American Brain Tumor Association Conference to Help...

Chicago, IL (PRWEB) July 09, 2013

While recent advances in diagnosis and treatment have improved brain tumor survival rates, persistent neurological and cognitive deficits are common according to “A New Reality: Long-Term Survivorship With a Malignant Brain Tumor,” a recently published study funded by the American Brain Tumor Association. Lead investigator of the study Mary Lovely, PhD, RN, CNRN, is among presenters scheduled to address survivorship issues at the American Brain Tumor Association’s annual Patient & Family Conference Fri., July 26 and Sat., July 27.

According to Lovely, who is also a senior advisor for the ABTA’s national programs and services, “some of these deficits prevent survivors from resuming previously routine activities and lead to profound challenges as both patients and caregivers struggle to regain control of their lives.”

Lovely will present her findings on common challenges confronting brain tumor survivors including safety concern, seizures, emotional and behavioral changes, and loss of intimacy, and how all of these issues factor into both the patient’s and the family’s new normal.

Managing post-treatment cognitive and physical side effects, regaining and maintaining strength through nutrition and fitness, the decision of “if and when” to return to work, and reconciling with limitations when resuming daily activities will also be discussed.

“For many patients and families, surviving a brain tumor is the beginning of the journey,” said Elizabeth Wilson, president and CEO of the American Brain Tumor Association. “After a brain tumor diagnosis and completion of treatments, the road to wellness can be ongoing for both the patient and the caregiver as each learns to adjust and adapt to their brain tumor survivorship. This conference features professionals from a range of disciplines who are expert in assisting individuals, couples and families in this process.”

Conference attendees will have the opportunity to hear from and speak with prominent national experts from such prestigious institutions as Cleveland Clinic, Duke University, Emory University, Mayo Clinic, MD Anderson Cancer Center, The Ohio State University and Roswell Park Cancer Institute. The presenters will be available for Q&A sessions at the conclusion of their sessions.

The conference is being held at the Renaissance Chicago O’Hare Suites Hotel, 8500 W. Bryn Mawr Ave. in Chicago. To register, visit http://www.braintumorconference.org or call 800-886-ABTA (2282).

Sponsors for the 2013 Patient & Family Conference include Genentech, Inc., Northwest Biotherapeutics, The University of Chicago Medical Center, Alexian Brothers Neuroscience Institute, Cleveland Clinic Brain Tumor and Neuro-Oncology Center, NorthShore University HealthSystem, Novocure Inc., Procure Proton Therapy Center, The Northwestern Brain Tumor Institute and The Ohio State University.

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ABOUT THE AMERICAN BRAIN TUMOR ASSOCIATION
Founded in 1973, the American Brain Tumor Association was first and is now the only national organization committed to funding brain tumor research and providing support and education programs for all tumor types and all age groups. For more information, visit http://www.abta.org.

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World's Oldest Human Tumor Discovered - Over 120,000 Years Old

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Academic Journal
Main Category: Cancer / Oncology
Article Date: 07 Jun 2013 - 0:00 PDT Current ratings for:
World's Oldest Human Tumor Discovered - Over 120,000 Years Old

Researchers have just discovered the world’s oldest tumor, in the rib of a 120,000 year old Neanderthal in Croatia.

It is a very rare discovery considering that tumors were uncommon in prehistoric populations. Tumors in fleshy tissue decay quickly - making them difficult to identify.

Spelling: both "Neandertals" and "Neandertals" are correct.

The bone was originally excavated a hundred years ago and scientists have just found out that the it has a cavity, where a tumor, known as fibrous dysplasia, replaced what should have been inner bone structure.

Fibrous dysplasia is not considered to be cancerous, because the tumors do not spread to other tissues.

According to David Frayer, professor of anthropology at the University of Kansas, and co-author of the paper:

"It's evidence that Neanderthals suffered tumors - that they were susceptible to the same kinds of diseases that we see in modern humans. Before this, the earliest tumor in bone that we've seen goes back to an Egyptian mummy. So this is 100,000 years older than the previous tumor that has been found. There is no evidence of cancer older than this in the human fossil record."

The 30-millimeter-long left rib fragment was unearthed between 1899 and 1905 in a Croatian cave that contained around 900 Neanderthal bones - hundreds of thousands of years old.

Back in the 1980s, all the bones from the cave were x-rayed and published in a book which showed each radiogram, with the exception of the rig fragment - which appeared burned out in the x-ray image.

Finally, using new high quality X-rays, researchers have been able to look at the bone more clearly.

