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Recent Posts

  • E2F1?dependent pathways are involved in amonafide analogue 7?d?induced DNA damage, G2/M arrest and apoptosis in p53?deficient K562 cells
  • Medical conditions and risk of adult myeloid leukemia
  • Hematopoietic Interferon Regulatory Factor 8-Deficiency Accelerates Atherosclerosis in Mice.
  • BCR-JAK2 fusion as a result of a translocation (9;22)(p24;q11.2) in a patient with CML-like myeloproliferative disease
  • A novel five-way translocation t(7;11;9;22;9)(q22;q13;q34;q11.2;q34) involving Ph chromosome in a patient of chronic myeloid leukemia: a case report
  • Reduced intensity conditioning is superior to nonmyeloablative conditioning for older chronic myelogenous leukemia patients undergoing hematopoietic cell transplant during the tyrosine kinase inhibitor era
  • Gastric Antral Vascular Ectasia in a Patient with GIST after Treatment with Imatinib: Case Report and Literature Review
  • Spinophilin: a new tumor suppressor at 17q21.
  • Metastatic basal cell carcinoma in the era of hedgehog signaling pathway inhibitors
  • Genetic testing behavior and reporting patterns in electronic medical records for physicians trained in a primary care specialty or subspecialty.
  • Altered Microenvironmental Regulation of Leukemic and Normal Stem Cells in Chronic Myelogenous Leukemia
  • Long?term outcome following imatinib therapy for chronic myelogenous leukemia, with assessment of dosage and blood levels: the JALSG CML202 study
  • Somatic mutations in the HLA genes of patients with hematological malignancy
  • Leukapheresis in management hyperleucocytosis induced complications in two pediatric patients with chronic myelogenous leukemia
  • 2??Chloro?4??aminoflavone Derivatives Selectively Targeting Hepatocarcinoma Cells: Convenient Synthetic Process, G2/M Cell Cycle Arrest and Apoptosis Triggers

 

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The role of the K247R substitution in the ABL tyrosine kinase domain in sensitivity to imatinib.

Posted by rob on February 20, 2006 under Uncategorized | Be the First to Comment

Nicolini FE, Chabane K, Cayuela JM, Rousselot P, Thomas X, Hayette S
Haematologica. 2006 Jan ; 91(1): 137-8

Imatinib mesylate has become the gold standard front-line treatment of chronic myelogenous leukemia through its ability to inhibit ABL tyrosine kinase. Resistance to this inhibition may occur. We investigated the role of the K247R polymorphism in persistent sensitivity.

The role of the K247R substitution in the ABL tyrosine kinase domain in sensitivity to imatinib.

Coexistence of inversion 16 and the Philadelphia chromosome in acute and chronic myeloid leukemias : report of six cases and review of literature.

Posted by rob on February 18, 2006 under Uncategorized | Be the First to Comment

Wu Y, Slovak ML, Snyder DS, Arber DA
Am J Clin Pathol. 2006 Feb ; 125(2): 260-6

We report 5 cases of chronic myelogenous leukemia (CML) and 1 case of acute myeloid leukemia (AML) with the dual presence of t(9;22) and inv(16). The 6 patients were 5 men and 1 woman with a median age of 42.5 years. All cases were BCR-ABL+ with p210 products detected in all CML cases and a p190 product detected in the AML case. An increase in bone marrow eosinophils was detected in 3 of 5 cases, and abnormal eosinophils were identified in these 3 cases. The CBFbeta-MYH11 fusion gene was confirmed in all 3 CML cases and the 1 AML case tested, and this correlated with the presence of abnormal eosinophils with coarse basophilic granules. Of 5 patients with CML, 4 had a rapid transformation to myeloid accelerated phase of blast crisis. The coexistence of t(9;22) and inv(16) in CML seems to correlate with more rapid transformation.
Coexistence of inversion 16 and the Philadelphia chromosome in acute and chronic myeloid leukemias : report of six cases and review of literature.

Imatinib mesylate (STI571) abrogates the resistance to doxorubicin in human K562 chronic myeloid leukemia cells by inhibition of BCR/ABL kinase-mediat

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Majsterek I, Sliwinski T, Poplawski T, Pytel D, Kowalski M, Slupianek A, Skorski T, Blasiak J
Mutat Res. 2006 Jan 31; 603(1): 74-82

Imatinib mesylate (STI571), a specific inhibitor of BCR/ABL tyrosine kinase, exhibits potent antileukemic effects in the treatment of chronic myelogenous leukemia (CML). However, the precise mechanism by which inhibition of BCR/ABL activity results in pharmacological responses remains unknown. BCR/ABL-positive human K562 CML cells resistant to doxorubicin (K562DoxR) and their sensitive counterparts (K562DoxS) were used to determine the mechanism by which the STI571 inhibitor may overcome drug resistance. K562 wild type cells and CCRF-CEM lymphoblastic leukemia cells without BCR/ABL were used as controls. The STI571 specificity was examined by use of murine pro-B lymphoid Baf3 cells with or without BCR/ABL kinase expression. We examined kinetics of DNA repair after cell treatment with doxorubicin in the presence or absence of STI571 by the alkaline comet assay. The MTT assay was used to estimate resistance against doxorubicin and Western blot analysis with Crk-L antibody was performed to evaluate BCR/ABL kinase inhibition by STI571. We provide evidence that treatment of CML-derived BCR/ABL-expressing leukemia K562 cells with STI571 results in the inhibition of DNA repair and abrogation of the resistance of these cells to doxorubicin. We found that doxorubicin-resistant K562DoxR cells exhibited accelerated kinetics of DNA repair compared with doxorubicin-sensitive K562DoxS cells. Inhibition of BCR/ABL kinase in K562DoxR cells with 1muM STI571 decreased the kinetics of DNA repair and abrogated drug resistance. The results suggest that STI571-mediated inhibition of BCR/ABL kinase activity can affect the effectiveness of the DNA-repair pathways, which in turn may enhance drug sensitivity of leukemia cells.

Imatinib mesylate (STI571) abrogates the resistance to doxorubicin in human K562 chronic myeloid leukemia cells by inhibition of BCR/ABL kinase-mediated DNA repair.

BNP as a marker of the heart failure in the treatment of imatinib mesylate.

