Pic Of The Day

Posted by rob on January 31, 2005 under Uncategorized | Read the First Comment

A masked participant poses in San Marco square in Venice. Venice start its famous carnival with a festival of eastern delights featuring street theatre, parades, concerts and exhibits on a ‘mask parade and events in theatre’ theme.

Pic Of The Day

Posted by rob on January 30, 2005 under Uncategorized | Be the First to Comment

A masked person poses at San Marco square in Venice at the start of Carnival.

Add CML Newsire To Your Yahoo Daily News

Posted by rob on January 29, 2005 under Uncategorized | Be the First to Comment

Add to My Yahoo!

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CML Newswire is syndicated by Yahoo and other news sites. If you use Yahoo as your start page you can now add CML Newswire to your daily news feed so the latest information on CML will always be available to you when you read the news.

Role of Chk1 and Chk2 in Ara-C-induced differentiation of human leukemia K562 cells

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Genes Cells. 2005 Feb ; 10(2): 97-106
Human chronic myelogenous leukemia K562 cells are relatively resistant to the anti-metabolite cytosine arabinoside (Ara-C) and, when treated with Ara-C, they differentiate into erythrocytes without undergoing apoptosis. In this study we investigated the mechanism by which Ara-C induces K562 cells to differentiate. We first observed that Ara-C-induced differentiation of these cells is completely inhibited by the radiosensitizing agent caffeine, an inhibitor of ATM and ATR protein kinases. We next found that Ara-C activates Chk1 and Chk2 in the cells, and that the activation of Chk1, but not of Chk2, was almost completely inhibited by caffeine. Proteasome-mediated degradation of Cdc25A and phosphorylation of Cdc25C were induced by Ara-C treatment, presumably due to the activation of Chk2 and Chk1, respectively. To directly observe the effects of checkpoint kinase activation in Ara-C-induced differentiation, we suppressed Chk1 or Chk2 with the Chk1-specific inhibitor Go6976, by generating cell lines stably over-expressing dominant-negative forms of Chk2, or by siRNA-mediated knock-down of the Chk1 or the Chk2 gene. The results suggest that Ara-C-induced erythroid differentiation of K562 cells depends on both Chk1 and Chk2 pathways.

 

http://www.hubmed.org/display.cgi?issn=13569597;uids=15676021

Molecular and cytogenetic characterization of a novel rearrangement involving chromosomes 9, 12, and 17 resulting in ETV6 (TEL) and ABL fusion.

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Cancer Genet Cytogenet. 2005 Feb ; 157(1): 74-7
We performed chromosome analysis on the bone marrow of a patient with BCR/ABL negative chronic myelogenous leukemia (CML). By interphase fluorescence in situ hybridization (FISH), an extra ABL signal was present in interphase nuclei and appeared to be located at 17p in the metaphase cells. Chromosome analysis showed a subtle abnormality at 17p13 and 12p13 but no visible rearrangement at 9q34 (ABL). Additional FISH experiments disclosed a rearrangement between the short arms of chromosomes 12 and 17 at approximately bands 12p13 and 17p13, respectively. In addition, subtelomeric FISH analysis confirmed the presence of terminal 12p at 17p13 and showed terminal 9q34 to be intact on each chromosome 9. Taken together, these results indicated a rearrangement involving chromosomes 9, 12, and 17 that suggested the possibility of juxtaposition of part of the ETV6 (also known as TEL) locus (12p13) with a portion of ABL (9q34) together at 17p13. The ETV6/ABL fusion was confirmed by RT-PCR, which showed that the first 5 exons of ETV6 were fused in frame with ABL at exon 2. Wild-type ETV6 and ABL were also expressed, in accordance with the FISH results that showed no loss of the second ETV6 or ABL allele.

 

http://www.hubmed.org/display.cgi?issn=01654608;uids=15676152

Transcriptional regulation in myelopoiesis: Hematopoietic fate choice, myeloid differentiation, and leukemogenesis

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Exp Hematol. 2005 Feb ; 33(2): 131-43
Myeloid cells (granulocytes and monocytes) are derived from multipotent hematopoietic stem cells. Gene transcription plays a critical role in hematopoietic differentiation. However, there is no single transcription factor that is expressed exclusively by myeloid cells and that, alone, acts as a “master” regulator of myeloid fate choice. Rather, myeloid gene expression is controlled by the combinatorial effects of several key transcription factors. Hematopoiesis has traditionally been viewed as linear and hierarchical, but there is increasing evidence of plasticity during blood cell development. Transcription factors strongly influence cellular lineage during hematopoiesis and expression of some transcription factors can alter the fate of developing hematopoietic progenitor cells. PU.1 and CCAAT/enhancer-binding protein alpha (C/EBPalpha) regulate expression of numerous myeloid genes, and gene disruption studies have shown that they play essential, nonredundant roles in myeloid cell development. They function in cooperation with other transcription factors, co-activators, and co-repressors to regulate genes in the context of chromatin. Because of their essential roles in regulating myeloid genes and in myeloid cell development, it has been hypothesized that abnormal expression of PU.1 and C/EBPalpha would contribute to aberrant myeloid differentiation, i.e. acute leukemia. Such a direct link has been elusive until recently. However, there is now persuasive evidence that mutations in both PU.1 and C/EBPalpha contribute directly to development of acute myelogenous leukemia. Thus, normal myeloid development and acute leukemia are now understood to represent opposite sides of the same hematopoietic coin.