They found that the rib contained a cavity 18 millimeters in length and 7.6 millimeters wide. After thorough analysis with radiograph and CT scans, the scientists concluded that the cavity was the site of a benign tumor associated with Fibrous dysplasia, which "is a developmental disorder of bone in which lesions develop fibrous tissue and spicules of woven bone."

Frayer said:

"It wasn't a small tumor. It was a fairly large one, probably bulging at the base of the rib. We're not sure how far along it was, but it was well-expressed in the bone. It was in the upper third of the back, and muscles attach there that are associated with raising the arm."

Frayer also mentioned that there may have been other bones involved, but they have not been identified. Adding that, although the site contained more than 900 bones "very few of them are associated one with the other. And while there are other pathologies, none of the others show evidence of a tumor."

Neanderthals are more similar to modern day humans than previously thought.

Scientists were once sure that Neanderthals had no influence on the evolutionary line of modern day humans., However, although Neanderthals died out 30,000 years ago and were a different species of human compared to modern day homo sapiens, we share much of the same DNA.

Frayer concluded:

"We have actual nuclear DNA from a number of different Neanderthals - not complete sequences - but segments of nuclear DNA. So we know that Neanderthals have a set of unique genes that were passed on to modern humans. It's about 4 percent of our genetic makeup."

By analyzing DNA extracted from three Neanderthal bones over 40,000 years old, European and the US researchers revealed that some Neanderthal DNA were passed on to humans.

Written by Joseph Nordqvist
Copyright: Medical News Today
Not to be reproduced without permission of Medical News Today

Visit our cancer / oncology section for the latest news on this subject. "Fibrous Dysplasia in a 120,000+ Year Old Neandertal from Krapina, Croatia"
Janet Monge, Morrie Kricun, Jakov Radov?i?, Davorka Radov?i?, Alan Mann, David W. Frayer
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Virus Combination Effective Against Deadly Brain Tumor, Moffitt Cancer Center Study Shows

Main Category: Cancer / Oncology
Also Included In: Neurology / Neuroscience
Article Date: 24 Jun 2013 - 1:00 PDT Current ratings for:
Virus Combination Effective Against Deadly Brain Tumor, Moffitt Cancer Center Study Shows

A combination of the myxoma virus and the immune suppressant rapamycin can kill glioblastoma multiforme, the most common and deadliest malignant brain tumor, according to Moffitt Cancer Center research. Peter A. Forsyth, M.D., of Moffitt's Neuro-Oncology Program, says the combination has been shown to infect and kill both brain cancer stem cells and differentiated compartments of glioblastoma multiforme.

The finding means that barriers to treating the disease, such as resistance to the drug temozolomide, may be overcome. The study, by Forsyth and colleagues in Canada, Texas and Florida, appeared in a recent issue of Neuro-Oncology.

"Although temozolomide improves survival for patients with glioblastoma multiforme, drug resistance is a significant obstacle," said Forsyth, the study lead author. "Oncolytic viruses that infect and break down cancer cells offer promising possibilities for overcoming resistance to targeted therapies."

The authors note that oncolytic viruses have the potential to provoke a multipronged attack on a tumor, with the potential to kill cancer cells directly through viral infection and possibly through inducing the immune system to attack the tumor. The multipronged approach might get around some of the classical resistance mechanisms that have plagued both targeted therapies and conventional chemotherapies.

Several oncolytic viruses, both alone or in combination with small molecule inhibitors, have been tested and show promise for malignant gliomas. However, most have not been effective in killing cancer cells. Two likely obstacles may be the patient's own anti-viral immune response and limited virus distribution.

"Based on our previous work with myxoma virus, we considered it to be an excellent oncolytic virus candidate against brain cancer stem cells," explained Forsyth.

The researchers found that brain cancer stem cells were susceptible to myxoma virus in the laboratory cultures (in vitro) and in animal models (in vivo), including in temozolomide-resistant cell lines.

"We also found that myxoma virus with rapamycin is a potentially useful combination. The idea that cancer cells can be killed by a harmless virus is an exciting prospect for therapy," Forsyth said.

The precise mechanism rapamycin uses to enhance infection in brain cancer stem cells is unknown, and the combination therapy does not result in cures. However, researchers are investigating other drugs that may improve the effectiveness of myxoma virus when used in combination, and they are evaluating the use of other strains of myxoma virus that might be more effective.

"Although our study adds myxoma virus to the list of oncolytic viruses capable of infecting and killing these cells, which strengthens its candidacy for clinical application, our model will need clinical application to determine its safety for patients," concluded the authors. "We expect that intracranial injections of myxoma virus will be safe based on our extensive preclinical work and the demonstrated safety of other oncolytic viruses in clinical trials."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our cancer / oncology section for the latest news on this subject. This study was supported by grants from the National Institutes of Health (R01 AI080607, R21 CA149869, and R01 CA138541).

