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December 27, 2005

Mechanisms Of Cancer Generation

Mechanisms Of Cancer Generation
Johns Hopkins researcher, with colleagues in Sweden and at the Fred Hutchinson Cancer Research Center, suggests that the traditional view of cancer as a group of diseases with markedly different biological properties arising from a series of alterations within a cell's nuclear DNA may have to give way to a more complicated view. In the recent issue of Nature Reviews Genetics, available online Dec. 21, he and colleagues suggest that cancers instead begin with "epigenetic" alterations to stem cells.

"We're not contradicting the view that genetic changes occur in the development of cancers, but there also are epigenetic changes and those come first," says lead author Andrew Feinberg, M.D., M.P.H., King Fahd Professor of Medicine and director of the Center for Epigenetics in Common Human Disease at Johns Hopkins.

Cells affected by epigenetic changes look normal under a microscope at low levels of resolution, Feinberg says, "but if you look carefully at the genome, you find there are subtle changes." By tracking these changes, he suggests, doctors potentially could treat people before tumors develop in much the same way as cardiologists prescribe cholesterol-lowering drugs to help prevent heart disease.

Epigenetic changes -- those that don't affect the gene's sequence of DNA but change the gene in other ways -- influence a wide variety of human diseases, including cancer, birth defects and psychiatric conditions. Epigenetic alterations include the turning off or quieting of genes that normally suppress cancer and the turning on of oncogenes to produce proteins that set off cancerous behavior.

Epigenetic changes are found in normal cells of patients with cancer and are associated with cancer risk, Feinberg notes.

As one example, as per a research findings published in the Feb. 24, 2005, online version of Science, Feinberg and his colleagues in the United States, Sweden and Japan reported that mice engineered to have a double dose of insulin-like growth factor 2 (IGF2) had more primitive precursor cells in the lining of the colon than normal mice. When these mice also carried a colon-cancer-causing genetic mutation, they developed twice as a number of tumors as mice with normal IGF2 levels. The extra IGF2 stemmed not from a genetic problem, or mutation, but from an epigenetic problem that improperly turned on the copy of the IGF2 gene that should have remained off.........

Daniel      Permalink

December 27, 2005

Breast Cancer Numbers Increase Among New Zealand Women

Breast Cancer Numbers Increase Among New Zealand Women Evans Bay New Zealand
The number of women in the upper South Island diagnosed with breast cancer is soaring as access to screening services improves.

Pressure is now on therapy providers who are faced with an influx of newly diagnosed cancer patients seeking radiotherapy or chemotherapy.

Mammographies provided by BreastScreen South led to 244 women in Canterbury, Nelson, Marlborough and the West Coast being diagnosed with breast cancer in the year to November. That figure compares with 159 the prior year and 143 the year before that.

A Canterbury District Health Board manager says the extra costs of treating the women with chemotherapy have added to a $2.48 million budget overrun in Christchurch Hospital's medical and surgical services division this financial year.

The age range for Government- funded breast cancer screening was extended in July last year to include all women aged 45 to 69.

However, a lack of staff and equipment meant women in the younger age bracket have only recently been able to access the programme.

Breast cancer is the leading cause of cancer deaths among New Zealand women. About 2200 women develop the disease each year and 640 die from it.

BreastScreen South clinical director Richard Chisholm said the higher number of diagnoses showed the screening extension had been a success. "It's a predictable increase, but over all we're pleased that we're detecting breast cancers".

He said some of the extra women would have been picked up anyway through private screening or by going to their GP after finding a lump.........

Emily      Permalink

December 25, 2005, 10:32 AM CT

Merry Christmas To All Our Readers

Merry Christmas To All Our Readers
Medicineworld wishes all our readers merry Christmas.

Oh, jingle bells, jingle bells

Jingle all the way

Oh, what fun it is to ride

In a one horse open sleigh

Jingle bells, jingle bells

Jingle all the way

Oh, what fun it is to ride

In a one horse open sleigh........

Daniel      Permalink

December 23, 2005

Langerhans Cells And Immune System

Langerhans Cells And Immune System Langerhans cells in red
The langerhans cells are marked in red and another cell type are in green. Wild-type mice are on the bottom and have both the red and green cells. Then transgenic mice are on the top and still have the green cells but the red cells are missing.

