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New Drug Helps Children Fight Leukemia
Paper Cut Leads To Cancer Diagnosis For Teen

HOUSTON - February 15, 2005 - For the first time in more than a decade, there's a new drug to help children fight leukemia, Local 2 reported Tuesday.

The Food and Drug Administration recently approved clolar for children who did not respond to traditional therapies.

It has already made a difference for Houstonian Heather Carpenter, 18. She was diagnosed with leukemia in December 2002. "Everybody jokes about paper cuts and I am like, 'Hey, those paper cuts can be deadly,'" she said.

That's how Carpenter found out she had cancer -- through a simple paper cut. "It swelled up and turned black and it got infected and started going up my arm, so I had to go into immediate hand surgery.

Two days later, she began chemotherapy to beat a rare childhood cancer, AML, which is an adult form of leukemia. "It was a complete shock," Carpenter said.

After six months of chemo, Carpenter went into remission until one year later. "Complete devastation once again," she said. Her cancer was back.

This time, Dr. Terzah Horton, with Texas Children's Hospital, gave Carpenter clolar, which was a new drug still in the trial phase. "One nice thing about this drug is that it doesn't have as many heart side effects," Horton said.

That was a perfect fit for Carpenter, who had experienced heart trouble with previous drugs. "It's a significant breakthrough," Horton said.

"That was probably my favorite chemo, out of all the chemos. I know that sounds kind of weird to say," Carpenter said. It also did not affect her as much. "I didn't get too sick with it. I didn't lose my hair," Carpenter said.

Clolar helped kill Carpenter's cancer enough to allow her to have a bone marrow transplant. "I am in remission doing very well," she said.

Now in college and majoring in nursing, Carpenter hopes to make a difference in someone else's life, like one nurse at Texas Children's did for her.

"She was perfect and so nice. She made everything OK and made cancer seem not so bad," Carpenter said.

Natco Pharma launches leukemia drug

2/16/2005 - Hyderabad-based Natco Pharma Ltd. said on Wednesday that it has launched Lukatret - a medicine used in the treatment of a rare form of leukemia.

With this launch, the Company expects to further consolidate its position in the oncology segment, Natco Pharma said in a statement.

Lukatret available in the form of 10 mg. capsules (in a pack of 100 capsules) is used in the treatment of Acute Promyelocytic Leukemia (APL), according to Natco Pharma.

Lukatret is a treatment option for remission induction in newly diagnosed, relapsed and/or refractory, chemotherapy non-responsive patients and for patients where anthracycline based chemotherapy is contraindicated, said Natco Pharma.

Natco's Lukatret, which replaces the hitherto imported brands, is available at an MRP of Rs.7,000 (for a bottle of 100 capsules of 10 mg. each), against the imported medicine price varying between Rs.10,000 to Rs.12,000.

GPCA to Participate in Leukemia & Lymphoma Society Fundraiser

5/27/2005 - ATLANTA The Leukemia & Lymphoma Society announced today that the Georgia Pest Control Association (GPCA) aims to raise $100,000 statewide for the Georgia Chapters 2005 Annual Light The Night ® Walks. Thirteen GPCA companies in the Atlanta area will join as sponsors in the fight against blood cancers by forming corporate teams and participating in Atlantas Walk on Saturday, Oct. 8, at Centennial Olympic Park.

Atlanta-area GPCA sponsors include Allgood Pest Solutions, Northwest Exterminating, Arrow Exterminators, Peachtree Pest Control, Bug Busters, Carroll Exterminating, Chemical Technologies of Georgia, Corsello & Sons, Expest, Garland Services, North Fulton Exterminating, Stewart Services and Abel Tru Kill.

For more information about GPCA, visit www.gpca.org.

Study finds enzyme activity promotes rare form of leukemia, offers potential target for new drugs

CHAPEL HILL - 21-Apr-2005 - Scientists at the University of North Carolina at Chapel Hill have identified an enzyme that helps trigger the development of leukemia, a cancer of blood cells.

The enzyme hDOT1L activates a set of genes that plays a key role in the rare and largely incurable acute myeloid leukemia (AML). This disease affects less than 2 percent of the estimated 16,000 individuals diagnosed with acute leukemia nationwide each year. The discovery, based on research using bone marrow cells from mice, offers a potential target for new drugs against this form of leukemia, the researchers said.