Researchers from the University of Florida, University of Calgary, University of Texas and Ottawa Regional Cancer Centre Research Laboratories contributed to this work and publication.

H. Lee Moffitt Cancer Center & Research Institute

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Sorafenib Stops Tumor Growth And Provides The First Effective Treatment For Thyroid Cancer Patients Who Progress Following Standard Therapies

Main Category: Cancer / Oncology
Also Included In: Endocrinology;??Ear, Nose and Throat
Article Date: 04 Jun 2013 - 0:00 PDT Current ratings for:
Sorafenib Stops Tumor Growth And Provides The First Effective Treatment For Thyroid Cancer Patients Who Progress Following Standard Therapies

The kidney and liver cancer drug sorafenib holds metastatic thyroid cancer at bay for nearly twice as long as a placebo, according to results of a randomized phase III trial, which was presented by a researcher from the Abramson Cancer Center and the Perelman School of Medicine at the University of Pennsylvania in a plenary session during the American Society of Clinical Oncology's annual meeting (Abstract #4).

If approved for use in thyroid cancer patients by the Food and Drug Administration, sorafenib (Nexavar), a kinase inhibitor that mediates tumor cell division and growth of tumor blood vessels, would be the first effective agent for this patient population. Thyroid cancer is highly curable through surgery and radioactive iodine treatment, but about 10 percent of the 60,000 patients who are diagnosed with the disease each year fail to respond to standard therapies, with tumors eventually appearing in the lymph nodes, bones, lungs, and other sites. The only other drug for advanced thyroid cancer, doxorubicin, which was approved in 1974, is not used because it is highly toxic and is not effective.

"Until we began using sorafenib, we had no medical options for these patients who suffered due to progression of their disease," said Marcia S. Brose, MD, PhD, an assistant professor of Otolaryngology and Head and Neck Surgery and Hematology/Oncology, who led the study, which is known as DECISION. "Now, we can give patients hope - a breakthrough medication that can stop the progression of the disease for 5 months. This trial is the first step in a promising series of clinical trials to identify new drugs that are shifting the horizon for patients with advanced thyroid cancer."

Of the 417 metastatic thyroid cancer patients studied in the multicenter, international trial, 207 were randomized to take sorafenib, an oral drug, and 210 to a placebo arm. Twelve percent of patients experienced tumor shrinkage in the sorafenib arm, compared to 0.5 percent of patients taking a placebo. Importantly, the therapy also appeared to thwart disease progression even among many of those whose tumors did not regress: 42 patients who took sorafenib had stable disease after six months, compared to 33 percent of those in the placebo group.

Among patients taking sorafenib, median progression-free survival was 10.8 months, compared to 5.8 months among the placebo group. Patients taking the placebo were allowed to cross over into the sorafenib arm once their disease progressed; 70 percent of them did so. Overall survival data is not yet available.

The most common adverse events observed among patients taking sorafenib included hand-foot skin reaction, diarrhea, alopecia, rash, fatigue, weight loss and hypertension, all of which are consistent with findings from previous trials of the drug for its approved indications.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our cancer / oncology section for the latest news on this subject. Bayer HealthCare Pharmaceuticals and Onyx Pharmaceuticals provided funding for the trial. Editor's note: Dr. Brose has received consulting fees and honoraria from these companies.
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University of Pennsylvania School of Medicine. (2013, June 4). "Sorafenib Stops Tumor Growth And Provides The First Effective Treatment For Thyroid Cancer Patients Who Progress Following Standard Therapies." Medical News Today. Retrieved from
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Researchers reveal new potential means to suppress tumor growth

Main category: Cancer / Oncology
Also included in: genetics
Article Date: June 5, 2013-0:00 PDT current ratings for:
Researchers reveal new potential means to suppress tumor growth

Researchers at the University of California, San Diego School of Medicine, with colleagues at the University of Rochester Medical Center have identified a new mechanism that seems to remove the tumor growth, opening up the possibility of developing a new class of anti-cancer drugs.

Written in first editions online this week by the proceedings of the Academy national of Sciences (PNAS), Willis X. Li, Ph.d., Professor in the Department of medicine at UC San Diego, reports that a particular form of signaling called STAT5A protein stabilizes the formation of heterochromatin (a form of chromosomal DNA), which in turn removes the ability of cancer cells to give instructions to multiply and grow.

