Author: Beth

News Release

LITTLE ROCK, Ark., Dec. 24 /PRNewswire/ — Scientists at the Universityof Arkansas for Medical Sciences (UAMS) have discovered the mechanism that destroys bone in the deadly cancer multiple myeloma and are developing a drug to stop or reverse the process.

John Shaughnessy, Jr., Ph.D., and his research team in the Myeloma Institute for Research and Therapy at UAMS report in the New England Journal of Medicine today that they have identified a gene, called DKK1, which causes bone lesions in multiple myeloma, leading to debilitating and intractable bone pain and a higher risk of bone fractures, spinal cord compression, and life- threatening levels of calcium in the blood.

Shaughnessy is developing a drug that will act like a sponge in the bloodstream to absorb DKK1, potentially arresting and reversing the bone destruction that is the primary effect of multiple myeloma. Almost always fatal, multiple myeloma strikes about 15,000 people in the United States each year.

“We can do it. We have the strategy. The soluble receptor should stop DKK1 from binding to bone cells,” Shaughnessy said. The potential UAMS treatments include soluble receptor therapy or monoclonal antibody therapy. Pharmaceutical companies have developed similar approaches to treat leukemias and breast cancer.

Shaughnessy’s team in the Donna D. and Donald M. Lambert Laboratory of Myeloma Genetics at UAMS found that DKK1 inactivates osteoblasts, the naturally occurring cells that cause bone growth, altering the natural balance of action between osteoblasts and bone-destroying cells called osteoclasts. “The paralysis of the bone-forming cells and the hyperactivation of osteoclasts result in a net loss of bone in patients with myeloma,” Shaughnessy said.

The UAMS research group is one of the first to use gene expression profiling to discover how a disease process works. Other researchers
have shown that mutations in the receptor for DKK1 cause two inherited bone syndromes, but the UAMS team is the first to trace elevated levels of DKK1 to multiple myeloma. Shaughnessy’s team also is exploring whether DKK1 is elevated in women with postmenopausal osteoporosis — a possibility that another UAMS scientist, Stavros Manologas, M.D., Ph.D., first suggested in the journal Science last year — or in other cancers that cause bone loss.

Shaughnessy is an associate professor of medicine in the UAMS College of Medicine and a member of the Arkansas Cancer Research Center (ACRC) at UAMS. Myeloma Institute Director Bart Barlogie, M.D., Ph.D., and researchers Yupo Ma, Ronald Walker, Fenghuang Zhan, and Erming Tian, all of UAMS, and Erik Rasmussem of Cancer Research and Biostatistics in Seattle collaborated on the study that led to identification of DKK1. Shaughnessy and Barlogie have received research funding from the National Cancer Institute, part of the National Institutes of Health, and the Fund to Cure Myeloma and the Penninsula Community Foundation.

Shaughnessy linked DKK1 to bone disease using microarray technology, which measures the activity of all 35,000 human genes in each tumor sample in an experiment. In a related project, Shaughnessy is comparing variation in gene expression with variation in response to different drug treatments in patients with myeloma, using a technique he described in the journal Blood earlier this year. Now completing a larger, more definitive study of the technique, Shaughnessy anticipates establishing a method for “personalizing” treatment of multiple myeloma on the basis of individual patients’ gene profiles in 2004.

UAMS has the largest myeloma treatment and research centers in the world. Led by Barlogie, the Myeloma Institute, located in the ACRC at UAMS, has achieved a median survival rate of six to seven years, even though the national median survival rate is roughly 2.5 to three years. Anti-DKK1 therapy may complement or even replace the current standard therapy, called autologous transplantation, which is to remove hematopoietic stem cells from the patient’s bone marrow, treat the patient with high doses of chemotherapy, and then replace the stem cells.

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I’ve set up an online cookbook to get some of the favorite recipes of MM’ers and our families and friends. Please add your recipe! When it gets well populated, I would like to try to get it printed so we can sell it to raise money for research. Let’s get some good recipes in there!

2 Men Facing Felony Spam Charges Surrender In VA

If you’re as sick of spam as I am, this will make you happy!

LEESBURG, Va. — Two men charged with running one of the most prolific spamming operations in the world surrendered Friday to Virginia authorities.

Jeremy Jaynes, of Raleigh, N.C., turned himself in to Loudoun County authorities on Friday, as did Richard Rutkowski of Cary, N.C. Both men had been free on bonds set by North Carolina authorities.

Both men were indicted last week, becoming the first people in the U.S. charged with felonies accusing them of sending unsolicited bulk e-mails. Virginia prosecutors charged them under a tough new state anti-spam law that took effect July 1.

They are accused of sending hundreds of thousands of unsolicited e-mail messages hawking everything from mortgage rates to stock schemes.

More than 50 percent of all Internet traffic across the world passes through Virginia because American Online and 1,300 other service providers or technology companies are located in northern Virginia.

Jaynes posted $125,000 bond and Rutkowski posted $60,000 bond. Both are due back in court Feb. 13.

If convicted, each could get up to 20 years in prison fines as high as $10,000.

Someone keeps sitting in my chair

Collie and PyeI took this picture of my dog & cat today. Aren’t they cute? Their names are Collie and Pye.

I saw my local oncologist yesterday. I see him every 2 months. He just asks some questions and they check my blood pressure. I asked him about the second m-spike that showed up on the last labs I had drawn there. He said that this time the second number didn’t seem significant, and may even be an error. He thought that my m-spike of 0.3 g/dL was good. Obviously, none is best! You can see my labs here.

Add Biaxin?

I emailed my doctor, asking what I can do about the small increases in my IgA. First of all, he did say that the increase can be from polyclonal IgA (the good ones). This is a possibility, since my IgG is also going up. He should be back from the ASH meeting now, and hopefully I’ll have an appointment soon. Anyway, I asked him if I should do another 4 days on/4 days off of dex, and he said he’d rather see me increase my dose of Thalomid. Hmm. Not me. I’m already feeling the effects of peripheral neuropathy from the 50 mg/day I’ve been taking since last April. I can forget I have cancer all day long, but I can’t forget I have nerve damage. So, based on the experiences of others, I am going to ask for the addition of Biaxin to my meds.

Adding Biaxin

IgA Creeping Up

My IgA is creeping up a bit. It’s back up in the 900s again, where it hasn’t been since May/June, 2003. I have emailed Dr. O. and asked if I can proceed with 4 rounds of dex at 4 days on/4 days off. No response from him yet, but I hope to hear from him soon. I expect not to have any disagreement from him. After that, I may choose to add Biaxin to my regimen.

Have you read this article?

Monthly appointment

I missed my regulary scheduled appointment because of bad weather a few weeks back, so I rescheduled for last Wednesday. That appointment was cancelled, due to the fact that my doctor was in the hospital! They said he had a virus. They’ll get in touch with me to reschedule my appointment. I’m hoping it’s soon. I missed getting my lab reports from a few weeks ago. I suppose I can call and ask them to fax the report to me.

I’m on my second day of dex and am not feeling that well from it. I have a headache and am crabby and tired! Look out everyone!

I’m thinking of asking the doc if I can add Biaxin to my treatment, to see if it’ll help get my numbers in the normal range.