New Haven, Conn. - Scientists at Yale School of Medicine have demonstrated that Langerhans cells in the skin, which had been thought to alert the immune system to pathogens, instead dampen the skin's reaction to infection and inflammation.

This has the potential to significantly alter understanding of the mechanisms underlying a number of skin disorders such as psoriasis, lupus and skin cancer.

Dendritic cells are found throughout the body and are extremely efficient at alerting the immune system to the presence of pathogens and other foreign materials. Langerhans cells are dendritic cells in the skin. Skin is an important barrier to infection and it has been generally assumed that the Langerhans cells only serve to warn the immune system of skin pathogens.

According to the study, featured on the cover of the December 15 issue of Immunity, Langerhans cells are not mandatory and, in fact, inhibit or modulate immune responses in the skin.

Daniel H. Kaplan, M.D., and Mark J. Shlomchik, M.D., used a technology called Bacterial Artificial Chromosome transgenics to develop a mouse model that lacks Langerhans cells in the skin from birth. They stimulated the skin of these mice to create hypersensitivity similar to a poison ivy reaction. They expected that mice without Langerhans cells would have less immune response in the skin.

"Unexpectedly, instead of a decreased immune response to contact hypersensitivity, we found a reproducible and significant increase," said first author Kaplan, assistant professor in the Department of Dermatology at Yale School of Medicine. "Langerhans cells are thus not mandatory to generate immune responses in the skin and more profoundly, they actually regulate immune responses in the skin".........

JoAnn      Permalink

December 23, 2005

Chinese Remedy For Breast Cancer

Chinese Remedy For Breast Cancer
A derivative of the sweet wormwood plant used since ancient times to fight malaria and shown to precisely target and kill cancer cells may someday aid in stopping breast cancer before it gets a toehold.

In a new study, two University of Washington bioengineers found that the substance, artemisinin, appeared to prevent the onset of breast cancer in rats that had been given a cancer-causing agent. The study appears in the latest issue of the journal Cancer Letters.

"Based on earlier studies, artemisinin is selectively toxic to cancer cells and is effective orally," according to Henry Lai, research professor in the Department of Bioengineering, who conducted the study with fellow UW bioengineer Narendra P. Singh, a research associate professor in the department. "With the results of this study, it's an attractive candidate for cancer prevention".

The properties that make artemisinin an effective antimalarial agent also appear responsible for its anti-cancer clout. When artemisinin comes into contact with iron, a chemical reaction ensues that spawns free radicals -- highly reactive chemicals that, when formed inside a cell, attack the cell membrane and other structures, killing the cell.

The malaria parasite can't eliminate iron in the blood cells it eats, and stores it. Artemisinin makes that stored iron toxic to the parasite.

The same appears to be true for cancer. Because they multiply so rapidly, most cancer cells have a high rate of iron uptake. Their surfaces have large numbers of receptors, which transport iron into the cells. That appears to allow the artemisinin to selectively target and kill the cancer cells, based on their higher iron content.

In the latest study, the researchers administered to rats a single oral dose of 7,12-dimethylbenz[a]anthracene, a substance known to induce multiple breast tumors. Half of the rats then were fed regular food, while the other half were fed food with 0.02 percent artemisinin added. For 40 weeks, researchers monitored each group for the formation of breast tumors.........

Emily      Permalink

December 23, 2005

Epstein-Barr Virus In Blood Cancers

Epstein-Barr Virus In Blood Cancers
Earlier this year, scientists at the University of Pennsylvania School of Medicine identified a link between a critical cancer pathway and an Epstein-Barr Virus (EBV) protein known to be expressed in many EBV-associated cancers. Their findings demonstrated a new mechanism by which EBV can transform human B cells from the immune system into malignant cells, which can lead to B-cell lymphomas. Now, they have found that the viral protein--called EBNA3C (for EBV nuclear antigen)--mediates the degradation of the retinoblastoma protein, an important molecular brake for cell proliferation.