Posted by rob on under Uncategorized | Be the First to Comment

Park YH, Park HJ, Kim BS, Ha E, Jung KH, Yoon SH, Yim SV, Chung JH
Cancer Lett. 2005 Dec 30;

Since its introduction 6 years ago, imatinib mesylate, a selective tyrosine kinase inhibitor, has been a phenomenon in treating chronic myelogenous leukemia (CML) with remarkably superior cytogenetic and molecular response rates at all stages of CML followed by longer progression free survival. Despite its extraordinarily high efficacy, adverse effects of imatinib mesylate such as edema, liver toxicity and fluid retention syndromes have been reported. Here we, for the first time, report development of heart failure in patients on imatinib mesylate medication and the possibility of brain natriuretic peptide (BNP) as a potential diagnostic (or predicting) marker for heart failure. Since plasma BNP levels in the two patients were exceptionally high, we then explored the possibility of genetic association of BNP with the development of heart failure to find no positive association.
BNP as a marker of the heart failure in the treatment of imatinib mesylate.

Synthesis of a novel series of 2-methylsulfanyl fatty acids and their toxicity on the human K-562 and U-937 leukemia cell lines.

Posted by rob on under Uncategorized | Be the First to Comment

Carballeira NM, Miranda C, Orellano EA, González FA
Lipids. 2005 Oct ; 40(10): 1063-8

The hitherto unknown 2-methylsulfanyldecanoic acid and 2-methylsulfanyldodecanoic acid were synthesized from methyl decanoate and methyl dodecanoate, respectively, through the reaction of lithium diisopropylamide and dimethyldisulfide in THF followed by saponification with potassium hydroxide in ethanol. Both alpha-methylsulfanylated FA were cytotoxic to the human chronic myelogenous leukemia K-562 and the human histiocytic lymphoma U-937 cell lines with EC50 values in the 200-300 microM range, which makes them more cytotoxic to these cell lines than decanoic and/or dodecanoic acid. The cytotoxicity of the studied FA toward K-562 followed the order 2-SCH3-12:0 > 2-SCH3-10:0 > 10:0 > 12:0 > 2-OCH3-12:0, whereas toward U-937 the cytotoxicity was 2-SCH3-10:0 > 2-SCH3-12:0 > 12:0 > 10:0 > 2-OCH3-12:0. These results indicate that the alpha-methylsulfanyl substitution increases the cytotoxicity of the C10 and C12 FA toward the studied leukemia cell lines.
Synthesis of a novel series of 2-methylsulfanyl fatty acids and their toxicity on the human K-562 and U-937 leukemia cell lines.

[Disease transformation in imatinib mesylate treated Philadelphia chromosome-positive chronic myelogenous leukemia patients achieved cytogenetic remis

Posted by rob on under Uncategorized | Be the First to Comment

Jiang Q, Chen SS, Jiang B, Jiang H, Lu Y, Lu DP
Beijing Da Xue Xue Bao. 2005 Dec 18; 37(6): 612-5

OBJECTIVE: To report disease transformation in 3 imatinib mesylate treated Philadelphia chromosome-positive chronic myelogenous leukemia (Ph(+)CML) patients who achieved cytogenetic response. METHODS: Hematologic examinations and bone marrow G-banding karyotyping were evaluated at regular intervals in 3 patients with Ph(+)CML who achieved hematologic responses during continuous imatinib therapy, including 1 patient in first chronic phase (case 1), 1 patient in second chronic phase (case 2) and 1 patient in accelerated phase (case 3). RESULTS: Case 1, case 2 and case 3 achieved complete cytogenetic response after 4, 3 and 6 months of imatinib therapy respectively. Though under continuously imatinib treatment, they developed acute lymphoblastic leukemia, acute myelogenous leukemia and extramedullary blast crisis in the following 12, 6 and 0 months respectively. Cytogenetic studies of bone marrow in the crisis period showed that cells in case 1 and case 3 had a complete cytogenetic response (Ph(+)cell=0), but case 2 had 20% Ph(+) cells. CONCLUSION: Acute leukemia or extramedullary blast crisis with Ph(-) cells or dominant Ph(-) cells in bone marrow may occur in the patients with Ph(+)CML after imatinib therapy.
[Disease transformation in imatinib mesylate treated Philadelphia chromosome-positive chronic myelogenous leukemia patients achieved cytogenetic remissions]

Jumping translocation of 17q11 approximately qter and 3q25 approximately q28 duplication in a variant Philadelphia t(9;14;22)(q34;q32;q11) in a childh

Posted by rob on under Uncategorized | Be the First to Comment

Haltrich I, Kost-Alimova M, Kovács G, Kriván G, Tamáska J, Klein G, Fekete G, Imreh S
Cancer Genet Cytogenet. 2006 Jan 1; 164(1): 74-80

The virtually obligatory presence of the Philadelphia chromosome may suggest a causal homogeneity, but chronic myelogenous leukemia (CML) is a clinically heterogeneous disease. This may be a consequence of the variable BCR breakpoints on chromosome 22 and of nonrandom secondary chromosomal abnormalities. We present the case of a boy, age 12, investigated in blastic phase of CML. Karyotyping with conventional and multiplex fluorescence in situ hybridization (FISH and M-FISH) karyotyping, complemented with reverse transcriptase-polymerase chain reaction, identified a variant Philadelphia translocation t(9;14;22)(q34;q32;q11) involving a cryptic BCR/ABL fusion with formation of the p190(Bcr-Abl) oncoprotein. M-FISH revealed also an unbalanced jumping translocation of 17q11 approximately qter alternatively present on chromosomes 14 or 20, apparently hithertofore unreported in hematological malignancies. Another secondary aberration, dup(3)(q25q28), was revealed by multipoint interphase FISH (mpI-FISH). Gain of this region is known in adult hematological malignancies and solid tumors, suggesting its general involvement in tumor initiation or progression (or both), regardless of tissue origin.
Jumping translocation of 17q11 approximately qter and 3q25 approximately q28 duplication in a variant Philadelphia t(9;14;22)(q34;q32;q11) in a childhood chronic myelogenous leukemia.

