Wednesday, July 23, 2014

What Doctors Tell Their Friends About Preventing Cancer
By Lisa Mulcahy
Photo by Redbook
You don’t have to give up sweets"Lots of people I know think that sugar causes cancer so you should avoid it at all costs. It’s true that cancer cells do utilize sugar to grow, but when friends tell me proudly, ‘I’ve cut sweets out of my diet completely,’ I tell them, ‘You don’t need to do that.’ Now, that’s not to say you should indulge in all the soda and cupcakes you want, because data shows that a diet packed with empty calories from sugar-filled processed foods or soft drinks can up your cancer risk. But if you’re eating right, filling your plate with healthy food, it’s fine to have the occasional sweet treat. A close friend was recently diagnosed with brain cancer, and even in her situation, enjoying, say, a cookie or slice of pie is more than okay." -Nam Tran, M.D., neuro-oncologist and surgeon at H. Lee Moffitt Cancer Center and Research Institute in Tampa, FL
Related: The Magic Food Formula That Makes You Lose 

Got an abnormal pap smear? Stop smoking, pronto!

“Up to 80 percent of women have been exposed to the HPV virus by the time they hit middle age, so it’s not surprising for me to hear about this diagnosis from my friends. Most women with HPV do not develop cervical cancer. However, it’s not unusual for someone to go in for their Pap test and get abnormal results that can indicate precancer. More than one has said to me, ‘There’s nothing I can do though, right?’ My reply? ‘Uh—yeah, there is!’ Once the precancerous cells are removed, you should stop smoking to minimize the chance of a recurrence. Research has shown that carcinogens found in tobacco actually show up in a woman’s cervical mucus, and those carcinogens create a greater likelihood that HPV will be persistent, upping your risk of developing full-blown cervical cancer. Another reason to ditch the cigs!” -Lauren Streicher, M.D., associate clinical professor of obstetrics and gynecology at Northwestern University in Chicago and author of The Essential Guide to Hysterectomy

Play mole detective with your pals

“Last summer, I was having a lovely time with some houseguests by a pool, and one of my friends walked past me in his swim trunks. Suddenly, I noticed a dark spot on his back. ‘I think you have a melanoma!’ I blurted out. ‘That little mole?’ he replied. ‘I haven’t had time for a doctor to take a look at it, but I’m not worried.’ I told him, ‘That’s not just a mole. Come into my office and we’ll find out what it is for sure.’ It did turn out to be melanoma. Only a doctor can diagnose a suspicious mole as skin cancer, but really anyone can spot one. That’s why monthly self-exams are so important—and friends can examine areas we may not see, like the back and scalp. So be sensitive to your own instincts that tell you something on a friend or spouse has changed. Any mole that looks suspicious, appears out of nowhere, or changes in color or size should be checked by a physician.” -Sandra Read, M.D., spokesperson for the Skin Cancer Foundation
Related: The 25 Best Snacks for Weight Loss 

Snack on some cancer-fighting nuts

“I tell my family and friends to eat an ounce of any kind of nut they like per day; research I’ve just done shows this may powerfully prevent you from getting cancer. My study showed an 11-percent drop in cancer risk for those who ate 160 calories’ worth of tree nuts or peanuts [about an ounce, and no, peanut butter doesn’t count] on a daily, consistent basis. We think this could be because one or more minerals in nuts affect the metabolic pathways in your body in a good way-say, nuts may reduce the inflammation that directly causes some cancer cells to grow. Our study also suggested that people who eat nuts are less likely to put on weight. That’s great, because obesity is another cancer risk, so there’s an additional layer of cancer prevention for you.” -Charles Fuchs, M.D., professor at Harvard Medical School and director of the Gastrointestinal Cancer Treatment Center at Dana-Farber Cancer Institute in Boston
Don’t avoid this lifesaving test
“Friends of mine who haven’t had a colonoscopy worry about how uncomfortable the procedure is. But I tell them that’s no reason to gamble with their health. Screening can spot polyps and other changes in the colon so early that you can be treated before they even develop into cancer. You should have the test starting at age 50, or earlier if your doctor feels that your family history warrants it. I also tell my pals: The procedure is the easy part; you’re safely put under sedation so you’ll be feeling no pain. Truthfully, by the time you’re done preparing for the test-especially drinking that liquid you’re given beforehand—the most uncomfortable part is over. So schedule that appointment, and go through with it.” -Armando Sardi, M.D., surgical oncologist at Mercy Medical Center in Baltimore
Related: 9 Secret Calorie Bombs Lurking in Your Diet 