Erle S. Robertson, PhD, an Associate Professor of Microbiology who leads the Tumor Virology Program at Penn's Abramson Cancer Center, and MD/PhD student Jason Knight, published their results last week in the Proceedings of the National Academy of Sciences.

The retinoblastoma protein (Rb) is a major regulator of several genes in charge of cell proliferation and cell-cycle regulation. In the nucleus, Rb normally binds to E2F, turning off genes involved with cell proliferation. Using human cell cultures infected with the Epstein-Barr virus, the researchers found that EBNA3C recruits a group of molecules called the SCF complex, which attaches ubiquitin to Rb. This inadvertently tags Rb for degradation by the proteosome machinery, the cell's recycling plant. With Rb out of the way, the cell now reproduces uncontrollably.

"It's as simple as that, but it's a major mystery solved that a number of scientists have been working on for at least 15 years," says Robertson.

EBV, a member of the herpesvirus family and one of the most common human viruses, plays a role in cancers such as lymphoproliferative diseases in transplant or AIDS patients, Burkitt's lymphoma, Hodgkin's lymphoma, and nasopharyngeal carcinoma, and also causes the well-known disease infectious mononucleosis. As a number of as 95 percent of adults 20 years and older have been infected with EBV, but show no symptoms.........

Daniel      Permalink

December 23, 2005

Test For Patients With Colorectal Cancer

Test For Patients With Colorectal Cancer
University of Chicago scientists have licensed a genetic test that determines which patients are likely to have a serious adverse reaction to irinotecan hydrochloride (Camptosarandreg;), a key component of the standard first-line therapy for advanced cancers of the colon and rectum, to Mayo Clinic.

Until now, the UGT1A1 test has only been available to patients enrolled in studies at the University of Chicago. Third Wave had received FDA approval for its UGT1A1 test kit in August, but the test had still not been made available to patients.

Through this licensing agreement, Mayo Clinic's reference laboratory, Mayo Medical Laboratories (MML), will make the test available to patients nationwide, starting this month.

The UGT1A1 test was developed and patented by Mark J. Ratain, MD, the Leon O. Jacobson Professor of Medicine and Chairman of the Committee on Clinical Pharmacology and Pharmacogenomics at the University of Chicago, and his colleagues. It gives doctors advance knowledge of an individual's risk for toxicity from irinotecan by revealing whether patients have one of two common versions of a gene that encodes for a protein involved in the metabolism of irinotecan.

"Eventhough most patients tolerate the drug quite well, some patients are genetically predisposed to severe side effects from irinotecan therapy," said Ratain. "The UGT1A1 test enables us to know in advance which patients are at risk. Those patients could be given reduced doses of irinotecan or other chemotherapy drugs".

This kind of customized dosing based on a person's genetic makeup is known as pharmacogenomics and is at the forefront of 21st century medicine. The UGT1A1 test is part of a growing list of pharmacogenomic tests designed to help physicians personalize therapy options.........

Sue      Permalink

December 21, 2005

It's never too late to quit smoking

It's never too late to quit smoking
There is never a bad time to stop smoking, but there is no time like the present to quit. November is Lung Cancer Awareness month, and with the holiday season approaching, quitting smoking is the best gift smokers can give themselves, their families and their friends.

According to the American Cancer Society, smoking is the most preventable cause of death in the United States, accounting for 440,000 deaths, or nearly one of every five deaths, each year. It also causes more than 80 percent of all lung cancers and increases the risk for a number of other types of cancer, including oral, throat pancreatic, uterine, bladder, and kidney cancers.

"Our most effective tool for treating lung cancer is to prevent it from ever happening," explains Bruce E. Johnson, MD, director of the Lowe Center for Thoracic Oncology at Dana-Farber Cancer Institute in Boston.

Johnson emphasizes that it is never too late to quit. People who stop and remain a nonsmoker for at least 10 to 20 years can cut their risk of developing lung cancer in half. Even those who quit smoking in their 60s, 70s, and 80s benefit by reducing their risk of dying from a heart attack or from developing lung or head and neck cancer, says Johnson.

Johnson offers the following tips to help people to quit smoking:

First, commit to quit

  • Remember reason for wanting to quit: Family, children, personal health

  • Tell friends and family

  • Recruit the help, support and encouragement of family and friends
  • ........