Two single-nucleotide polymorphisms with linkage disequilibrium in the human programmed cell death 5 gene 5′ regulatory region affect promoter activit

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Ma X, Ruan G, Wang Y, Li Q, Zhu P, Qin YZ, Li JL, Liu YR, Ma D, Zhao H
Clin Cancer Res. 2005 Dec 15; 11(24 Pt 1): 8592-9

PURPOSE: Chronic myelogenous leukemia (CML) is a disease characterized cytogenetically by the presence of the Philadelphia chromosome. Recent studies suggested that altered PDCD5 expression may have significant implications in CML progression. The aim of this study was to identify single-nucleotide polymorphisms (SNP) within the programmed cell death 5 (PDCD5) promoter region and show their functional relevance to PDCD5 expression as well as their genetic susceptibility to CML. EXPERIMENTAL DESIGN: One hundred twenty-nine CML subjects and 211 healthy controls were recruited for identification of SNPs and subsequent genetic analysis. Luciferase reporter assays were carried out to show the functional significance of the SNPs located in the promoter region to PDCD5 expression. Real-time quantitative PCR and Western blot analysis were done to determine the expression differences of PDCD5 in CML patients with different genotypes. RESULTS: Two SNPs were identified within the PDCD5 promoter. They are -27A>G and -11G>A (transcription start site as position 1), respectively. The complete linkage disequilibrium was found between these two polymorphisms. The frequencies of -27G+/-11A+ genotype and -27G/-11A allele were significantly higher in CML patients than in healthy controls (genotype: 26.36% versus 11.85%, chi2=11.75, PHubMed Abstracts

PharmaLive: SGX Pharmaceuticals Presenting Data at Keystone Symposia

Posted by rob on February 15, 2006 under Uncategorized | Read the First Comment

SAN DIEGO, February 15, 2006 /PRNewswire-FirstCall/ — SGX Pharmaceuticals announced that it will present data today at the Keystone Symposia in Santa Fe, New Mexico entitled “Cancer and Kinases: Lessons from the Clinic” showing that, in vitro, compounds discovered by applying its FAST(TM) lead discovery platform potently inhibit wild-type and Gleevec-resistant BCR-ABL, including the most clinically challenging mutation T315I.


<A HREF=”http://ad.doubleclick.net/jump/PharmaLive/main;sz=300×250;abr=!ie4;abr=!ie5;ord=1140027193828?”> <IMG SRC=”http://ad.doubleclick.net/ad/PharmaLive/main;sz=300×250;abr=!ie4;abr=!ie5;ord=1140027193828?” width=”300″ height=”250″ border=0 ALT=”"></A>

The clinical success of Gleevec has demonstrated that BCR-ABL kinase inhibitors can provide effective treatment of Chronic Myelogenous Leukemia (CML). However, some patients develop resistance to Gleevec therapy, which occurs due to point mutations in the BCR-ABL kinase. There is currently no approved pharmaceutical treatment for such Gleevec-resistant CML. Although effective against many of the other clinically relevant mutants, second- generation BCR-ABL inhibitors currently in clinical studies have not been shown to inhibit T315I, which represents about 20 percent of clinically observed mutations and is one of the most common causes of resistance to treatment with Gleevec.

During an oral presentation in the session entitled “Structural Chemistry of Kinases and Profiling Kinase Inhibitors,” taking place today at 5:00 p.m., Stephen K. Burley, M.D., D.Phil., SGX Pharmaceuticals’ Chief Scientific Officer and Senior Vice President, Research, will present in vitro data showing that compounds in SGX’s most advanced lead series potently inhibit proliferation of K562 cells and Ba/F3 cells with wild-type BCR-ABL and most clinically-relevant mutations, including T315I.

SGX expects to file an IND in late 2006 to permit clinical development of a compound from its lead series of BCR-ABL kinase inhibitors for treatment of drug-resistant CML.

About SGX Pharmaceuticals

SGX Pharmaceuticals is a biotechnology company focused on the discovery, development and commercialization of innovative cancer therapeutics. More information can be found at www.sgxpharma.com.

Forward-Looking Statements

Statements in this press release that are not strictly historical in nature are forward-looking statements. These statements include but are not limited to statements related to the progress, timing and potential success of SGX’s research and drug discovery and development programs, including the expected timing of filing an IND for a compound in its BCR-ABL program, the safety and efficacy of SGX’s potential development candidates, including the potential potency of SGX’s compounds, and the potential benefits to be derived from SGX’s technology and development candidates, in each case, including any compounds discovered in its BCR-ABL program. These statements are only predictions based on current information and expectations and involve a number of risks and uncertainties. Actual events or results may differ materially from those projected in any of such statements due to various factors, including the risks and uncertainties inherent in drug discovery, development and commercialization, collaborations with others, and litigation. For a discussion of these and other factors, please refer to the risk factors section of the final prospectus from SGX’s initial public offering filed with the United States Securities and Exchange Commission on February 1, 2006 as well as other subsequent filings with the Securities and Exchange Commission. You are cautioned not to place undue reliance on these forward-looking statements, which speak only as of the date hereof. This caution is made under the safe harbor provisions of the Private Securities Litigation Reform Act of 1995. All forward-looking statements are qualified in their entirety by this cautionary statement and SGX undertakes no obligation to revise or update this press release to reflect events or circumstances after the date hereof.

CONTACT: Jason Spark of Porter Novelli Life Sciences, +1-858-527-3491,, for SGX jspark@pnlifesciences.com

Web site: http://www.sgxpharma.com/

Ticker Symbol: (NASDAQ-NMS:SGXP)

Terms and conditions of use apply
Copyright © 2006 PR Newswire Association LLC. All rights reserved.
A United Business Media Company

PharmaLive: SGX Pharmaceuticals Presenting Data at Keystone Symposia

Power3’s Invited Review on Biomarkers and Test for ALS, Parkinson’s, and Alzheimer’s is Published by Expert Reviews of Proteomics

Posted by rob on February 14, 2006 under Uncategorized | Be the First to Comment

2/14/2006 10:00:00 AM EST

Power3 Medical Products, Inc. (Pink Sheets:PWRM), a leader in the development of blood serum-based diagnostic tests for early-detection of cancer and neurodegenerative diseases, announced today the publication of an invited review co-authored by its chief scientific officer and other key members of its senior technical management team.

The invited review, “2D Gel Blood Serum Biomarkers Reveal Differential Clinical Proteomics of the Neurodegenerative Diseases” is in the current issue of “Expert Reviews of Proteomics,” and outlines the scientific groundwork for Power3’s NuroPro(R) suite of blood serum tests for neurodegenerative diseases, including ALS, Parkinson’s and Alzheimer’s.

Power3 currently has 19 provisional and utility patent applications pending with the U.S. Patent and Trademark Office involving biomarker discovery and test designs for breast, stomach and esophageal cancer, neurodegenerative disease, and drug targets for resistance to chemotherapy.

Steven B. Rash, chairman and CEO of Power3, said he was “very proud that this important review was invited and published.

“To have our company and our innovative work recognized by scientific and healthcare industry peers is very rewarding and satisfying,” he said.

