Despite Recommendations Against it, Men Still Plan to Get PSA Tests

Washington, DC (PRWEB) July 09, 2013

Men plan to continue getting prostate-specific antigen (PSA) tests despite recommendations that suggests men should not be screened, according to a new study by researchers at RTI International.

In October 2011, the U.S. Preventive Services Task Force, an independent panel of experts in primary care and prevention, released a new recommendation advising men against getting a PSA test, which screens for prostate cancer. The task force concluded that many men are harmed as a result of prostate cancer screening and few, if any, benefit.

The study, published as an early release of the August issue of the American Journal of Preventive Medicine, surveyed 1,089 men who did not have a history of prostate cancer and were 40 to 74 years old. The survey, conducted about one month after the task force released the new recommendation, measured men’s initial response to the recommendation. Men were shown the recommendation and asked to what extent they agreed or disagreed with it and when/if they planned to get a PSA test. Men were also asked whether or not they were confident that the recommendation was based on the latest research.

The researchers found that despite the fact that most participants (61 percent) agreed with the new PSA testing recommendation and were confident that the recommendation was based on the latest research (69 percent), only 13 percent intended to follow it and not get a PSA test. More than half of men (54 percent) surveyed still plan to get a PSA test in the future, and one-third of participants were undecided.

“Since cancer screening has been promoted as a way to save lives, this recommendation may seem counterintuitive to many people,” said Linda Squiers, Ph.D., senior health communication scientist at RTI and the paper's lead author.

Men who were in their 50s were significantly more likely than men in their 40s to disagree with the recommendation not to get screened. Black men, men with higher incomes, those who had had a PSA in the previous two years, and men who were somewhat or very worried about getting prostate cancer were also more likely to say they will not follow the new recommendation.

More than 70 percent of participants did not discuss the potential benefits or harm of screening with their healthcare provider. Those who did remember such a discussion only remember hearing of the benefits of testing.

"We need to do a better job of presenting both the benefits and harms of screening to all patients and explaining the science behind the recommendation in plain language so everyone can understand it," Squiers said.

In May 2013, the American Urological Association altered its position, recommending against routine screening among men age 40 to 54 years and age 70 and older, but it continues to advocate for informed decision-making for men age 55 to 69 years.

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About RTI International
RTI International is one of the world's leading research institutes, dedicated to improving the human condition by turning knowledge into practice. Our staff of more than 3,700 provides research and technical services to governments and businesses in more than 75 countries in the areas of health and pharmaceuticals, education and training, surveys and statistics, advanced technology, international development, economic and social policy, energy and the environment, and laboratory testing and chemical analysis. For more information, visit http://www.rti.org.

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Vote against brain cancer comments on discovering the cause of...

New York, NY (press BOX) 10 July 2013

An organization dedicated to the 10th of July, voices against brain cancer, cancer, brain research and advocacy, commented a discovery by scientists who identified a cause of resistance to the therapy in cases of brain cancer.

After a 26 June 2013 ScienceDaily.com article with the title "brain cancer: A cumbersome way to therapy resistance," scientists of the German Cancer Research Center (DKFZ) and University of Heidelberg discovered that migrate microglia cells in tumors and deliver the cancer cells with a substance necessary for the repair of DNA damage. These cancer cells can then escape programmed cell death. Is this resistance mechanism to block, can lead to more effective treatments for malignant brain cancer.

Neurooncologist Professor Dr. Michael sheets which hospital conducts a cooperation unit DKFZ and Heidelberg University, says: "in the treatment of malignant gliomas, we currently radiotherapy the cancer drug Temozolomide combined with. In some patients, tumors become swiftly resistant to both treatments. We therefore need urgent new methods of treating diseases more effectively."

Michael Clipper, Chairman of voices against brain cancer, an organization for cancer brain research and advocacy, pays tribute to the scientists for this ground-breaking discovery. "This discovery is promising news for those who are affected by this terrible disease. It is reassuring to know that scientists work around the clock to find a cure for brain tumors."

VABC has a variety of initiatives for brain cancer research, awareness and support. The Organization grants research research programs of the Fund which will be monumental on the diagnosis and treatment of brain tumors. VABC funds currently research at several prestigious institutions such as Brookhaven National Laboratory, Cleveland Clinic, Columbia, Cornell, Duke, Harvard, John Hopkins, Memorial Sloan-Kettering and Yale, to name a few.