Specifically, Li and his colleagues concluded that the place of STAT form promotes and stabilizes the heterochromatin, which keeps DNA closely packed and inaccessible to transcription factors. "As a result, genes 'buried' in heterochromatin are not expressed," said Li.

Phosphorylation is a fundamental cellular function in which a phosphate group is added to a protein or molecule, the cause to activate or disable or modify its function. A STAT place lack of this phosphate group.

Li said that in previous studies with the fruit flies, the place of STAT caused chromatin form to condense in heterochromatin, while the phosphorylated version prompted the dispersal and loss of the heterochromatin, promoting the expression of genes.

"STAT site promotes and stabilizes the formation of heterochromatin, which in turn removes the gene transcription," Li said. "when we have expressed either HP1 (the central element of the heterochromatin) or place STAT5A in human cancer cells, several genes important for the growth of the cancer are removed." These cancer cells do not grow as fast or as large as their cancer cells parental control in xenograft models mouse."

Most suppressors tumor known, such as p53 or Rb function by inhibiting the progression of the cell cycle or by stimulating cell death or apoptosis. Li said their findings indicate a potential new way to inhibit the expression of the genes of cancer and could constitute a new class of tumour suppressors.

"We are trying to identify drugs to small molecules that can promote the formation of heterochromatin without stopping cell division or causing the death of the cell," he said. "These drugs, if found, may be effective in treating cancer with fewer side effects."

Article adapted by Medical News Today press release original. Click on "references" tab above for the source.
Visit our cancer / Oncology section for the latest news on this subject. Co-authors are Xiaoyu Hu, Amy Tsurumi and Hartmut Land, Department of biomedical genetics, University of Rochester Medical Center; Pranabananda Dutta, Jinghong Li and Jingtong Wang, Department of medicine, UCSD.
Funding of this research came, in part, grants from the National Institutes of Health R01CA131326 and RO1CA138249 and a leukemia & Lymphoma Society Research Scholar grant.
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Link Suggested Between Tumor Suppressors And Starvation Survival

Main Category: Cancer / Oncology
Also Included In: Genetics;??Eye Health / Blindness;??Pediatrics / Children's Health
Article Date: 14 May 2013 - 0:00 PDT Current ratings for:
Link Suggested Between Tumor Suppressors And Starvation Survival

A particular tumor suppressor gene* that fights cancer cells does more than clamp down on unabated cell division -- the hallmark of the disease -- it also can help make cells more fit by allowing them to fend off stress, says a University of Colorado Boulder study.

CU-Boulder Professor Min Han said the research team was interested in how a common tumor suppressor gene known as Retinoblastoma 1, or Rb, behaved under conditions of starvation. The question is important, said Han, because it may help researchers understand why many cancer cells are more susceptible to starvation or fasting than ordinary cells.

Han and his team studied a popular lab organism called C. elegans, a translucent nematode smaller than an eyelash. Many of the C. elegansC. elegans in the absence of food to look at the corresponding stress response.

"We found the tumor suppressor Rb is a critical regulator of the starvation response," said Han, who also is a Howard Hughes Medical Investigator. "Rb is known for doing more than just suppressing cell division associated with cancer -- it carries out a host of other cellular tasks including regulating development. The new findings by our group and research by other groups suggest organisms survive longer when they encounter starvation by regulating the expression of a large number of genes."

A paper on the subject was published online in Current Biology, a publication of Cell Press. The co-authors on the study, Mingxue Cui, Max Cohen and Cindy Teng, are all researchers associated with both CU-Boulder and HHMI. The study was funded by HHMI and the National Institutes of Health.

As part of the study, the researchers monitored the two- to three-week survival time of hundreds of C. elegans hatchlings in an environment with no food, which caused immediate "developmental arrest," said Han, a professor in CU-Boulder's molecular, cellular and developmental biology department. "The survival time of the young nematodes is dramatically shorter when the Rb gene is mutated, which causes changes in the activities of multiple cell signaling pathways."

The study suggests that Rb plays a critical role in maintaining a starvation-induced "transcriptome," which is the transcription of DNA to corresponding bits of RNA that allow researchers to pinpoint when and where each gene is turned on or off in the cells, he said. Under starved conditions, for example, Rb represses some responses induced by other physical stressors like pathogens and toxins.

Han said the Rb gene is mutated in a large percentage of human cancers. Hundreds of mutations in the RB gene have been identified in people with retinoblastoma, a rare type of eye cancer that usually strikes young children.

"Altogether, these findings identify Rb as a critical regulator of the starvation response and suggest a link between functions of tumor suppressors and starvation survival," the team wrote in Current Biology. "These results may provide mechanistic insights into why cancer cells are often hypersensitive to starvation treatment."