The 18-page article was written by Dr. Ira Goldknopf, Power3’s chief scientific officer, Dr. Essam A. Sheta, its director of biochemistry, and Dr. Stanley H. Appel. A member of Power3’s Scientific Advisory Board, Dr. Appel is former chairman of the Department of Neurology, past director of the Vicki Appel MDA/ALS Clinic, past-director of the Alzheimer’s Disease Research Center at Baylor College of Medicine, past director of the Jerry Lewis Neuromuscular Research Center in Houston and director of the Methodist Neurological Institute in Houston.

Monitoring Multiple Blood Serum Protein Biomarkers

Dr. Goldknopf said the review, which was invited by Expert Reviews of Proteomics, “shows how Power3’s tests obtained superior performance by monitoring multiple blood serum protein biomarkers and multivariate biostatistics.

“Power3 was able to define the disease mechanisms for ALS and Parkinson’s that can be measured by the blood tests,” he said. “The review places our patent-pending technology and methods within the context of overall research as having the only blood protein biomarkers and test for neurodegenerative diseases. We believe the leadership of Power3 Medical in clinical proteomics for differential diagnosis of neurodegenerative diseases is clearly delineated and demonstrated within this review.

Information and reprints are available by contacting reprints@future-drugs.com.

Presentations Set, More Findings to be Published

Power3 is also scheduled to deliver presentations at major scientific conferences this spring and will soon have more of its scientific findings published.

“Blood Serum Biomarkers for Differential Diagnosis of Parkinson’s Disease” and “Biomarkers for Diagnosis and Targeting of Resistance and Sensitivity to Imatinib Mesylate in Chronic Myelogenous Leukemia” will be delivered at Experimental Biology 2006 in San Francisco in early April, and “Convergence of Proteome-Diagnostics and Pharmaco-Proteomics toward Personalized Medicine — Examples from Breast Cancer and Leukemia” will be given at the OncoProteomics World Congress in San Francisco in late April.

In addition, “C3c and Related Protein Biomarkers in Amyotrophic Lateral Sclerosis and Parkinson’s Disease,” written by Drs. Goldknopf, Sheta and Appel, along with Jennifer Bryson, Brian Folsom, Chris Wilson, Jeff Duty, and Albert A. Yen, has been accepted for publication and is expected to appear in the March or April issue of “Biochemical and Biophysical Research Communications.” The article is the result of a collaboration between Power3 Medical Products and the Methodist Neurological Institute of Houston.

About Power3 Medical Products, Inc.

Power3 Medical Products, Inc. (Pink Sheets:PWRM) is a leading proteomics company engaged in the discovery of protein footprints, pathways, and mechanisms of diseases. Power3’s patent-pending technologies are being used to develop screening and diagnostic tests for the early detection and treatment of disease, and its identified protein biomarkers, drug targets, and diagnostic tests are targeted toward markets with critical unmet needs in areas such as breast cancer and neurodegenerative disease. Power3 operates a state-of-the-art proteomics laboratory in The Woodlands (Houston), Texas.

This press release contains forward-looking statements within the meaning of section 27A of the Securities Act of 1933 and Section 21E of the Securities Exchange Act of 1934. With the exception of historical information contained herein, the matters discussed in this press release involve risk and uncertainties. Actual results could differ materially from those expressed in any forward-looking statement.

CONTACT:

Power3 Medical Products, Inc. Steven B. Rash, 281-466-1600 srash@power3medical.com or The Kaminer Group David A. Kaminer, 914-684-1934 dkaminer@kamgrp.com

Breaking News: Power3’s Invited Review on Biomarkers and Test for ALS, Parkinson’s, and Alzheimer’s is Published by Expert Reviews of Proteomics

Our towns – news from our local communities

Posted by rob on February 12, 2006 under Uncategorized | Be the First to Comment

Members of the Potterville and Charlotte Lions clubs are inviting the public to a pancake breakfast benefit for Rocky and Tammy White and their children – Kamryn, 4, and Peyton, 11 months.
Advertisement

Rocky, 37, is being treated for chronic myelogenous leukemia
Lansing State Journal: Our towns – news from our local communities

Man Dies After Insurance Co. Refuses To Cover Treatment on Yahoo! News

Posted by rob on February 11, 2006 under Uncategorized | Be the First to Comment

Tracy Pierce, 37, lived a full life. He grew up with family and faith. He went to a Catholic school, got married, had a son, and he even had the car of his dreams. It was the perfect life.

“He’s been strong. He has,” his wife, Julie Pierce, said.

Two years ago, Tracy Pierce’s life changed dramatically when he was diagnosed with kidney cancer.

“I have no treatment. Three months has gone by and I haven’t had any treatment,” Tracy Pierce told KMBC’s Jim Flink in May 2005.

When Flink talked to Tracy Pierce, his cancer was attacking his body. Despite being fully insured, every treatment his doctors sought for him was denied by his insurance provider. First-Health Coventry deemed the treatments were either not a medical necessity or experimental.

“I don’t know what else to do but just wait,” Tracy Pierce said last May.

As he waited, his doctors appealed again and again, including a 27-page appeal spelling out that Tracy Pierce would die without care. Coventry dismissed each request.

“It’s purely economical. You never see an insurance company try to block an inexpensive test,” said William Soper.

Soper leads a group of doctors who filed a lawsuit last year against insurance providers. This week, Soper went to Jefferson City to lobby legislators for change.

“And you know, it’s not going to get better anytime soon. It’s going to get worse,” said Myra Christopher, who is the president and chief executive officer of the Center for Practical Bioethics.

Christopher told Flink that change won’t happen until there’s a change in the entire medical model.

“I just believe strongly that we need to start being honest about what’s going on here,” Christopher said.

What is going on is that some insurance companies deny even routine treatments because insurance companies treat their patients as costs, not as clients, Christopher said.

“Some of these companies are just unethical the way they treat both subscribers and providers, doctors and hospitals,” Soper said.

Two weeks ago, Tracy Pierce talked with Flink again.

“Just holding a lot of anger in,” Pierce said.

Cancer ravaged his body, moving from his kidney to his lungs and to his brain.

“Now, we’re just to the point where we’re trying to make him comfortable,” Julie Pierce said.

Even as he was dying, for more than a week, his insurance company denied him oral morphine, which had been prescribed to reduce his pain.

“That’s unacceptable because in this day and age, no one should be in pain,” Pierce said.

“I just hope we can get something done about it, that’s all. We just have to get something done,” Tracy Pierce said.

An hour and a half after Tracy Pierce talked to Flink, he took a nap and never woke up. His family calls his case death by denial.

“They just wrote a prescription for him to die,” Julie Pierce said.

