The federal agency announced that it will temporarily allow the importing of a replacement drug for Doxil, a drug used in the treatment of ovarian and other cancers that has been unavailable for new patients for months.

It also said it has approved another supplier for a preservative-free version of methotrexate, a drug used for children with one type of leukemia and for treatment of bone cancer. Preservatives can cause problems for children and for those getting high doses as part of their cancer treatment. Adequate methotrexate supplies have been a problem since about 2008.

WASHINGTON — The government regulator for Fannie Mae and Freddie Mac has submitted a plan to Congress that would shrink the mortgage giants’ role in the housing market.

The Federal Housing Finance Agency’s proposal was released Tuesday and would mean fewer mortgages are backed by the government. Under the plan, Fannie and Freddie could also increase its prices to guarantee loans and establish agreements with private investors to take on added credit risk.

WASHINGTON — The $143 billion payroll tax cut won by President Barack Obama may be the last significant measure he receives from a deeply divided Congress that promises to only get more polarized as Election Day approaches.

Mr. Obama’s coveted renewal of the payroll tax cut for 160 million workers and jobless benefits for millions more caps a five-month campaign-style drive against reluctant Republicans who were eager to wipe the issue from the election-year agenda.

WASHINGTON — A noted California scientist and environmental activist has admitted that he assumed a false identity to obtain and distribute internal documents from a libertarian group that questions climate change.

In a statement published on The Huffington Post, Peter Gleick apologized for his actions, and said his judgment was clouded by his “frustration with the ongoing efforts — often anonymous, well-funded and coordinated — to attack climate science and scientists … and by the lack of transparency of the organizations involved.”

WASHINGTON — Mick Jagger, B.B. King, Buddy Guy and Jeff Beck were among the blues artists performing Tuesday in the eighth installment of the “In Performance at the White House” series in honor of Black History Month.

The concert comes a day before President Barack Obama is to speak at the construction site for the Smithsonian’s National Museum of African American History and Culture, to open in 2015.

Fans who were killed and injured last Aug. 13 when stage rigging and sound equipment collapsed onto them as they awaited a Sugarland concert at the Indiana State Fair failed to take steps to ensure their own safety, the country duo’s attorneys said in response to a civil suit. … One of four versions of Edvard Munch’s celebrated work “The Scream” will be for sale at Sotheby’s in New York on May 2, the auction house announced Tuesday.

– Compiled from news services

Article source: http://www.post-gazette.com/pg/12053/1211733-84.stm?cmpid=nationworld.xml

Transplantation of human ovarian cancer cells that were molecularly engineered to have a reduced expression of opioid growth factor receptor (OGFr), into immunocompromised mice resulted in ovarian tumours that grew rapidly.

This discovery by the researchers at The Pennsylvania State University College of Medicine, Hershey, Pennsylvania, provides fresh new insights into the pathogenesis and therapy of a lethal cancer that is the fifth leading cause of cancer-related mortality among women in the USA, and has a death rate that is unchanged for over 75 years.

The opioid growth factor (OGF)(also-termed [Met5]-enkephalin)-OGFr axis plays a fundamental role in cancer, development, and cellular renewal by regulating cell proliferation.

An important question addressed in this study relates to the requirement of this peptide-receptor system for the progression of carcinogenesis.

Human ovarian cancer cell lines that were genetically modified to underexpress OGFr grew far more rapidly in tissue culture than control (empty vector/wildtype) cell lines.

Moreover, the addition of OGF to cultures of these genetically modified cells did not respond to the inhibitory peptide and change cell number, indicating that the loss of OGFr interfered with the function of the OGF-OGFr axis with respect to regulating cell proliferation.

Immunocompromised mice injected with ovarian cancer cells that had a reduction in OGFr displayed tumours much earlier than controls, and these tumours grew faster than controls.

Putting this information together with knowledge that the pathway for OGF-OGFr regulation of cell proliferation in ovarian cancer is by way of increasing the cyclin-dependent inhibitory kinase proteins p16 and p21, we now can understand that minimizing the quantity of OGFr results in an increase in the number of cells entering the G1/S phase of the cell cycle.