Quotes

"We found the tumor suppressor Rb is a critical regulator of the starvation response," said Min Han, a professor in CU-Boulder's molecular, cellular and developmental biology department. "Rb is known for doing more than just suppressing cell division associated with cancer -- it carries out a host of other cellular tasks including regulating development. The new findings by our group and research by other groups suggest organisms survive longer when they encounter starvation by regulating the expression of a large number of genes."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our cancer / oncology section for the latest news on this subject.
A tumor supressor gene found in the common laboratory nematode, C. elegans, has been shown to not only shut down cancerous cell division but also to fend off stress, according to a new University of Colorado Boulder study.

There are about 330 HHMI Investigators in the nation, including 15 Nobel laureates and 157 members of the National Academy of Sciences. Other HHMI Investigators at CU-Boulder include Natalie Ahn, Kristi Anseth, Tom Cech (also a Nobel laureate) and Roy Parker. In addition, HHMI Investigator Lee Niswander is at the University of Colorado Denver School of Medicine.

University of Colorado at Boulder

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Metastases from Breast Cancer May Differ from Primary Tumor

It appears that in metastatic breast cancer, the biologic characteristics of liver metastases sometimes differ from those of the primary tumor. This finding may affect treatment choices for metastases. Results of this retrospective study were presented at the 2010 annual meeting of the American Society of Clinical Oncology.

Three key biologic markers are used to determine treatment for breast cancer. These are estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2) status. These markers are expressed as positive or negative and affect the way the cancer grows. Because certain drugs are designed to stop the growth of cancer according to these markers, ER, PR, and HER2 status guide treatment choices.

The treatment of metastatic cancer (cancer that has spread to other parts of the body), is often based on the biologic markers of the primary tumor. Metastatic cancer is not always biopsied to determine its own biologic markers. If, however, metastatic cancer, such as liver metastases, has markers that differ from those of the primary tumor, the original treatment plan may not be as effective.

To evaluate the extent to which characteristics between primary breast tumors and metastases to the liver may differ, researchers in Italy compared tumor biopsies from 255 women.

Changes in ER status (from ER-negative to ER-positive and vice versa) were observed in 14.5% of liver metastases.Changes in PR status were observed in 48.6%.Changes in HER2 status were observed in 13.9%.Changes in tumor characteristics from primary to metastatic tumors resulted in changes in treatment plan for 12.1% of women.

The researchers concluded that because biologic markers of liver metastases may differ from those of primary breast tumors, biopsy of liver metastases should be considered. Accurate classification of secondary tumors by these markers may influence treatment choices.

Reference: Locatelli MA, Curigliano G, Fumagalli L, et al. Should liver metastases of breast cancer be biopsied to improve treatment choice? Presented at the 2010 annual meeting of the American Society of Clinical Oncology. June 4-8, 2010. Chicago, IL. Abstract CRA 1004.

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Identification Of Inhibitors Of Human Proteins That Promote Tumor Formation May Lead To Novel Anti-Cancer Therapeutics

Main Category: Cancer / Oncology
Also Included In: Genetics
Article Date: 07 May 2013 - 1:00 PDT Current ratings for:
Identification Of Inhibitors Of Human Proteins That Promote Tumor Formation May Lead To Novel Anti-Cancer Therapeutics

Tumor repressor genes, which inhibit tumor formation, can be "turned off" due to undesirable molecular changes affecting the chromosomes on which the genes reside. Understanding and being able to control these alterations could lead to new approaches for activating or inactivating genes linked to cancer. A novel, high-throughput screening method used to identify agents that can block one chemical modifier that plays a key role in some forms of cancer is described in ASSAY and Drug Development Technologies, a peer-reviewed journal published from Mary Ann Liebert, Inc., publishers. The article is available on the ASSAY and Drug Development Technologies website.*

Jeffrey Simard, Matthew Plant, Renee Emkey, and Violeta Yu, Amgen, Inc. (Cambridge, MA) present an optimized, robust assay for screening large numbers of chemical compounds against EZH2 methyltransferase. This enzyme is part of a multi-protein complex which can alter the methylation state of chromosomal proteins. Increased EZH2 methyltransferase activity has been associated with reduced expression of tumor repressor genes.

In the article "Development and Implementation of a High-Throughput AlphaLISA Assay for Identifying Inhibitors of EZH2 Methyltransferase" the authors describe the use of AlphaLisa technology to detect methylation by EZH2 and emphasize that this approach should accelerate the identification of small molecule inhibitors for use as research tools and for development as novel anti-cancer therapeutics.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
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