The family is begging for change.

“The reality is the blame-and-shame game isn’t going to get us anywhere. We are all at fault,” Christopher said.

Insurance companies, hospitals, doctors, patients and politicians all need to work together, she said.

“We have to have the moral will. We have to have the intelligence. We have to have the political leadership to change this,” Christopher said.

For Julie Pierce, it was 15 months of watching her husband die slowly, painfully and helplessly with no chance at lifesaving treatment, Flink reported.

“My mother always told me to get a good job with insurance. For what? It hasn’t done anything,” Julie Pierce said.

Julie Pierce said that she understands that we will all die. What is expected, she said, is that if you have health insurance, you’ll be given every fighting chance. She said that is not happening.

Leukemia Story

Last fall, 12-year-old Nathan Crabtree was an outgoing child getting ready for a new school year. But his father says Nathan often played sick to extend summer vacation by a day or two.

To prove a point, his dad took Nathan to a doctor for test, which showed that Nathan had an aggressive form of leukemia — one that needed immediate treatment.

Flink reported that a hospital room has become Nathan’s classroom. He spent just two days of his sixth-grade year with classmates; mostly, he’s been at Children’s Mercy Hospital.

“It’s not going away, so they were going to send me to Minnesota,” Nathan said.

Doctors wrote to Nathan’s insurance company, urging it to send him to the nation’s foremost research hospital. Nathan’s bags were packed, when his father’s insurance company, Coventry, refused to pay for that care, calling it “experimental.”

“You don’t have anyone to fight for you,” said Lee Crabtree, Nathan’s father.

Lee Crabtree said he’s desperate.

“I have to go out and find private grants, because for all intents and purposes, I have to assume I have no medical coverage,” Lee Crabtree said.

“I think they expect or depend on people giving up after the first phone call,” said Dr. William Soper, the executive director of Mid-America Medical Affiliates.

Soper said his group is so upset with insurance companies that it has filed a lawsuit alleging insurers block patient care.

“We have patients who say, ‘I want a complete physical,’ and we’ll look at their insurance coverage and we have to say, ‘Sorry, but your plan doesn’t cover a complete physical,’” Soper said.

Flink reported that many people don’t realize what isn’t covered by health insurance until it is too late.

Lee Crabtree said he has a helpless feeling when he looks at his son and tries to explain why he can’t help him live.

“The feeling of this is beyond words. It makes you feel hollow,” Lee Crabtree said.

Late Friday, KMBC learned that Nathan’s mother found out she could apply for coverage with Blue Cross Blue Shield at her workplace, and so she had applied. What Coventry spent months denying and calling experimental, Blue Cross Blue Shield approved on the first request.

Nathan Crabtree leaves for Minnesota on Sunday morning.

More Info

Coventry Health Care Statement

Health Insurance Opinion Survey Summary

Be a part of an online discussion about insurance companies and your health care by clicking here.

E-Mail: Contact Jim Flink

Print Story: Man Dies After Insurance Co. Refuses To Cover Treatment on Yahoo! News

Filipina Researcher Who Worked On Gleevec

Posted by rob on under Uncategorized | Be the First to Comment

World-class Filipina
First posted 04:57am (Mla time) Feb 11, 2006
By Queena Lee-Chua
Inquirer

IN JUNE 1990, 18-year-old high school senior Mercedes “Tata” Escano Gorre vowed in her valedictory speech that she would find a cure for cancer. Her mother Lisa, a research chemist at the Hughes Laboratory in Malibu, California, had died of cancer a few months earlier. In August 2001, Tata’s promise came true. Her paper from her doctoral dissertation on molecular mechanisms in chronic leukemia was published in the prestigious journal Science.

Tata’s work aimed to thresh out what exactly was happening with the cancer drug called Gleevec, developed in 2000.

Gleevec seemed to work very well with leukemia patients, at first. However, the drug would seem to stop working. Why?

Protein mutation

Tata eventually found that certain leukemia patients have a mutation in a certain protein that would not make the drug work, and this discovery was the basis of her paper.

At first, other researchers were skeptical, but now her discovery is widely accepted, and Tata and her adviser (Dr. Charles Sawyers) have filed a patent claim for their discovery.

But Gleevec can work with other patients. It is relatively inexpensive (just one pill a day) and has little side effects (it targets the abnormal protein and nothing else). Currently, Tata and her team are working on alternative ways to help Gleevec-resistant patients, and other researchers have found that their study could be applied to other cancers besides leukemia.

Line of scientists

Tata hails from a line of scientists. Aside from her mother, her physicist uncle and my friend Dr. Gregory Tangonan used to work in Hughes Labs. As principal research Scientist at Quest Diagnostics Nichols Institute, a huge medical diagnostics firm in California, Tata heads a laboratory in the Hematology-Oncology R&D Department.

Tata’s aunt, writer Paulynn Sicam, says there was only one other Filipina in Tata’s graduate class at the University of California, Los Angeles. Tata did not let this matter, and at heart she remains a Pinay.

Making Filipinos proud

In an e-mail to her aunt, Tata says, “I am certain that whatever accomplishments I have achieved are largely due to my Filipino family and its strong emphasis on education, discipline and social responsibility. I only hope that I can continue to make them and other Filipinos proud.”

For more information on Tata, e-mail psicam@cyberdyaryo.com.

Science humor

Another physicist friend, Alan Batongbacal, e-mailed this bit of science humor:

A math professor noticed that his kitchen sink broke down. He called a plumber. The plumber came the next day, sealed a few screws and everything was working as before. The professor was delighted.

However, when the plumber gave him the bill a minute later, he was shocked. “This is one third of my monthly salary!” he yelled.

The plumber consoled him, “I understand. Why don’t you come to our company and apply as a plumber? You will earn three times as much as a professor. But remember, when you apply, tell them that you completed only grade school. They don’t like educated people.”

The professor became a plumber, and his salary went up significantly. One day, the boss decided that every plumber has to go to evening classes to complete high school.

The first class was math. The teacher asked for the formula for the area of a circle. The professor went to the board but realized he forgot the formula.

So he started to reason it out and soon filled the board with integrals, differentials and other advanced formulas to derive the formula. Then he got “negative pi times r squared.” He didn’t like the negative, so he started all over again. No matter how many times he tried, he always got a negative.

He was frustrated and looked helplessly at his classmates. Then all the plumbers whispered, “Switch the limits of the integral!!”

For more science humor, go to http://ask.slashdot.org/askslashdot/04/03/03/2125257.shtml.



