Pic Of The Day
Posted by rob on May 20, 2005 under Uncategorized | 
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A hummingbird hovers near a drinking fountain in Manizales, Colombia.
Pic Of The Day
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Indian boys sit on the roof of a house during sunset in the northern Indian city of Jammu.
Pterostilbene and 3′-hydroxypterostilbene are effective apoptosis-inducing agents in MDR and BCR-ABL-expressing leukemia cells.
Posted by rob on May 18, 2005 under Uncategorized | Be the First to Comment
Tolomeo M, Grimaudo S, Cristina AD, Roberti M, Pizzirani D, Meli M, Dusonchet L, Gebbia N, Abbadessa V, Crosta L, Barucchello R, Grisolia G, Invidiata F, Simoni D
Int J Biochem Cell Biol. 2005 Aug ; 37(8): 1709-26
Pterostilbene and 3,5-hydroxypterostilbene are the natural 3,5-dimethoxy analogs of trans-resveratrol and piceatannol, two compounds which can induce apoptosis in tumor cells. In previous studies we demonstrated the importance of a 3,5-dimethoxy motif in conferring pro-apoptotic activity to stilbene based compounds so we now wanted to evaluate the ability of pterostilbene and 3,5-hydroxypterostilbene in inducing apoptosis in sensitive and resistant leukemia cells. When tested in sensitive cell lines, HL60 and HUT78, 3′-hydroxypterostilbene was 50-97 times more potent than trans-resveratrol in inducing apoptosis, while pterostilbene appeared barely active. However, both compounds, but not trans-resveratrol and piceatannol, were able to induce apoptosis in the two Fas-ligand resistant lymphoma cell lines, HUT78B1 and HUT78B3, and the multi drug-resistant leukemia cell lines HL60-R and K562-ADR (a Bcr-Abl-expressing cell line resistant to imatinib mesylate). Of note, pterostilbene-induced apoptosis was not inhibited by the pancaspase-inhibitor Z-VAD-fmk, suggesting that this compound acts through a caspase-independent pathway. On the contrary, 3′-hydroxypterostilbene seemed to trigger apoptosis through the intrinsic apoptotic pathway: indeed, it caused a marked disruption of the mitochondrial membrane potential DeltaPsi and its apoptotic effects were inhibited by Z-VAD-fmk and the caspase-9-inhibitor Z-LEHD-fmk. Moreover, pterostilbene and 3′-hydroxypterostilbene, when used at concentrations that elicit significant apoptotic effects in tumor cell lines, did not show any cytotoxicity in normal hemopoietic stem cells. In conclusion, our data show that pterostilbene and particularly 3′-hydroxypterostilbene are interesting antitumor natural compounds that may be useful in the treatment of resistant hematological malignancies, including imatinib, non-responsive neoplasms.
Lonafarnib reduces the resistance of primitive quiescent CML cells to imatinib mesylate in vitro.
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Jørgensen HG, Allan EK, Graham SM, Godden JL, Richmond L, Elliott MA, Mountford JC, Eaves CJ, Holyoake TL
Leukemia. 2005 May 12;
Recent studies indicate that a rare population of primitive quiescent BCR-ABL(+) cells are innately insensitive to imatinib mesylate (IM) and persist after IM therapy of patients with chronic myeloid leukemia (CML). New approaches to the eradication of these cells are therefore likely to be crucial to the development of curative therapies for CML. We have now found that Ara-C, LY294002 (a PI-3 (phosphatidylinositol-3′ kinase) kinase inhibitor), 17AAG (a heat-shock protein (HSP)-90 antagonist) and lonafarnib (a farnesyltransfease inhibitor) all enhance the toxicity of IM on K562 cells and on the total CD34(+) leukemic cell population from chronic phase CML patients. However, for quiescent CD34(+) leukemic cells, this was achieved only by concomitant exposure of the cells to lonafarnib. Ara-C or LY294002 alone blocked the proliferation of these cells but did not kill them, and Ara-C, LY294002 or 17AAG in combination with IM enhanced the cytostatic effect of IM but did not prevent the subsequent regrowth of the surviving leukemic cells. These studies demonstrate the importance of in vitro testing of novel agents on the subset of primary leukemic cells most likely to determine long-term treatment outcomes in vivo.Leukemia advance online publication, 12 May 2005; doi:10.1038/sj.leu.2403785.