This has the net effect of increasing the progression of tumorigenic events.

These results reveal the critical nature of OGFr in human ovarian cancer, and that the receptor along with its ligand, OGF, is essential for determining the course of these neoplasias.

Dr. Ian S. Zagon and Dr. Patricia J. McLaughlin discovered that endogenous opioids serve as growth factors, and have been pioneers in translating their findings from the bench to the bedside.

“Ovarian cancers frequently have a methylation of p16 that is associated with an increased progression of ovarian cancer and a loss of OGFr in ovarian tumors,” Dr. Renee N. Donahue in the Department of Neural and Behavioral Sciences, who conducted the ovarian cancer studies and its relationship to the OGF-OGFr axis, stated.

“The diminished expression of OGFr and its repercussions on tumorigenesis, only adds to the concern about the need for information concerning genetic and epigenetic changes that may impact the course of disease and its treatment.

“Our findings also hold potentially ominous overtones for those individuals taking naltrexone for addictive disorders. The dosage used for treatment of addiction blocks opioid receptors continually. The present findings that diminishing the OGF-OGFr axis by depleting the receptor exacerbates tumorigenesis, could place these patients using naltrexone at risk for accelerating disease processes that involve cell proliferation,” Dr. Donahue added.

Dr. Steven R. Goodman, Editor-in-Chief of Experimental Biology and Medicine, added that this compelling evidence confirmed the absolute requirement for OGFr (and OGF) as a tonically active inhibitory regulatory mechanism in ovarian cancer.

“As a corollary, amplifying the OGF-OGFr pathway is a novel and highly effective biotherapeutic strategy to suppress the progression of these deadly cancers,” Dr Goodman added.

The study has been published in Experimental Biology and Medicine. (ANI)

Article source: http://in.news.yahoo.com/key-understand-biology-treatment-ovarian-cancer-identified-112659247.html

SCHAUMBURG, Ill.–(BUSINESS WIRE)–

Renowned international investment and management executive Colin
Low has been named to the board of directors of Cancer
Treatment Centers of America (CTCA).

Schaumburg, Ill. (U.S.A.)-based CTCA is a rapidly growing network of
regional destination hospitals specializing in treating complex and
advanced-stage cancer with a seamlessly integrated and comprehensive
“whole person” approach to care.

“We are honored to have Mr. Low join our board,” said Richard J
Stephenson, CTCA founder and chairman. “Colin brings a wealth of
knowledge and experience about the dynamic markets in the Asia Pacific
region. He’ll help diversify the CTCA board’s commitment to deliver on
Our Mission to never stop searching for and providing powerful and
innovative therapies to heal the whole person, improve quality of life
and restore hope.”

Mr. Low is the president and chief executive officer of Singapore
Investment Development Corporation. He heads a partnership in the
private equity and capital markets sector focusing on investments and
funding for high growth companies. He was previously president of GE
International and regional growth executive in the ASEAN region for this
global firm.

“It’s an honor to join Mr. Stephenson and the CTCA team,” said Mr. Low.
“Cancer is a disease that knows no borders, nor does it recognize you by
culture or language. It devastates patients and their families in so
many ways.

I’ve never seen an organization so focused on delivering what their
customers value most. For cancer patients, it means whole-person care
that meets their individual needs. CTCA is committed to delivering the
Mother Standard® of care and Patient Empowerment Medicine®. But, when
all is said and done, it’s just the right way to do it.”