©2006 www.inq7.net all rights reserved
World-class Filipina – INQ7.net

Novartis denied patent for cancer drug

Posted by rob on February 10, 2006 under Uncategorized | Be the First to Comment

C H Unnikrishnan in Mumbai | February 10, 2006 01:46 IST

The Patent Controller Office of India has rejected the patent application of Novartis AG for its cancer drug Gleevec.

Assistant Controller of Patents & Designs V Rengasamy rejected the application on January 25 on the ground that the drug, Imatinib Mesylate, did not qualify for patenting in India as the novelty of the drug was objected to by a host of Indian companies, including Cipla.?

The patent office heard the pre-grant opposition on October 14, 2005, filed by Cipla. This is the first major decision on patent application after India complied with the TRIPS regime in 2005.?

Norvatis officials were not available for comment. Novartis was likely to challenge the patent controller’s decision in the Madras high court, industry sources said.?

With this, the generic manufacturers in India, including the Hyderabad-based Natco Pharma, Cipla, Ranbaxy, Torrent Pharma, Sun Pharma and many more can re-enter the Rs 400 crore market with their generic versions of this product.

Novartis denied patent for cancer drug

Patent remedy for India’s health

Posted by rob on under Uncategorized | Be the First to Comment

Priti Radhakrishnan
Just how wealthy do you have to be to buy medicines in India? The UPA government is about to decide. After the controversial Patent Amendment Act was passed in March 2005, the government is now about to take critical decisions impacting access to health. Its position will affirm or negate its commitment to the promises of the Doha Declaration on Public Health, the Common Minimum Programme and the health of ordinary Indians.

A few days ago, cancer patients won a stunning victory in Chennai. The patent controller ruled against multinational conglomerate Novartis AG in the Gleevec case, stating that Novartis had not shown any improvement over a known compound. Controversy raged last year after Novartis was granted an exclusive marketing right for the anti-cancer drug imatinib mesylate, commonly known as Gleevec. This prevented other domestic companies from making the drug and resulted in the price of Gleevec rising from Rs 10,000 per month (already out of reach for most Indians) to Rs 1.2 lakh per month.

Prices of other drugs are also expected to rise. One study estimates price increases in one therapeutic class alone will be between 100-400 per cent. The controller’s ruling is significant as it sends a clear message to drug companies that they can’t obtain frivolous patents through chicanery: patents will be granted only for real inventions. Last year, various ministers stated that if medicine prices increase excessively in India due to the patent regime, the government will intervene. In the case of Gleevec, it was the unparalleled determination of the Cancer Patients Aid Association, with the support of civil society and Indian drug companies, that led to this adjudication. The government’s only response was inaction.

It is time to demonstrate a commitment to health. The commerce and chemicals ministries could begin by taking the inputs of the health ministry on issues connected to pharmaceutical patents. The rebirth of the product patent regime sounded the death knell for affordable generic medicines. Monopolies on medicines, heretofore considered unacceptable for India, will now be the norm as India complies with its WTO/TRIPS obligations in a manner that goes beyond the call of duty. It is an open question as to which drugs will be patentable, as the patent controller decides on issues of ‘efficacy’ and ‘economic significance’, standards that no country has employed. As a result, without patent opposition from domestic patients and manufacturers, there is scope for abuse and ‘evergreening’ to extend monopolies on medicines.

Difficult decisions lie ahead. After the patent act passed, one of the open issues was referred to a technical committee headed by Dr A.R. Mashelkar. The committee will recommend whether the scope of patentability for drugs will be limited to new chemical entities or expanded to include mere modifications. Civil society groups have written to the PMO asserting that the patent controller’s grant of pharmaceutical patents will be ultra vires (beyond his powers) and should be enjoined until the issue is decided. It remains to be seen what action the PMO takes. The pressure is on.

The government, however, has some options. First, it can take decisive action to check the scope of patentability and data protection. Health groups are watching to see if the UPA is committed to protecting health as promised. Thus far, there have been no mechanisms introduced to safeguard the rights of patients. The defunct Drug Price Control Order can hardly be used as a shield for the government to hide behind, even with a new pharmaceutical policy on the anvil. Demonstrating commitment to open, consultative processes on issues impacting access will be an important step in the right direction.

Second, the UPA can ensure that flexibilities are utilised. In the event of grant of a patent they can order immediately a licence under Section 92 for public health crises such as HIV, TB or potentially the ‘bird flu’ pandemic. Alternatively, they can override patents for “government use” purposes. The health ministry must act swiftly to ensure licences are granted for drugs desperately required in the next stage of India’s HIV/AIDS epidemic.

The government would be wise to note that even these measures are merely preliminary safeguards. It is hardly effective as a public health measure to put a patient on TB medicines if she will thereafter succumb to another disease such as diarrhoea. But for now, the question is, how seriously will the government take its immediate commitment to public health?

The writer is coordinator, the Affordable Medicines & Treatment Campaign

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Generics Hail Novartis Loss

Posted by rob on under Uncategorized | Be the First to Comment

Cancer drug patent outcome elates Indian pharma industry as generics hike production.
February 10, 2006

What could be a major setback to the Swiss drug maker Novartis has proven to be a victory for the Indian pharmaceutical industry.

After Novartis lost its patent claim on Gleevec in India late last month, more than half a dozen Indian drug companies are ready to launch the generic version of Imatinib Mesylate, a lifesaving drug used to treat chronic myeloid leukemia, and tap the $100-million-plus domestic market.

‘We got chemical tests done… which proved contrary to the claims of Novartis.’

-Adi Narayana,

Natco Pharmaceutical

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Cancer at 23 – Dateline NBC – MSNBC.com

Posted by rob on February 7, 2006 under Uncategorized | Be the First to Comment

Updated: 5:54 p.m. ET Feb. 5, 2006

23 years old and fresh out of college, in love with her boyfriend Nick, and having just started a great new job as assistant editor at Glamour magazine, Erin Zammett was looking forward to a future of unlimited promise.

A routine checkup by her doctor seemed to indicate that she was in perfect health, until she was called back just a day later to be told that a blood test revealed she had a type of cancer, Chronic Myelogenous Leukemia, the only known treatment for which was a bone marrow transplant; without treatment, she had roughly five years to live.

After the initial shock wore off, and with the support of her family and friends, her own inner strength, and a recently approved experimental drug, Erin Zammett immediately began the journey that would lead her to recovery. Below, is an excerpt of her book.