Making just one diet change can cut your cancer risk

“I tell my friends and relatives that fresh fruit absolutely needs to be in their daily diet; studies have suggested that consuming it is associated with a reduced risk of cancer. The most potent fruits are strawberries, blackberries, raspberries, blueberries, oranges, grapefruits, lemons, cherries, and red grapes. To make getting them in even easier, pick up those prepared fresh fruit cups at the grocery store. I buy them every week for my clinic staff and walk around delivering them personally, saying, ‘This is the way you can prevent cancer!’” -Gerald Gehr, M.D., oncologist/hematologist at Dartmouth-Hitchcock Norris Cotton Cancer Center in Nashua, NH

Saturday, July 19, 2014

HPV test better than Pap for assessing cervical cancer risk: study

Reuters 
By Andrew M. Seaman
NEW YORK (Reuters Health) - Testing for human papillomavirus (HPV) may be the best way to know whether a woman is at risk of developing cervical cancer in the near future, according to a new study.
Negative HPV tests provided women with more reliable assurance that they wouldn’t develop cancer or other abnormal cervical changes in the next three years, compared to traditional Pap tests, researchers report.
“Primary HPV screening might be a viable alternative to Pap screening alone,” said Julia Gage, the study’s lead author from the National Institutes of Health’s National Cancer Institute in Bethesda, Maryland.
About 12,000 U.S. women were diagnosed with cervical cancer in 2010 and about 4,000 died from the disease, according to the Centers for Disease Control and Prevention. Roughly 91 percent of cervical cancers are thought to be caused by HPV.
Pap smears, which require doctors to collect cells from the cervix to look for abnormalities, have traditionally been used to determine whether a woman is at risk of developing cancer in the near future.
In 2012, the government-backed U.S. Preventive Services Task Force recommended women between ages 21 and 65 years be screened using a Pap test every three years and said those ages 30 to 65 years could instead opt for cotesting, which is a Pap test in combination with a HPV test, every five years.
HPV is the most common sexually transmitted infection and affects both men and women. About 79 million people have the infection but most people don’t know they’re infected because symptoms are uncommon.
HPV testing also requires doctors to collect cells like they would during a Pap test but the end result is whether the woman has the virus - not abnormal cells.
“What we wanted to see is whether primary HPV screening could be a good alternative to Pap and compare it to cotesting,” Gage said.
For the new study, the researchers used data from over one million women who were between ages 30 and 64 years and screened for cervical cancer at Kaiser Permanente Northern California since 2003.
The researchers followed women who had a negative Pap or HPV test to see whether they developed cervical cancer during the next three years. They also looked at how many women developed cervical cancer in the five years following cotesting.
Overall, about 20 women out of 100,000 developed cervical cancer in the three years following a negative Pap test. That compared to 11 women out of 100,000 who developed the cancer during the three years after receiving a negative HPV test.
About 14 women out of 100,000 developed cervical cancer in the five years following negative cotests, according to results published in the Journal of the National Cancer Institute.
Gage said the findings were not surprising, since HPV is the cause of most cervical cancers.
She cautioned that the results do not foreshadow the death of Pap smears. The tests may still have a role in monitoring whether women with HPV, who are at an increased risk of cancer, go on to develop abnormal cervical cells.
“We always have to reconsider how we’re screening patients and focus on the best way to screen for certain cancer,” said Dr. Mario Leitao Jr., a gynecological surgeon at Memorial Sloan Kettering Cancer Center in New York City.
“I think this is very interesting because instead of doing (Pap tests) every three years you could do HPV (tests) every three years,” said Leitao, who was not involved with the new study.
He said there will be a lot of variables in deciding which test is best for women.
“The best way to do it is still to be determined but it’s important they have some form of cervical cancer screening at least every three years,” Leitao said.
He added that women also have to be their own advocates and tell their doctors that they don’t need Pap tests every year.
“It shouldn’t be done more frequently than every three years,” he said.
SOURCE: http://bit.ly/UckC33 Journal of the National Cancer Institute, online July 18, 2014.

US regulators fast-track novel leukemia therapy

AFP 
Nurses walk in a corridor on September 20, 2013 in a hospital in France
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View photo
Nurses walk in a corridor on September 20, 2013 in a hospital in France (AFP Photo/Philippe Huguen)
Washington (AFP) - US regulators on Monday put an experimental immunotherapy agent on the fast track to market approval, after 89 percent of leukemia patients in early trials saw their cancers disappear.
The personalized immunotherapy known as CTL019 was developed by the University of Pennsylvania and was designated a "breakthrough therapy" by the US Food and Drug Administration.
That means the experimental therapy will benefit from a speedier than average review process and will get extra attention from the FDA toward development for market.
It is the first cancer immunotherapy to receive the breakthrough designation, and only the fifth biologic agent so far.
The approach works by extracting a patient's T-cells, then genetically programming them in the lab to target cancer cells that produce a protein called CD19.
The altered T-cells are then re-injected into the patient's body, where they multiply and attack cancer.
Researchers reported last year that of 27 patients, including 22 children and five adults, with acute lymphoblastic leukemia, 89 percent had a complete response to the therapy, meaning their cancer became undetectable.
The first child to receive the treatment, Emily Whitehead, in May marked two years of being in remission, and the first adult patient has been in remission for one year.
"Our early findings reveal tremendous promise for a desperate group of patients, many of whom have been able to return to their normal lives at school and work after receiving this new, personalized immunotherapy," said the Penn research team's leader, Carl June.
The university in 2012 teamed up with pharmaceutical company Novartis to develop and license personalized chimeric antigen receptor (CAR) T cell therapies for the treatment of cancers.
In addition to the ongoing trials for acute lymphoblastic leukemia, trials using CTL019 began in the summer of 2010 in patients with relapsed and refractory chronic lymphocytic leukemia.
It is also being tried in patients with non-Hodgkin lymphoma and myeloma.
More research is also under way into CAR therapies for mesothelioma, ovarian, breast and pancreatic cancers.