VABC's mission is to find, through the promotion of scientific research, raise awareness within the medical community and supporting patients, their families and carers with this devastating disease suffer from a cure for brain cancer.

For press inquiries, please contact: 5W-Offentlichkeitsarbeit

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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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Olaparib Active Against Advanced Ovarian Cancer and Breast Cancer with BRCA Mutations

Previously treated advanced breast and ovarian cancer patients with BRCA1 or BRCA2 gene mutation may benefit from treatment with the oral investigational drug olaparib. These findings were recently published in the journal The Lancet.[1],[2]

Although most ovarian cancer patients initially respond to platinum-based chemotherapy, most will eventually experience a return (relapse) of their cancer. Treatment of metastatic breast cancer often includes chemotherapy, but options can become limited when the cancer stops responding to conventional chemotherapy regimens. Outcomes remain poor after treatment of relapsed disease, and researchers continue to explore new approaches to treatment.

Targeted therapies are anticancer drugs that interfere with specific pathways involved in cancer cell growth or survival. Some targeted therapies block growth signals from reaching cancer cells; others reduce the blood supply to cancer cells; and still others stimulate the immune system to recognize and attack the cancer cell. Depending on the specific “target,” targeted therapies may slow cancer cell growth or increase cancer cell death.

Olaparib is an oral investigational drug called a PARP inhibitor. The PARP enzyme plays a role in DNA repair, including the repair of DNA damage from chemotherapy. Drugs that inhibit this enzyme may contribute to cancer cell death and increased sensitivity to chemotherapy.

Cancers that result from BRCA1 or BRCA2 gene mutations may be particularly responsive to PARP inhibitors. The BRCA genes provide another source of DNA repair. BRCA gene mutations result in a loss of this DNA repair capability and may make cells particularly vulnerable to the loss of other DNA repair mechanisms such as those provided by PARP.

The current Phase II studies evaluated low and high doses of olaparib in previously treated breast cancer and ovarian cancer patients with BRCA1 or BRCA2 gene mutations. Patients in both studies were treated with either 100 mg or 400 mg of oral olaparib twice a day. The studies was designed to determine overall response rate in 57 ovarian cancer patients and 54 breast cancer patients in order to validate the concept of targeting treatment for the BRCA1 or BRCA2 gene mutation, regardless of disease.

Overall response rate in the ovarian cancer study was 33% in the high-dose group and 13% in the low-dose group. Patients in the low-dose group were reported to have prognostic factors somewhat worse than the patients in the high-dose group in this study.Overall response rate in the breast cancer study was 41% in the high-dose group and 22% in the low-dose group.Side effects were tolerable in both groups.

The researchers concluded that olaparib was active in previously treated ovarian and breast cancer patients and that BRCA1 or BRCA2 mutations may play a role as a predictor for responsiveness to olaparib. Further studies are warranted to confirm these data and determine the role of BRCA mutation as a predictive biomarker that may help individualize treatment strategies for optimal results.

References:

[1] Audeh MW, Carmichael J, Penson RT, et al. Oral poly(ADP-ribose) polymerase inhibitor olaparib in patients with BRCA1 or BRCA2 mutations and recurrent ovarian cancer: a proof-of-concept trial. The Lancet [early online publication]. July 6, 2010.

[2] Tutt A, Robson M, Garber JE, et al. Oral poly(ADP-ribose) polymerase inhibitor olaparib in patients with BRCA1 or BRCA2 mutations and advanced breast cancer: a proof-of-concept trial. The Lancet [early online publication]. July 6, 2010.

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T-DM1 Produces Promising Results Against Advanced HER2-Positive Breast Cancer

Among women with metastatic, HER2-positive breast cancer, trastuzumab emtansine (T-DM1)—an investigational drug that combines HerceptinR (trastuzumab) and a chemotherapy drug—resulted in better progression-free survival than standard chemotherapy and Herceptin. The results of this Phase II clinical trial were presented at the 2011 European Multidisciplinary Cancer Congress.??

Approximately 20-25% of breast cancers overexpress (make too much of) the HER2 protein. HER2-targeted therapies such as Herceptin have dramatically improved outcomes for women with HER2-positive breast cancer, but researchers continue to explore new approaches to treatment.???