About Cancer Treatment Centers of America

Cancer Treatment Centers of America®, Inc. (CTCA) is a network of
all-digital hospitals providing a comprehensive, fully integrated
approach to cancer treatment. Independent surveys herald CTCA’s
industry-leading service-centrism and unrelenting patient focus, with
more than 95 percent of cancer patients they have helped recommending
CTCA to family members and other patients. CTCA serves patients with
complex and advanced-stage cancer from all 50 states and many foreign
countries at facilities located in suburban Chicago, Philadelphia,
Tulsa, suburban Phoenix and Atlanta (August 2012). The Patient
Empowered Care^® model at CTCA places patients at the
center of their care, encouraging and enabling patients and their
families to take an active role in treatment decision-making. For more
information about CTCA, visit www.cancercenter.com.

Cancer Treatment Centers of America
Kristin Schaner, 847-342-6454
kristin.schaner@ctca-hope.com

Article source: http://finance.yahoo.com/news/international-investment-management-executive-colin-150500474.html

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Contact: Dr. Ian Zagon
isz1@psu.edu
Society for Experimental Biology and Medicine

Researchers at The Pennsylvania State University College of Medicine, Hershey, Pennsylvania have discovered that the presence and integrity of the opioid growth factor receptor (OGFr), which mediates the inhibitory action of opioid growth factor (OGF) on cell proliferation, is a key to understanding the progression and treatment of human ovarian cancer. Transplantation of human ovarian cancer cells that were molecularly engineered to have a reduced expression of OGFr, into immunocompromised mice resulted in ovarian tumors that grew rapidly. This discovery, reported in the February 2012 issue of Experimental Biology and Medicine, provides fresh new insights into the pathogenesis and therapy of a lethal cancer that is the fifth leading cause of cancer-related mortality among women in the USA, and has a death rate that is unchanged for over 75 years.

The OGF (also-termed [Met5]-enkephalin)-OGFr axis plays a fundamental role in cancer, development, and cellular renewal by regulating cell proliferation. An important question addressed in this study relates to the requirement of this peptide-receptor system for the progression of carcinogenesis. Human ovarian cancer cell lines that were genetically modified to underexpress OGFr grew far more rapidly in tissue culture than control (empty vector/wildtype) cell lines. Moreover, the addition of OGF to cultures of these genetically modified cells did not respond to the inhibitory peptide and change cell number, indicating that the loss of OGFr interfered with the function of the OGF-OGFr axis with respect to regulating cell proliferation. Immunocompromised mice injected with ovarian cancer cells that had a reduction in OGFr displayed tumors much earlier than controls, and these tumors grew faster than controls. Putting this information together with knowledge that the pathway for OGF-OGFr regulation of cell proliferation in ovarian cancer is by way of increasing the cyclin-dependent inhibitory kinase proteins p16 and p21, we now can understand that minimizing the quantity of OGFr results in an increase in the number of cells entering the G1/S phase of the cell cycle. This has the net effect of increasing the progression of tumorigenic events. These results reveal the critical nature of OGFr in human ovarian cancer, and that the receptor along with its ligand, OGF, is essential for determining the course of these neoplasias.

The research team was comprised of Dr. Ian S. Zagon, Distinguished University Professor, and Dr. Patricia J. McLaughlin, Professor, along with Dr. Renee N. Donahue in the Department of Neural Behavioral Sciences. Drs. Zagon and McLaughlin discovered that endogenous opioids serve as growth factors, and have been pioneers in translating their findings from the bench to the bedside. Dr. Zagon states that “Over 75% of women are initially diagnosed with advanced ovarian cancer. Despite excellent initial response to cytoreductive surgery and adjuvant chemotherapy, 65% of these patients relapse within two years. However, only palliative care is available for these patients. With evidence from Phase I and II clinical trials as to the success of OGF for the treatment of advanced pancreatic cancer and knowledge presented herein that the OGF-OGFr axis is a critical determinant of the course of ovarian neoplasia, the present study raises the possibility of using this information to modulate the OGF-OGFr pathway with i) exogenous OGF, ii) imiquimod to upregulate OGFr, and/or iii) low dose naltrexone (LDN) to increase OGF and OGFr, as a therapeutic strategy for ovarian carcinoma.” Co-author Dr. McLaughlin adds that “A major problem in ovarian cancer is the need for diagnostic markers – both for early diagnosis and to monitor treatment modalities. Since some of the signaling pathways for OGF-OGFr are known (e.g., karyopherin β, Ran, p16, p21), the components of this system would represent a worthwhile focus in designing diagnostic assays.” Dr. Donahue, who conducted the ovarian cancer studies and its relationship to the OGF-OGFr axis for her doctoral dissertation, states that “Ovarian cancers frequently have a methylation of p16 that is associated with an increased progression of ovarian cancer and a loss of OGFr in ovarian tumors. The diminished expression of OGFr and its repercussions on tumorigenesis, only adds to the concern about the need for information concerning genetic and epigenetic changes that may impact the course of disease and its treatment. Our findings also hold potentially ominous overtones for those individuals taking naltrexone for addictive disorders. The dosage used for treatment of addiction blocks opioid receptors continually. The present findings that diminishing the OGF-OGFr axis by depleting the receptor exacerbates tumorigenesis, could place these patients using naltrexone at risk for accelerating disease processes that involve cell proliferation.”