Friday, July 18, 2014

Trial uses TheraSphere for the treatment of liver metastases

Living with cancer blog

Trial uses TheraSphere for the treatment of liver metastases

By Sheryl M. Ness, R.N. July 10, 2014
Mayo Clinic is studying a new way of treating colorectal cancers that have spread to the liver.
TheraSphere is a targeted way of delivering radiation through tiny glass beads containing radioactive yttrium-90.
The radioactive glass beads are only about 20-30 micrometers in diameter — about a third of the width of a human hair — and are delivered directly into the liver tumors.
TheraSphere uses radioactive microspheres that emit radiation over a period of several weeks. TheraSphere treatment is also referred to as radioembolization or selective internal radiation therapy.
TheraSphere is delivered into the hepatic artery of the liver through a catheter. The tiny radioactive beads flow directly to the liver tumor via the blood where they lodge into the small blood vessels of the tumor. The radiation destroys the tumor cells from within the tumor with minimal impact to the surrounding healthy tissue of the liver.
A new study is open at Mayo Clinic Cancer Center and others around the country using TheraSphere to treat people who have a diagnosis of colorectal cancer that has spread to the liver.
For this study, people who have disease progression with oxaliplatin or irinotecan based first line chemotherapy and are eligible for treatment will receive second-line standard-of-care chemotherapy with either an oxaliplatin-based or an irinotecan-based chemotherapy regimen. The patient's primary tumor (the colorectal cancer) must be unresectable and stable.
Those with previous radiation therapy to the liver aren't eligible. Neither are people who have cancer that has spread to other parts of the body. Additional inclusion and exclusion criteria apply.
For more information, please call the Mayo Clinic Clinical Trials Referral Office at (855) 776-0015. If you'd like to see if this trial is offered in your area, you can search for clinical trial NCT01483027 on clinicaltrials.gov.

The Future of Cancer Genomics

A new era of NGS has begun with the focus shifted from discovery to integration into the clinic.
  • Dan Koboldt
As you have probably noticed, there’s been a major shift in the focus of next-gen sequencing over the past couple of years. First it was all about new genomes, new techniques, and discovery. Now it’s all about translation. We are entering a new era in next-gen sequencing, one in which NGS technologies will not only be used for discovery, but will be integrated into clinical care.
A review in the latest issue of Human Molecular Genetics discusses NGS-enabled cancer genomics from the clinician’s point of view. In it, the authors highlight recent findings from large-scale cancer genomics efforts—such as the Cancer Genome Atlas—and offer their perspectives on the significant challenge facing us: translating the knowledge from such massive “oncogenomic” datasets to the clinic.