Lonafarnib reduces the resistance of primitive quiescent CML cells to imatinib mesylate in vitro.
[Cardiac manifestations of the idiopathic hypereosinophilic syndrome.]
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Harzy T, Allali F, Amine B, Rahmouni R, Hajjaj-Hassouni N
Rev Med Interne. 2005 May ; 26(5): 386-392
Back ground. – The aim of our study is to describe the more common cardiac manifestations of idiopathic hypereosinophilic syndrome representing the major cause of mortality. Main points. – Current therapy consists of corticosteroid, hydroxyurea and interferon alpha. Recent publications confirm the activity of imatinib mesylate, a selective tyrosine kinase inhibitor, in patients with idiopathic hypereosinophilic syndrome. In cases with marked valvular compromise or with endomyocardial thrombosis or fibrosis, cardiac surgery can provide substantial benefits. Perspectives. – A better understanding of the pathophysiology of this syndrome could lead to the development of new therapeutic agents.
[Cardiac manifestations of the idiopathic hypereosinophilic syndrome.]
Cost Effectiveness of Imatinib Compared with Interferon-alpha or Hydroxycarbamide for First-Line Treatment of Chronic Myeloid Leukaemia.
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Dalziel K, Round A, Garside R, Stein K
Pharmacoeconomics. 2005; 23(5): 515-26
OBJECTIVE: To evaluate the cost utility of imatinib compared with interferon (IFN)-alpha or hydroxycarbamide (hydroxyurea) for first-line treatment of chronic myeloid leukaemia. DESIGN AND SETTING: A cost-utility (Markov) model within the setting of the UK NHS and viewed from a health system perspective was adopted. Transition probabilities and relative risks were estimated from published literature. Costs of drug treatment, outpatient care, bone marrow biopsies, radiography, blood transfusions and inpatient care were obtained from the British National Formulary and local hospital databases. Costs ( pound, year 2001-03 values) were discounted at 6%. Quality-of-life (QOL) data were obtained from the published literature and discounted at 1.5%. The main outcome measure was cost per QALY gained. Extensive one-way sensitivity analyses were performed along with probabilistic (stochastic) analysis. RESULTS: The incremental cost-effectiveness ratio (ICER) of imatinib, compared with IFNalpha, was pound26 180 per QALY gained (one-way sensitivity analyses ranged from pound19 449 to pound51 870) and compared with hydroxycarbamide was pound86 934 per QALY (one-way sensitivity analyses ranged from pound69 701 to pound147 095) [ pound1 = $US1.691 = euro1.535 as at 31 December 2002].Based on the probabilistic sensitivity analysis, 50% of the ICERs for imatinib, compared with IFNalpha, fell below a threshold of approximately pound31 000 per QALY gained. Fifty percent of ICERs for imatinib, compared with hydroxycarbamide, fell below approximately pound95 000 per QALY gained. CONCLUSIONS: This model suggests, given its underlying data and assumptions, that imatinib may be moderately cost effective when compared with IFNalpha but considerably less cost effective when compared with hydroxycarbamide. There are, however, many uncertainties due to the lack of long-term data.
Expression of c-Fes protein isoforms correlates with differentiation in myeloid leukemias.
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Carlson A, Berkowitz JM, Browning D, Slamon DJ, Gasson JC, Yates KE
DNA Cell Biol. 2005 May ; 24(5): 311-6
The cellular fes gene encodes a 93-kilodalton protein-tyrosine kinase (p93) that is expressed in both normal and neoplastic myeloid cells. Increased c-Fes expression is associated with differentiation in normal myeloid cells and cell lines. Our hypothesis was that primary leukemia cells would show a similar pattern of increased expression in more differentiated cells. Therefore, we compared c-Fes expression in cells with an undifferentiated, blast phenotype (acute myelogenous leukemia–AML) to cells with a differentiated phenotype (chronic myelogenous leukemia–CML). Instead of differences in p93 expression levels, we found complex patterns of c-Fes immunoreactive proteins that corresponded with differentiation in normal and leukemic myeloid cells. The “blast” pattern consisted of c-Fes immunoreactive proteins p93, p74, and p70; the “differentiated” pattern showed two additional c-Fes immunoreactive proteins, p67 and p62. Using mRNA from mouse and human cell lines, we found deletion of one or more exons in the c-fes mRNA. Those deletions predicted truncation of conserved domains (CDC15/FCH and SH2) involved in protein-protein interactions. No deletions were found, however, within the kinase domain. We infer that alternative splicing generates a family of c-Fes proteins. This may be a mechanism to direct the c-Fes kinase domain to different subcellular locations and/or substrates at specific stages of myeloid cell differentiation.
