Jean-Sebastien Hoffmann at the Cancer Research Center of Toulouse, France.

The research was funded by grants from the Competitive Medical Research Fund and Stimulating Pittsburgh Research in Geroscience at the University of Pittsburgh, National Institutes of Health grants and La Ligue contre le Cancer.

Dr Fredda Branyon