Chapter 1: A Fork In the Road
I was living the life I’d always said I wanted. But I was afraid if I slowed down to really enjoy that life, I might not be able to get enough items checked off my to-do list. I might not be a huge success, and nothing could be worse than that. Then, when I was 23, busy plotting my next move, stockpiling my hopes and dreams, I was diagnosed with cancer. So much for my big plans. There is no preparing for news like that, no penciling it in to your otherwise packed schedule. It just happens, without warning. No symptoms, no heads-up, just cancer handed to me on a perfectly nice Tuesday afternoon.

On Monday, November 12, 2001 I went to the doctor for a checkup. I wasn’t sick, but I hadn’t been to a regular physician in a while so I made an appointment. He was a brand new doctor for me, and I figured it would be a good opportunity to get to know him in case I ever really needed him, for a real reason. A friend from work had recommended him: Eric Lutsky, nice, smart, close to the office, took my insurance. Perfect. I also wanted a referral to go to physical therapy for the herniated disc in my back, which I thought was just about the worst thing that could happen to a 23-year-old. I’d been an athlete my whole life-I played Division I volleyball in college-so I’d always taken great care of myself. I ate right, I slept right, I exercised. I figured the doctor would just give me a pat on the back, a “keep up the good work!” Approval and reassurance were two of my favorite things.

I can handle this, I thought, as I walked out of his office. I had no idea what it was I’d have to handle but I told myself I could do it. In a way, I was prepared for something like this, expecting it even. My whole life I’d lain awake at night having horrible thoughts about my parents and my grandparents and my sisters-plane crashes, car crashes, heart attacks, cancer. My family had it pretty good, and I always felt like our number would have to be up sooner or later, like it was only a matter of time before the dreaded phone call came. I just never thought I’d be the one that call was about.

Desperate to talk to my mom, I scanned the streets for a payphone. Of course I had walked out of my apartment without my cell phone that morning. I crossed the street and fumbled through my bag for some change.

“He thinks it could be something bad,” I told her, unable to just say the word.

“Did he say what?” she asked.

“Yes,” I said.

“What did he say, Erin?” she was getting annoyed.

“He said that it wasn’t good, and it could be really bad if it wasn’t a mistake,” I said, desperately trying to come up with a way to sugarcoat the news. I suddenly understood how Dr. Lutsky must have felt.

“How bad, Erin?” she pressed.

I leaned into the phone booth and whispered, not wanting anyone-especially myself-to hear me say the words out loud.

“Like . . . leukemia, Mom.”

And just like that, it was real. “What?” my mom shrieked. “Holy shit. What’s the doctor’s number?” She sounded like she was going to yell at him, like it was his fault. Then we were interrupted: “Please deposit 10 cents. Ten cents please.” I pumped dimes into the phone and tried to relay every detail. On the third interruption by the operator, my mom got really frustrated. “Don’t you have a goddamn quarter?” she fumed. I knew she wasn’t mad, just scared, like the time she yelled at me for getting lost on our Brownie field trip to Radio City Music Hall (I hadn’t actually been lost, I just followed the other leader into the bathroom without telling my mom). I told her that Dr. Lutsky didn’t want to talk until he knew more, and that I wished she wouldn’t bother him. But I knew she’d call. She’d ask a million questions and get some answers too. Then she’d talk to more doctors. My mom works in a hospital and makes friends with every janitor, X-ray technician and surgeon she meets. She was going to use her connections.

My mom is a tough lady, and she’s great in emergencies-medical, fashion and otherwise. She always knows the right thing to do or say and manages to stay relatively calm. In a crisis, my two sisters and I would usually go to my mom, who’s the far more rational of our two parents. Then she’d decide if it was worth telling my dad. Certain things-my 12 parking tickets sophomore year, Meghan’s shamrock tattoo, the price of Melissa’s wedding dress-were better kept between the girls. My dad is a complete alarmist and just a tad temperamental. When Meghan, my younger sister, tore up her knee on a ski slope in Vermont a few years back, my dad was so upset, he took her skis, snapped them in half over his knee and heaved them into the woods. He hasn’t skied since. My mom and I decided it would be best if we waited until my dad was back from his business trip to tell him in person. We hung up and I headed back to work.

As people on the sidewalk bumped past me with cigarettes burning, I wanted to shout, watch where you put that thing, I have cancer! But I had a sudden sympathy for these strangers. Who knew what was going on in their lives, if they had just gotten similar news. I certainly looked like a normal person, but I wasn’t. Not anymore. I put on my sunglasses and let myself cry.

From the book My (So-Called) Normal Life, copyright (c) 2005 by Erin Zammett. Used with the permission of The Overlook Press.

c 2006 MSNBC.com

URL: http://www.msnbc.msn.com/id/11191259/

Cancer at 23 – Dateline NBC – MSNBC.com

Posted by rob on under Uncategorized | Be the First to Comment

Updated: 5:54 p.m. ET Feb. 5, 2006

23 years old and fresh out of college, in love with her boyfriend Nick, and having just started a great new job as assistant editor at Glamour magazine, Erin Zammett was looking forward to a future of unlimited promise.

A routine checkup by her doctor seemed to indicate that she was in perfect health, until she was called back just a day later to be told that a blood test revealed she had a type of cancer, Chronic Myelogenous Leukemia, the only known treatment for which was a bone marrow transplant; without treatment, she had roughly five years to live.

After the initial shock wore off, and with the support of her family and friends, her own inner strength, and a recently approved experimental drug, Erin Zammett immediately began the journey that would lead her to recovery. Below, is an excerpt of her book.

Chapter 1: A Fork In the Road
I was living the life I’d always said I wanted. But I was afraid if I slowed down to really enjoy that life, I might not be able to get enough items checked off my to-do list. I might not be a huge success, and nothing could be worse than that. Then, when I was 23, busy plotting my next move, stockpiling my hopes and dreams, I was diagnosed with cancer. So much for my big plans. There is no preparing for news like that, no penciling it in to your otherwise packed schedule. It just happens, without warning. No symptoms, no heads-up, just cancer handed to me on a perfectly nice Tuesday afternoon.

On Monday, November 12, 2001 I went to the doctor for a checkup. I wasn’t sick, but I hadn’t been to a regular physician in a while so I made an appointment. He was a brand new doctor for me, and I figured it would be a good opportunity to get to know him in case I ever really needed him, for a real reason. A friend from work had recommended him: Eric Lutsky, nice, smart, close to the office, took my insurance. Perfect. I also wanted a referral to go to physical therapy for the herniated disc in my back, which I thought was just about the worst thing that could happen to a 23-year-old. I’d been an athlete my whole life—I played Division I volleyball in college—so I’d always taken great care of myself. I ate right, I slept right, I exercised. I figured the doctor would just give me a pat on the back, a “keep up the good work!” Approval and reassurance were two of my favorite things.