Expression of c-Fes protein isoforms correlates with differentiation in myeloid leukemias.
Pic Of The Day
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A Chinese opera mask is displayed during ‘Beijing’s Night’ ceremony for the Fortune Global Forum
Pic Of The Day
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Asiatic lioness Rossy plays with her three new born cubs inside their enclosure at the Assam State Zoo in Guwahati.
Pic Of The Day
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Indian farmer Bhaan Singh tends to his crop of sunflowers in a field on the outskirts of Amritsar, India. |
Pic Of The Day
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Hands are visible through the Europe Gate, which is a light transmitting concrete statue made in 2004 to celebrate Hungary’s European Union membership.
Partnership for Prescription Assistance | CMLHope.Com (Beta)
Posted by rob on May 14, 2005 under Uncategorized | Be the First to Comment
A new site to apply for free or reduced cost prescription drugs and other services.
Partnership for Prescription Assistance | CMLHope.Com (Beta)
Pic Of The Day
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A pedestrian walks under a Dragon’s-blood tree, a member of the Dracaenaceae family, in Sydney’s Royal Botanic Gardens. (
Cancer Drugs On The Way, But Who Pays?
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Matthew Herper, 05.13.05, 4:05 PM ET
This year’s annual meeting of the American Society of Clinical Oncology unveils new data on an unprecedented number of drugs targeted at the genetic quirks that cause cancer.
Some of these drugs will not help patients. But those that will help could lead to another problem: Their high cost could create an even bigger crisis for the U.S. health care system. Consider that treating one patient with one drug can easily cost tens of thousands of dollars.
“Totaling up how many dollars are involved here is quite staggering,” says Leonard Saltz, an oncologist at Memorial Sloan-Kettering Cancer Center, who conducted trials on many big-name cancer drugs. “The fact is these are extraordinarily expensive therapies that lead to real but modest improvements, and we as a society are going to confront the cost and how to pay for it.”
Drug companies, meanwhile, are racing to develop new targeted drugs that will further increase costs while prolonging the lives of cancer patients a little bit at a time.
The big winner this year may be Genentech (nyse: DNA – news – people ). Geoffrey Porges at Sanford C. Bernstein writes in a note to investors that the drug company has more presentations at ASCO this year than the rest of the biotech industry combined. The most important presentation shows studies that its Avastin drug works against certain lung and breast tumors and that Herceptin, a breast cancer drug, is effective in preventing tumors from returning. The lung cancer data is being presented Friday at a press briefing.
But big pharmaceutical firms aren’t content to let Genentech have the huge market for new cancer drugs to itself. One major challenger is Novartis (nyse: NVS – news – people ). The company jumpstarted the field of gene-targeted cancer pills with Gleevec, which showed stunning successes in certain forms of leukemia and stomach cancers. The drug giant has been hoping to repeat that success with PTK-787, a pill meant to work in the same way as Genentech’s Avastin. But initial results being presented at a press briefing at ASCO did not reach statistical significance in preventing colon cancer from progressing.
Novartis and partner Schering AG (nyse: SHR – news – people ) are still hopeful the drug will eventually prove effective.
“The development of oncology products is not often a straight line,” says David Epstein, head of oncology at Novartis. “I’m still relatively optimistic about PTK.”
One strategy that could goose sales and save lives is to use medicines not only to rid the body of cancer but also to prevent it from ever coming back. But this means patients can wind up taking drugs for years.