The new findings appear in today's (April 21) issue of the journal Cell. The report demonstrates that hDOT1L helps transform, or immortalize, bone marrow cells, causing their unrestrained growth, a hallmark of leukemia, the researchers said.

Dr. Yi Zhang, associate professor of biochemistry and biophysics at UNC's School of Medicine and a member of the UNC Lineberger Comprehensive Cancer Center, led the study. Zhang is the university's first Howard Hughes Medical Institute investigator, one of the most prestigious appointments among biomedical researchers.

"We demonstrate that not only is hDOT1L required for transformation of bone marrow cells, but, more importantly, that its enzymatic activity is required to maintain the transformed status," said Zhang. "That means if we have a way to prevent the activity of hDOT1L, then the affected cells of particular leukemia patients can be killed."

Zhang investigates a group of enzymes that modifies five core histone proteins forming the molecular scaffold that helps organize DNA within the nucleus of every cell. Histone modifications affect gene activity and include methylation, in which a methyl component is attached to the histone protein.

"The prevailing model is that methylation on histones serves as a docking site," Zhang said. "It will recruit proteins that 'read' this histone modification, and it's those proteins that directly have an impact on gene expression - either activating or silencing a gene."

As an enzyme that adds a methyl component to histone H3, hDOT1L activates the gene associated with that histone. Zhang and fellow researchers now provide evidence that in some leukemias, hDOT1L activates so-called Hox genes, whose increased activity is closely tied to AML.

Leukemia most often arises from a chromosomal translocation, a breaking and joining of two distinct chromosomes, that creates a hybrid gene. The product of the hybrid gene is called a "fusion protein," meaning that the newly formed gene encodes a protein made of fragments from each of the two genes that were fused together by the rearrangement.

Some leukemia patients carry rearrangements of a gene on chromosome 11 called the mixed lineage leukemia gene, or MLL. Translocations involving MLL are most often found in childhood leukemias and as a secondary cancer in adults who have undergone chemotherapy to treat a previous leukemia.

Individuals with MLL translocations have an especially poor prognosis, with less than a 50 percent survival rate.

"There are more than 40 proteins that have been found fused to MLL in leukemia patients, and different ones can cause leukemia by different mechanisms," Zhang said.

When MLL functions as it should, without a fusion partner, it binds to and controls the expression of Hox genes, which in turn control cell growth and maturation. Until now, the role of the MLL-AF10 fusion protein in causing leukemia was unknown.

"We show how at least one MLL fusion can lead to the over-expression of Hox genes in bone marrow cells. MLL-AF10 directs hDOT1L to the Hox genes, where it normally shouldn't be, causing a different pattern of histone methylation and, therefore, extraordinarily high activity of the Hox genes," Zhang said.

Treatments used for AML patients have been largely ineffective against cells harboring the MLL-AF10 fusion protein, drawing attention to the need for a new medication.

Zhang's study reveals that leukemia cells containing MLL-AF10 require hDOT1L to survive. When the researchers introduced into leukemia cells a defective form of hDOT1L, one that cannot methylate histone proteins, the cells were no longer able to grow. "This study highlights the potential of hDOT1L as a possible drug target," Zhang added.

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Co-authors on the study from Zhang's lab include postdoctoral fellow Dr. Yuki Okada and Dr. Qin Feng, a former graduate student. Also at UNC were Drs. Qi Jang and Vernon M. Coffield, both postdoctoral fellows in the lab of Dr. Lishan Su, associate professor of microbiology and immunology. Dr. Guoliang Xu, a professor at the Shanghai Institute of Biochemistry and Cell Biology, and his graduate students Yihui Lin and Yaqiang Li also contributed.

The study was supported by a grant from the National Institutes of Health.

By STUART SHUMWAY
UNC School of Medicine

Note: Contact Zhang at (919) 966-3036 or [email protected].

Contact: L. H. Lang
[email protected]
919-843-9687
University of North Carolina School of Medicine

School of Medicine contact: Les Lang, (919) 843-9687 or [email protected]
UNC Lineberger contact: Dianne Shaw, (919) 966-7834 or [email protected]

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