I can handle this, I thought, as I walked out of his office. I had no idea what it was I’d have to handle but I told myself I could do it. In a way, I was prepared for something like this, expecting it even. My whole life I’d lain awake at night having horrible thoughts about my parents and my grandparents and my sisters—plane crashes, car crashes, heart attacks, cancer. My family had it pretty good, and I always felt like our number would have to be up sooner or later, like it was only a matter of time before the dreaded phone call came. I just never thought I’d be the one that call was about.

Desperate to talk to my mom, I scanned the streets for a payphone. Of course I had walked out of my apartment without my cell phone that morning. I crossed the street and fumbled through my bag for some change.

“He thinks it could be something bad,” I told her, unable to just say the word.

“Did he say what?” she asked.

“Yes,” I said.

“What did he say, Erin?” she was getting annoyed.

“He said that it wasn’t good, and it could be really bad if it wasn’t a mistake,” I said, desperately trying to come up with a way to sugarcoat the news. I suddenly understood how Dr. Lutsky must have felt.

“How bad, Erin?” she pressed.

I leaned into the phone booth and whispered, not wanting anyone—especially myself—to hear me say the words out loud.

“Like . . . leukemia, Mom.”

And just like that, it was real. “What?” my mom shrieked. “Holy shit. What’s the doctor’s number?” She sounded like she was going to yell at him, like it was his fault. Then we were interrupted: “Please deposit 10 cents. Ten cents please.” I pumped dimes into the phone and tried to relay every detail. On the third interruption by the operator, my mom got really frustrated. “Don’t you have a goddamn quarter?” she fumed. I knew she wasn’t mad, just scared, like the time she yelled at me for getting lost on our Brownie field trip to Radio City Music Hall (I hadn’t actually been lost, I just followed the other leader into the bathroom without telling my mom). I told her that Dr. Lutsky didn’t want to talk until he knew more, and that I wished she wouldn’t bother him. But I knew she’d call. She’d ask a million questions and get some answers too. Then she’d talk to more doctors. My mom works in a hospital and makes friends with every janitor, X-ray technician and surgeon she meets. She was going to use her connections.

My mom is a tough lady, and she’s great in emergencies—medical, fashion and otherwise. She always knows the right thing to do or say and manages to stay relatively calm. In a crisis, my two sisters and I would usually go to my mom, who’s the far more rational of our two parents. Then she’d decide if it was worth telling my dad. Certain things—my 12 parking tickets sophomore year, Meghan’s shamrock tattoo, the price of Melissa’s wedding dress—were better kept between the girls. My dad is a complete alarmist and just a tad temperamental. When Meghan, my younger sister, tore up her knee on a ski slope in Vermont a few years back, my dad was so upset, he took her skis, snapped them in half over his knee and heaved them into the woods. He hasn’t skied since. My mom and I decided it would be best if we waited until my dad was back from his business trip to tell him in person. We hung up and I headed back to work.

As people on the sidewalk bumped past me with cigarettes burning, I wanted to shout, watch where you put that thing, I have cancer! But I had a sudden sympathy for these strangers. Who knew what was going on in their lives, if they had just gotten similar news. I certainly looked like a normal person, but I wasn’t. Not anymore. I put on my sunglasses and let myself cry.

From the book My (So-Called) Normal Life, copyright (c) 2005 by Erin Zammett. Used with the permission of The Overlook Press.

pd_top(‘Story’,'handheld’,'11191259′,’Cancer at 23′,’How a young woman coped with leukemia’,'Dateline NBC’,”,”,”,”,’17:54, 05/02/06′,”,’handheld’,”,”,’3032599′,’70033′,”);pd_om(‘msnbcom’,'100′);

© 2006 MSNBC.com

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URL: http://www.msnbc.msn.com/id/11191259/

Cancer at 23 – Dateline NBC – MSNBC.com

[Psoriasis vulgaris exacerbated by imatinib therapy in chronic myelogenous leukemia]

Posted by rob on February 5, 2006 under Uncategorized | Be the First to Comment

Shimizu K, Kuroda H, Kida M, Watanabe H, Shirao S, Akiyama T, Fujimi A, Tanaka I, Sato T, Matsunaga T, Niitsu Y
Rinsho Ketsueki. 2005 Oct ; 46(10): 1152-5

Administration of imatinib exacerbated psoriasis vulgaris in a case of chronic myelogenous leukemia (CML). After the cessation of imatinib therapy, the psoriasis was alleviated. Upon readministration of imatinib, the psoriasis worsened despite the improvement of hematological and cytogenetic findings in the CML. Psoriasis is known to be an autoimmune skin disease characterized by Th1 cell-mediated hyperproliferation of keratinocytes, and the type 1 helper T (Th1) cell subset increased with imatinib therapy. Thus, the exacerbation of psoriasis was likely due to the increase in Th1 cells associated with imatinib therapy.

[Therapy-related acute promyelocytic leukemia with a t(9;22)(q34;q11) and t(15;17)(q22;q11 to approximately 12) subclone]

Posted by rob on under Uncategorized | Be the First to Comment

Mochiduki Y, Muramoto S
Rinsho Ketsueki. 2005 Nov ; 46(11): 1218-22

The translocation (15;17) is a typical marker of acute promyelocytic leukemia, whereas t(9;22) is predominantly associated with chronic myelogenous leukemia, and seldom with acute myelogenous leukemia. Furthermore, the association between t(15;17) and t(9;22) in the same cell is extremely rare. We present a case of therapy-related acute promyelocytic leukemia (t-APL) with a subclone accompanied by karyotype 46, XX, t(9; 22)(q34;q11), t(15 ;17)(q22;11 to approximately 12) at onset. A 75-year-old woman was diagnosed as having non-Hodgkin lymphoma of the thyroid gland in July 1997. She was treated with a CHOP-like regimen, but complete remission (CR) was not achieved. She then underwent surgical resection of her thyroid gland, and was treated with etoposide (total dose 16775 mg) from February 1998 to May 2000. In June 2000, having developed t-APL, she was referred to our department. The patient attained CR following treatment with chemotherapy containing all-trans retinoic acid. Ten months later she relapsed, but lost the t(9;22), while maintaining the t(15;17).
[Therapy-related acute promyelocytic leukemia with a t(9;22)(q34;q11) and t(15;17)(q22;q11 to approximately 12) subclone]

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