Dr. Steven R. Goodman, Editor-in-Chief of Experimental Biology and Medicine, said “This compelling evidence confirms the absolute requirement for OGFr (and OGF) as a tonically active inhibitory regulatory mechanism in ovarian cancer. As a corollary, amplifying the OGF-OGFr pathway is a novel and highly effective biotherapeutic strategy to suppress the progression of these deadly cancers.”

Experimental Biology and Medicine is the journal of the Society of Experimental Biology and Medicine. To learn about the benefits of society membership visit www.sebm.org. If you are interested in publishing in the journal please visit http://ebm.rsmjournals.com/.

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Article source: http://www.eurekalert.org/pub_releases/2012-02/sfeb-abi022112.php

]]> http://nepacancer.com/2012/02/22/a-breakthrough-in-understanding-the-biology-and-treatment-of-ovarian-cancer/feed/ 0 http://nepacancer.com/2012/02/22/drug-shortages-fda-fights-problem-oks-sources-of-2-cancer-drugs/ http://nepacancer.com/2012/02/22/drug-shortages-fda-fights-problem-oks-sources-of-2-cancer-drugs/#comments Wed, 22 Feb 2012 01:25:45 +0000 admin http://nepacancer.com/2012/02/22/drug-shortages-fda-fights-problem-oks-sources-of-2-cancer-drugs/ Continue reading →]]> The Food and Drug Administration has moved to increase the supplies of two needed cancer-treatment drugs and on Tuesday issued a draft guidance on how to cope with the problem of drug shortages.

The federal agency announced that it will temporarily allow the importing of a replacement drug for Doxil, a drug used in the treatment of ovarian and other cancers that has been unavailable for new patients for months.

It also said it has approved another supplier for a preservative-free version of methotrexate, a drug used for children with one type of leukemia and for treatment of bone cancer. Preservatives in the drug can cause problems for children and for those getting high doses as part of their cancer treatment. Adequate methotrexate supplies have been a problem since about 2008.

“A drug shortage can be a frightening prospect for patients, and President Obama made it clear that preventing these shortages from happening is a top priority of his administration,” FDA Commissioner Margaret A. Hamburg said in a prepared statement. “Through the collaborative work of FDA, industry and other stakeholders, patients and families waiting for these products or anxious about their availability should now be able to get the medication they need.”

Drug shortages are a periodic woe and the Obama administration has stepped up its efforts to deal with the problem by getting advance information of impending difficulties from manufacturers. On Tuesday, the FDA increased its requirements for mandatory and voluntary notification of issues that could disrupt the supply chain, a step building on the executive order signed by the president Oct. 31.

According to the FDA, 195 drug shortages were prevented in 2011, 114 of which came after the executive order.

More than 180 drugs have been in short supply in just the last year, with cancer treatment medications usually getting the most publicity. In addition to the executive order, there is legislation pending in Congress to toughen the reporting requirement for companies facing production problems.