Large-Scale Tumor Genomics Studies

Ambitious efforts by the Cancer Genome Atlas (TCGA) and the International Cancer Genomics Consortium (ICGC) have provided, in the last few years, comprehensive molecular profiles of the most common cancer types. Some of the key findings included:
Glioblastoma (GBM)—TCGA’s first integrative analysis, a study of 91 tumors, revealed:
  • Frequent mutations affecting TP53 (37% of tumors) and NF1 (14%).
  • A subset of tumors with epigenetic abnormalities (MGMT promoter methylation) and hypermutation.
  • Gene expression-based definition of four subtypes: proneural, neural, classical, and mesenchymal.
Ovarian Cancer—TCGA’s study on 489 patients with serous ovarian cancer reported:
  • Nearly all tumors had mutation and/or deletion of tumor suppressor TP53.
  • Nine further genes, including NF1, BRCA1/2, RB1, and CDK12 were significantly mutated.
  • Ovarian carcinomas also harbored extensive copy number alteration and promoter methylation.
Colorectal Cancer—A study of 276 colorectal carcinomas found that among these tumors:
  • 16% were hypermutated: 3/4 with microsatellite instability, hypermethylation, and MLH1 silencing; 1/4 with mutations in DNA repair genes.
  • Frequent alteration of the WNT, MAPK, PI3K, TGF-B, and TP53 pathways.
  • 24 significantly mutated genes, including known (APC, TP53, SMAD4, PIK3CA, and KRAS) as well as novel (ARID1A, SOX9, and FAM123B).
Lung Squamous Cell Carcinoma—TCGA also profiled 178 lung SqCCs, which exhibited:
  • Very high mutation rates (~360 coding mutations, ~165 rearrangements, and ~323 CNAs per tumor).
  • TP53 mutations in almost every tumor.
  • Frequent alteration of CDKN2A/RB1 (72%), PI3K/AKT (47%), and squamous differentiation (44%) pathways.
  • 7% of cases with EGFR amplification resulting in sensitivity to erlotinib and gefitinib.
  • Breast Carcinoma
  • The largest sequencing study from TCGA to date included a comprehensive molecular profile of 510 breast tumors. Some of the highlights:
  • Significantly mutated genes included classical ones (PIK3CA, PTEN, AKT1, TP43, etc.) as well as novel ones (TBX3, RUNX1, CBFB, etc.).
  • Key differences in mutation patterns between luminal A, luminal B, Her2-enriched, and basal-like subtypes.
  • Frequent mutation of TP53 and PIK3CA genes (29%).
Endometrial Cancer—TCGA’s extensive characterization of 373 endometrial carcinomas revealed that:
  • Uterine serous tumors and 25% of high-grade endometrioid tumors had many CNAs and frequent TP53 mutation, but low DNA methylation changes and progesterone/estrogen receptor expression.
  • Most endometrioid tumors had few copy number alterations or TP53 mutations, but frequent mutations in PTEN, CTNNB1, PIK3CA, ARID1A, KRAS, and novel SMG ARID5B.
  • A subset of endometrioid tumors had a markedly increased transversion mutation frequency and hotspot mutations in POLE.
  • Tumors fell into one of four groups: ultramutated, microsatellite instability hypermutated, copy-number low, and copy-number high.

Global Oncogenomics Findings

A systematic analysis of 3,281 tumors from 12 cancer types by Kandoth et al., offered a global picture of the genomics of common human cancers. Many tumor types had mutations in chromatin remodeling genes (MLL2, MLL4, or the ARID gene family). TP53 was the most common mutated gene overall. Mutations in that gene and six others (BAP1, DNMT3A, HGF, KDM5C, FBX7, and BRCA2) were significantly associated with poor survival. Large alterations (CNAs, SVs), clearly have an important role in tumor biology, and gene/miRNA expression profiling allows stratification of tumors into subtypes, often ones that correlate with clinical outcomes. Even within one tumor type, the mutational profiles suggested that few driver genes were shared across subtypes.
The broader conclusion from these and from so-called pan-can studies is that cancer represents a wide variety of diseases originating from different organs. Clustering genomic data across organs will therefore allow a biology-driven approach, focusing more on key genes and cellular pathways and less on simple tumor morphology.

Clinical Translation of Cancer Genomics

The real question, now that we’ve made considerable progress, is how to make use of that information in the clinic. Many institutions have launched personalized oncology programs, which consider tumor mutation and/or gene expression profiling. Early reports suggest that 30–70% of cases will harbor mutations that are “actionable” for targeted therapy or patient stratification. The poster child for this might be the identification of BRAF as a driver gene in melanoma, which led to the use of BRAF inhibitors in melanomas that harbor the V600E mutation. It’s a wonderful story, but the simple fact is that most targeted therapies didn’t emerge from large-scale genomics studies, but from a deep understanding of specific pathways involved in defined tumor types.
Further, the successful identification (and targeted therapy against) a driver mutation in one tumor type does not guarantee it will work in another type. Other factors—tissue specificity, genetic environment, and tumor micro-environment—must be considered as well.
In many current clinical trials, gene expression and mutation data are being concomitantly assessed for insight into patient stratification and therapeutic response. These sorts of trials are necessary to close the gap between new knowledge from large-scale cancer genomics and its application in the clinic. The feedback loop needs to work both ways: Clinical trial results should inform future oncogenomics studies as well.
It’s clear that we will both creativity and cross-discipline expertise to carry the mission forward from here. Specifically, we’ll need:
  • Continued efforts to develop large, high-resolution, clinical-genomics datasets
  • Better and earlier access to drugs
  • Cross-discipline expertise in cancer, genomics, and informatics (“onco-bioinformaticians”)
  • Integration of genomic data into clinical tumor board discussions
Beating cancer is an important but incredibly difficult mission, and it won’t be solved by one scientific discipline alone. Collaborative efforts by cross-discipline teams are going to be necessary. Let’s get going.

New gene discovered that stops the spread of deadly cancer

Salk scientists identify gene that fights metastasis of a common lung cancer.