At Friday’s press briefing, data is being presented from a five-year, 8,000 patient study of Novartis’ pill Femara, which is used to keep breast cancer from recurring after chemotherapy and surgery. Patients who took Femara for five years had 19% fewer breast cancer recurrences than those who took Tamoxifen, the current gold standard. All of the drugs work by affecting estrogen, which can help some breast tumors grow.
Pfizer (nyse: PFE – news – people ) and AstraZeneca (nyse: AZN – news – people ) sell similar drugs, but Matthew Ellis, director of medical oncology at the Washington University School of Medicine in St. Louis, argues that the medicines are different and that Femara may be the most potent, biochemically. The stage seems set for a marketing war between the three firms. Once a relatively small seller, Femara now has blockbuster potential despite its high price tag. The drug costs $224 per month, compared to $38 for generic Tamoxifen.
Data are also being made available on the infamous drug thalidomide, sold by Celgene (nasdaq: CELG – news – people ) as Thalomid. Though the drug was linked to birth defects in the 1950s, it has found a place as a powerful treatment for the blood cancer multiple myeloma. In a trial, 668 patients were given chemotherapy and a stem-cell transplant to replace their bone marrow. Half were also given Thalomid. After five years, 55% of patients on Thalomid had no cancer recurrence, compared to 40% of those who did not get the drug.
Forbes.com – Magazine Article
Myelodysplasic syndromes: A comprehensive review.
Posted by rob on May 13, 2005 under Uncategorized | Be the First to Comment
Catenacci DV, Schiller GJ
Blood Rev. 2005 May 6;
Myelodysplastic syndromes (MDS) are a set of oligoclonal disorders of hematopoietic stem cells characterized by ineffective hematopoiesis that manifest clinically as anemia, neutropenia, and/or thrombocytopenia of variable severity. The result often is transfusion-dependent anemia, an increased risk of infection or hemorrhage, and a potential to progress to acute myelogenous leukemia (AML). Although progression to acute leukemia can lead to death in patients with MDS, many deaths are consequences of cytopenias and marrow failure in the absence of transformation. Approximately 2/3 of patients succumb to the disease within 3-4 years after presentation, and individuals with high-risk MDS generally survive about 1 year. Given that the disease is more prevalent in the elderly who often have comorbid conditions, the current treatment of MDS consists mainly of supportive care. Curative treatments are restricted to younger, healthy individuals with histocompatible (HLA)-matched donors for allogenic transplant or those able to undergo intensive chemotherapeutic regimens. However, understanding of the pathophysiology of MDS and identification of potential cellular and molecular targets in recent years has led to novel therapeutic approaches. Encouraging results using these heterogeneous therapeutic approaches alone or in combination in Phase I and II trials, have, in turn, called into question previous classification systems and have confirmed the need for an all-encompassing molecular, diagnostic and prognostic staging system.
DRUG MAKERS AIM FOR A BULL’S-EYE – Firms such as Bristol-Myers Squibb focus on targeted therapies
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Friday, May 13, 2005
BY GEORGE E. JORDAN
Star-Ledger Staff
Elliott Sigal, Bristol-Myers Squibb’s chief science officer, says the pharmaceutical industry is entering an era of revolutionary breakthroughs in disease treatment.
The mapping of the human genome, the genetic blueprint of the body, and advances in laboratory techniques and information technology have opened potentially hundreds of new pathways to attack diseases.
Bristol is focused on 10 disease areas: cancer, diabetes, hepatitis, AIDS, Alzheimer’s disease, obesity, atherosclerosis, psychiatric disorders, rheumatoid arthritis and organ transplantation.
Two years ago, Sigal, a laboratory researcher by training, was appointed senior vice president in charge of Bristol’s drug discovery pipeline. Last year, he succeeded James Palmer, who died after suffering from non-Hodgkin’s lymphoma, as chief science officer.
Sigal, 53, said the entire pharmaceutical industry is vexed by the long, expensive road from research to drug discovery to final approval by the Food and Drug Administration. On average, he said, it takes 10 years and upward of $1.5 billion to bring a new drug to pharmacy shelves.
The Star-Ledger caught up with Sigal in his office at Bristol’s main research laboratories in Lawrenceville, where he discussed the direction of the company’s research.