Some of the difficulty is also at the manufacturing end rather than just informational, the FDA acknowledged.

 “While additional manufacturing capacity is necessary to fully address the drug shortage problem, additional early notification to FDA can have a significant, positive impact on addressing the incidence and duration of drug shortages,” according to the FDA statement.

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michael.muskal@latimes.com

Article source: http://www.latimes.com/news/la-na-nn-drug-shortages-20120221,0,5438287.story?track=rss

]]> http://nepacancer.com/2012/02/22/drug-shortages-fda-fights-problem-oks-sources-of-2-cancer-drugs/feed/ 0 http://nepacancer.com/2012/02/22/reentry-into-the-world-after-breast-cancer-treatment/ http://nepacancer.com/2012/02/22/reentry-into-the-world-after-breast-cancer-treatment/#comments Wed, 22 Feb 2012 01:25:44 +0000 admin http://nepacancer.com/2012/02/22/reentry-into-the-world-after-breast-cancer-treatment/ Continue reading →]]> The body image issues continued. How could they not? After breast cancer treatment, the woman in the mirror looked like a damaged mannequin. And even with breast implants, I felt like a creature that belonged on a different planet.

“I pity the guy who checks me out and dares to come up to me,” I told a guy friend over a text message. And when he asked why, I replied, “It’s like feeling sorry for a man who hits on a drag queen thinking he is a she.” He said I didn’t make any sense.

Three weeks after radiation therapy had ended, the injuries in my chest were starting to look like a sunburn. And nearly four months after the last chemo, my eyelashes were back, my nails were starting to grow stronger and my head had enough hair for people to assume that I was going for a rebellious punk look.

Never has the link to beauty and health been more obvious. I weighed 144 pounds; my ideal is 125. I hadn’t exercised in months, so I decided to show up to a spinning class at a gym in Miami Beach. I walked out of the class after 15 minutes and nearly fainted while walking back home.

“Are you kidding me? Why would you do that?” a friend asked. “You are not well. You really need to take care of yourself. Yes, now you don’t have to go to the hospital as often. Let’s keep it that way.”

She was right.

The past five months had felt like some one had thrown me into a pool, and I had been doing my best to swim back to the surface. But as much as I wanted to think that I was getting closer to the surface, I wasn’t.

I was in the gray zone. My energy level was low, but I was healthy enough to return to work part-time, and as I attempted to do so, I caught a nasty throat infection. I love and admire my co-workers. I wanted to hug, shake hands. A few days later, I had a fever. I showed up to Dr. Alicia Rodriguez-Jorge’s office without a voice.

She had not seen me since she had given me the green light for chemotherapy last year. As I attempted to whisper my course of treatment, I covered my face with both hands and broke down in tears. I couldn’t believe I had gone through everything I had gone through. I was terrified. I didn’t want to suffer any more.

“What’s important is that you survived,” said Rodriguez-Jorge, who has a private practice near Mercy Hospital in Coconut Grove. “If there was a good time to get cancer, this was the time. You are young, and have a capacity to recover. Not everybody does.”

According to the National Cancer Institute, an estimated 229,060 new cases will be diagnosed in the United States in 2012. One in 31 women will die.

“You can slowly increase your level of activity. You can start doing some weight training to work out your legs when you start to feel better. No spinning yet,” said Rodriguez-Jorge. “Pneumonia is not uncommon after treatment. You need to get some rest.” She sent me to get a chest X-ray, lab work and antibiotics.

Before the cancer treatment, Valentine’s Day week would have been a busy one. I would have worked long hours. I also would have networked at the Social Media Miami conference, celebrated my brother’s birthday, gone to the boat show in Miami Beach, people watched at Premios Lo Nuestro in downtown and explored the Coconut Grove Arts Festival.

Article source: http://www.miamiherald.com/2012/02/21/2651806/reentry-into-the-world-after-chemo.html

]]> http://nepacancer.com/2012/02/22/reentry-into-the-world-after-breast-cancer-treatment/feed/ 0