T-DM1 links Herceptin with a chemotherapy drug (DM1). T-DM1 delivers Herceptin and DM1 directly to HER2-positive cells, and limits exposure of the rest of the body to the chemotherapy.??

To evaluate T-DM1 for the initial treatment of metastatic, HER2-positive breast cancer, researchers conducted a Phase II clinical trial among 137 women. Study participants were treated with either T-DM1 or Herceptin plus TaxotereR (docetaxel).??

Survival without cancer progression was 14.2 months among women in the T-DM1 group and 9.2 months among women in the Herceptin plus Taxotere group.?In addition to delaying cancer progression, T-DM1 was also better tolerated by patients. Discontinuation of treatment due to side effects occurred in 7.2% of women in the T-DM1 group and 28.8% of women in the Herceptin plus Taxotere group.?

These results suggest that T-DM1 may be safe and effective for the treatment of advanced, HER2-positive breast cancer. Results from ongoing Phase III trials will provide additional information about this drug.?

Reference: Hurvitz S, Dirix L, Kocsis J et al. Trastuzumab emtansine (T-DM1) vs trastuzumab plus docetaxel (H+T) in previously untreated HER2-positive metastatic breast cancer (MBC): primary results of a randomized, multicenter, open-label phase II study (TDM4450g/BO21976). Presented at the 2011 European Multidisciplinary Cancer Conference. Stockholm, Sweden. September 23-27, 2011. Abstract 5001.?

Posted October 5, 2011?

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Cabozantinib Shows Promise against Bone Metastases

The investigational drug cabozantinib is showing promise against several types of advanced cancer, and may also reduce or eliminate bone metastases (cancer that has spread to the bone) in some patients. These results will be presented at the 2011 annual meeting of the American Society of Clinical Oncology.?

Metastatic cancer refers to cancer that has spread to distant sites in the body. Several types of cancer—including cancers of the prostate, lung, and breast—have a tendency to spread to the bone. Bone metastases can lead to serious problems such as fracture and spinal cord compression, and may require treatment with surgery or radiation therapy. ?

Cabozantinib is an investigational drug that targets two proteins—MET and VEGFR2—that play a role in the development and progression of many types of cancer. ?

To evaluate cabozantinib in the treatment of advanced cancer, researchers conducted a Phase II clinical trial among 398 patients. The nine types of cancer included in the study were breast, stomach/gastroesophageal junction, non-small cell lung, ovarian, pancreatic, hormone-refractory prostate, small cell lung, liver, and melanoma. At the start of the study, 39% of the patients had bone metastases.?

Patients were initially treated with 12 weeks of cabozantinib. After 12 weeks, patients who had a partial response to treatment (a reduction in detectable cancer) remained on cabozantinib, patients with stable disease (no significant change in the cancer) were randomly assigned to either continue with cabozantinib or to take a placebo, and patients with progressive (worsening) cancer were withdrawn from the study.?

By week 12, 9% of patients responded to treatment. ?For some types of cancer, cabozantinib produced high disease control rates (defined as either a reduction in cancer or stable disease). The disease control rates were 76% for liver cancer, 71% for prostate cancer, and 58% for ovarian cancer.?Among the 68 patients with bone metastases, 59 had partial or complete disappearance of the cancer on bone scans, often accompanied by significant pain relief. A majority of these patients had hormone-refractory prostate cancer, but patients with breast cancer and melanoma also experience a disappearance of bone metastases. The researchers had not expected this result.?The most common side effects were fatigue and hand-foot syndrome (pain, swelling, numbness, tingling, or redness of the hands or feet).?

In a prepared statement, the lead author of the study noted “Cabozantinib appears to have significant effects on several treatment-resistant tumors, as well as impressive effects on bone metastases. In addition, these effects are associated with rapid improvement in pain, a reduction in opiate narcotic requirements and improvement in anemia. The implications of these results are very exciting—it is unusual to find a targeted therapy, absent of a molecular mutation in tumors, that works in bony disease and has this activity.”?

Research on cabozantinib continues. ?

Reference: Gordon MS, Vogelzang NJ, Schoffski P et al. Cabozantinib (XL184) has activity in both soft tissue and bone: Results of a phase II randomized discontinuation trial (RDT) in patients (pts) w/ advanced solid tumors. Paper presented at: 2011 Annual Meeting of the American Society of Clinical Oncology; June 3-7, 2011; Chicago, IL. Abstract 3010.?

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