What’s happening in the laboratory today that’s different from just a few years ago?
We’re learning at a molecular level what’s important in health and disease. It started 25 years ago and has been rapidly accelerating with the mapping of the human genome. You have an explosion of opportunity to target the treatment of disease.
What’s a target?
All marketed drugs — and there are thousands of them — target about 400 basic disease mechanisms, or targets. Because of the human genome, and the expansion of our understanding of molecular medicine, we now have thousands of targets.
The ones that haven’t led to a drug are novel. In our business, we have to continually improve existing medicines but also find novel medicines.
Why did Bristol narrow its research to 10 disease areas?
We’ve focused on disease areas of great unmet need, rather than develop a drug in an already well-served area, such as blood pressure or cholesterol control. So, you have an opportunity to give some real benefit and can tolerate some risks.
We also focused on the areas that offer commercial opportunities and where we can be competitive.
But the discovery of blockbuster drugs used by tens of millions of people is rare, no?
Good business will follow good medicine. The definition of the blockbuster is going to change. I don’t think it will necessarily be a high-volume medicine with a huge patient base of one size fits all.
Does the expansion of knowledge mean luck has become less a factor in scientific discovery?
You have to be prepared for the serendipity that goes with scientific investigation.
We started out studying a family of enzymes called kinase that control several different functions. In your genome, there may be 500 or 600 of them. They are also involved in certain malignancy processes and tumors.
We started out studying something for rheumatoid arthritis and found out it also targets the very special enzyme that is a genetic defect in chronic myelogenous leukemia, CML.
So, we have a drug that comes out of immunology that applied to solid tumors.
What is personalized medicine?
Personalized medicine is the great holy grail and yet a grand experiment in the industry. Although it has taken longer than some people have predicted, I believe it is where we are going.
That is already true for cancer. We’re using pharmacogenomics, gene-based tests that guide the development and application of medicines.
What do you tell people who fear genomics and genetic engineering?
I think people object, and this is understandable, inserting genes into people in some type of way. I’m not talking about that. I’m talking about can I take laboratory measurements to help decide if you should get one medicine instead of another that I give to everyone else.
Why does it take so long to discover and test drugs?
The Achilles heel of this industry is attrition, the failure of good ideas at the start of the pipeline. It may take thousands of ideas, thousands of compounds, for every one that gets marketed.
The statistic to keep in mind is even after we do all the laboratory work, and we nominate one to take into clinical testing, from that point, nine out of 10 drugs fail. There is a 90 percent failure rate.
What, if anything, can be done to reduce attrition?
The whole industry is focused on this. Step One is picking the right target. Step Two is pick the right compound.
We’ve done a lot of work on predicting which compounds will run into safety issues. And then you pick the right development plan. You have to know where you’re going to match the medical needs with the direction of the company.
George E. Jordan can be reached at gjordan@starledger.com or (973) 392-1801.
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Dispatches from the War on Cancer
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MAY 13, 2005
NEWS ANALYSIS :TECH
By Catherine Arnst
At this year’s ASCO meeting, all eyes will be on Genentech’s latest findings on Avastin and new gene-inhibiting therapies
One in three Americans can expect to die from cancer. The enormous efforts of medical researchers seeking to change that grim statistic will be showcased May 13-17 in Orlando at the world’s largest cancer conference, the annual meeting of the American Society of Clinical Oncology.
This is the main forum for releasing data on clinical trials of the latest cancer drugs, particularly the new generation of targeted therapies that take aim at tumors without harming healthy tissue. Consequently, ASCO not only affects the care of patients but the fortunes of the companies reporting that data — particularly biotech firms, the leaders in cancer research.
This year, however, the traditonal Big Pharma companies will try to regain a place at the table. Some of the most closely watched studies — all embargoed until their release at the meeting — will come from Pfizer (PFE ), GlaxoSmithkline (GSK ), Bristol-Myers Squibb (BMS ), and Bayer (BAY ).
NEW BEST-SELLER? Nevertheless, the real heavyweight at the meeting will be Genentech (DNA ), which is having a very good year. Genentech has four of the most innovative cancer drugs on the market and will be represented by some 150 studies at ASCO, including 32 alone on Avastin, approved for colon cancer in February, 2004.