    Janet      Permalink

    December 21, 2005

    Marine Bacteria Compound For Multiple Myeloma

    Marine Bacteria Compound For Multiple Myeloma Dharminder Chauhan, PhD
    An anti-cancer compound derived from bacteria dwelling in ocean-bottom sediments appears in laboratory tests to be a potent killer of drug-resistant multiple myeloma cells, and potentially with less toxicity than current therapys, report Dana-Farber Cancer Institute scientists in the recent issue of Cancer Cell.

    The experimental compound, NPI-0052, has been found to block or inhibit cancer cells' proteasomes from working effectively. The proteasome work as a cell's "garbage disposal," chewing up and disposing of old, unwanted proteins. With their proteasome jammed, cells die from the backup of damaged proteins.

    "Proteasome inhibition is a key therapeutic target and bortezomib (Velcadeā„¢) was the first in a new class of compounds in multiple myeloma. NPI-0052 is a novel proteasome inhibitor with a chemical structure and action that is distinct from bortezomib, and has the promise of being even more effective for patients," says Kenneth Anderson, MD, director of the Jerome Lipper Multiple Myeloma Center at Dana-Farber, and senior author of the report.

    The compound will be moved into Phase I clinical trials in early 2006, say officials of Nereus Pharmaceuticals in San Diego, the developer of NPI-0052. The compound will be tested as a single agent and subsequently in combination with other therapys.

    Multiple myeloma is a currently incurable cancer of the bone marrow that causes a plunge in the production of vital red and white blood cells. Eventhough relatively rare, it is the second most common type of blood cancer and accounts for 11,000 deaths annually in the United States. Bortezomib, approved by the Food and Drug Administration in 2003 for relapsed myeloma patients and subsequently for patients who have received at least one previous therapy, demonstrated in clinical trials that it extended the time to disease progression and also improved survival.........

    Daniel      Permalink

    December 21, 2005

    Novel mechanism for blood disease

    Novel mechanism for blood disease
    Approximately 80,000 to 100,000 people in the United States suffer from myeloproliferative disease, a broad category of ailments characterized by overproduction of different types of blood cells. Often these diseases lead to cancers of blood cells. Scientists at Whitehead Institute for Biomedical Research and Brigham and Women's Hospital have discovered an unusual mechanism underlying this condition, and their findings may lay the foundation for future drug development.

    As people age, their genes acquire mutations. In a patient with myeloproliferative disease, a mutation occurs in a specific kind of protein called a kinase, that is, a protein that adds a small molecule called a phosphate to other proteins, in this case proteins involved in blood-cell growth. But the mutation alone will not produce the disease. The mutant kinase, named JAK2V617F, causes the condition only after binding to another molecule. This makes myeloproliferative disease an unusual disease of overproduction of cells, since a number of other kinase mutations lead directly to cell proliferation.

    "Surprisingly, this mutant kinase is completely dependent on a cell-surface protein for its transforming potential," says Whitehead Member Harvey Lodish, whose lab made the discovery in collaboration with D. Gary Gilliland of Brigham and Women's. Their results will be published online in Proceedings of the National Academy of Sciences during the week of December 19.

    "This paper provides new and important insights into how this gene contributes to the development of myeloproliferative disease and it should provide an important foundation for subsequent development of new drugs," says Gilliland, who is also a Howard Hughes Medical Institute investigator.

    Gilliland's lab was one of several to identify the precise genetic mutation responsible for myeloproliferative disease when they discovered that the exact same genetic mutation in a kinase called JAK2 causes many distinct disorders that fall under the myeloproliferative disease umbrella. After publishing this finding in Cancer Cell in April, Gilliland turned to Lodish lab researchers, who designed experiments that shed light on the mechanism behind the disease.........

    Daniel      Permalink

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    Did you know?
    Studies in monkeys and women suggest that unlike traditional estrogen therapy, a diet high in the natural plant estrogens found in soy does not increase the risk of uterine cancer in postmenopausal women, according to Mark Cline, D.V.M., Ph.D., an associate professor of comparative medicine at Wake Forest University Baptist Medical Center. Archives of cancer news blog

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