Avastin is the first of a promising class of drugs that block blood-vessel growth to cancer cells, and the first targeted therapy to extend the survival of late-stage colon cancer patients, one of the hardest groups to treat.
In April, Genentech announced that the drug also extended the lives of breast cancer patients, and details of that trial will be released at ASCO. Doctors and stock analysts alike will also be closely watching a study testing Avastin in combination with traditional chemotherapy for lung cancer. At this point, analysts expect Avastin to be the biggest-selling cancer drug ever if it keeps racking up successes against different types.
GENE PATROL. Genentech will also be releasing the results of studies involving its breast cancer drug Herceptin; Tarceva, which it jointly developed with OSI Pharmaceuticals (OSI ); and Rituxan, co-owned with Biogen-Idec (BIIB ).
Beyond the Genentech treatments, there’s a lot of interest this year in an emerging class of drugs that inhibit several different genes involved in cancer growth and mutations. These multitargeted drugs are being tested in some of the hardest-to-treat cancers, among them kidney, stomach, and a rare form of leukemia.
The two leading compounds are Pfizer’s Sutent and Bay-43-9006, jointly developed by Onyx Pharmaceuticals (ONXX ) and Bayer. Earlier this year, Pfizer reported that Sutent, which the company acquired through its takeover of Pharmacia, is effective in certain types of stomach cancer for patients who have grown resistant to Gleevec, a breakthrough Novartis (NVS ) drug. Oncologists were especially pleased with this result because it proves the principle that patients whose disease grows resistant to one targeted therapy can be switched to another.
WHO WILL PAY? Details of the Sutent stomach cancer trial will be presented at ASCO, as well as results from a test of the drug against kidney cancer. Attendees will be closely comparing the kidney results to those of a late-stage trial with the Onyx-Bayer drug. BristolMyers Squibb also has a drug in development in this category, BMS-354825.
GlaxoSmithKline has its own multitargeted drug, Lapatinib, that’s getting a lot of buzz. This treatment is for breast cancer, and the company is expected to seek Food & Drug Administration approval for it by yearend. Lapatinib is aiming for many of the patients now treated with Genentech’s Herceptin, which is most effective against the 25% to 30% of breast cancer tumors with the Her-2/neu genetic mutation. Herceptin, however, must be taken intravenously, while lapatinib is an oral drug, giving it an edge in ease of use.
Plenty of other innovative treatments will grab attention, including Telcyta from Telik (TELK ), for lung cancer, and Novartis’ PTK787 for colon cancer.
But perhaps one of the biggest general issues to be discussed at the meeting is how our the straining U.S. health-care system will pay for all these new cancer treatments, which tend to cost between $10,000 to $20,000 per course of treatment. The financial component is one area that is sorely lacking in research.
Pic Of The Day
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Felix Onondi, with his dog, Mkombozi (Savior) Thursday, May 12, 2005. The tale of how the stray dog reportedly rescued an infant _ given the name ‘Angel’ by hospital workers _ has attracted an outpouring of concern from Kenyans and well-wishers worldwide.
Pic Of The Day
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A dancer steps out of ‘the Europe Gate’ during celebrations marking the first anniversary of Hungary’s membership in the EU.
CML Articles With No Abstract
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Images in cardiology: Hypereosinophilic syndrome and effect of imatinib mesylate.
Images in cardiology: Hypereosinophilic syndrome and effect of imatinib mesylate.
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Clin Cardiol. 2005 Apr; 28(4): 188 |
Imatinib in pregnancy.
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Eur J Haematol. 2005 Jun; 74(6): 535-7 |
CML patient with rare b2a3 (e13a3) variant of BCR-ABL transcript: Complete molecular response to imatinib.
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Leuk Res. 2005 May 2; |
Loss of skin pigment caused by imatinib therapy.
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Br J Haematol. 2005 May; 129(4): 448 |
Resolution of atopic dermatitis following allogeneic bone marrow transplantation for chronic myelogenous leukemia.
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Bone Marrow Transplant. 2005 May 9; |