http://www.hubmed.org/display.cgi?issn=0301472X;uids=15676205

A non-ATP-competitive inhibitor of BCR-ABL overrides imatinib resistance

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Imatinib, which is an inhibitor of the BCR-ABL tyrosine kinase, has been a remarkable success for the treatment of Philadelphia chromosome-positive (Ph(+)) chronic myelogenous leukemias (CMLs). However, a significant proportion of patients chronically treated with imatinib develop resistance because of the acquisition of mutations in the kinase domain of BCR-ABL. Mutations occur at residues directly implicated in imatinib binding or, more commonly, at residues important for the ability of the kinase to adopt the specific closed (inactive) conformation to which imatinib binds. In our quest to develop new BCR-ABL inhibitors, we chose to target regions outside the ATP-binding site of this enzyme because these compounds offer the potential to be unaffected by mutations that make CML cells resistant to imatinib. Here we describe the activity of one compound, ON012380, that can specifically inhibit BCR-ABL and induce cell death of Ph(+) CML cells at a concentration of <10 nM. Kinetic studies demonstrate that this compound is not ATP-competitive but is substrate-competitive and works synergistically with imatinib in wild-type BCR-ABL inhibition. More importantly, ON012380 was found to induce apoptosis of all of the known imatinib-resistant mutants at concentrations of <10 nM concentration in vitro and cause regression of leukemias induced by i.v. injection of 32Dcl3 cells expressing the imatinib-resistant BCR-ABL isoform T315I. Daily i.v. dosing for up to 3 weeks with a >100 mg/kg concentration of this agent is well tolerated in rodents, without any hematotoxicity.

http://www.hubmed.org/display.cgi?issn=00278424;uids=15677719

Pic Of The Day

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Ice accumulates on the shore of the East River near the Brooklyn Bridge in New York on January 28, 2005 after several days of frigid weather in the city. The temperature is expected to climb to 35 degrees Fahrenheit (2 Celsius) over the weekend.

BCR/ABL-mediated downregulation of genes implicated in cell adhesion and motility leads

Posted by rob on January 28, 2005 under Uncategorized | Be the First to Comment

BCR/ABL-mediated downregulation of genes implicated in cell adhesion and motility leads to impaired migration toward CCR7 ligands CCL19 and CCL21 in primary BCR/ABL-positive cells.
Leukemia. 2005 Jan 13;
The mechanism underlying p210(BCR/ABL) oncoprotein-mediated transformation in chronic myelogenous leukemia (CML) is not fully understood. We hypothesized that p210(BCR/ABL) suppresses expression of genes which may explain at least some of the pathogenetic features of CML. A subtractive cDNA library was created between BCR/ABL-enhanced-green-fluorescent-protein (GFP)-transduced umbilical cord blood (UCB) CD34(+) cells and GFP-transduced UCB CD34(+) cells to identify genes whose expression is downregulated by p210(BCR/ABL). At least 100 genes were identified. We have confirmed for eight of these genes that expression was suppressed by quantitative real-time-RT-PCR (Q-RT-PCR) of additional p210(BCR/ABL)-transduced CD34(+) UCB cells as well as primary early chronic phase (CP) bone marrow (BM) CML CD34(+) cells. Imatinib mesylate reversed downregulation of some genes, to approximately normal levels. Several of the genes are implicated in cell adhesion and motility, including L-selectin, intercellular adhesion molecule-1 (ICAM-1), and the chemokine receptor, CCR7, consistent with the known defect in adhesion and migration of CML cells. Compared with GFP UCB or normal (NL) BM CD34(+) cells, p210 UCB and CML CD34(+) cells migrated poorly towards the CCR7 ligands, CCL19 and CCL21, suggesting a possible role for CCR7 in the abnormal migratory behavior of CML CD34(+) cells.Leukemia advance online publication, 13 January 2005; doi:10.1038/sj.leu.2403626.

http://www.hubmed.org/display.cgi?issn=08876924;uids=15674360

C/EBPdelta expression in a BCR-ABL-positive cell line induces growth arrest and myeloid differentiation.

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Oncogene. 2005 Jan 10;
CCAAT/enhancer-binding proteins (C/EBPs) are a family of highly conserved transcription factors that have important roles in normal myelopoiesis as well as associated with myeloid disorders. The chronic myelogenous leukemia (CML) cell lines, KCL22 and K562, express exceptionally low levels of endogenous C/EBPs and provide a good model to test the effects of C/EBPs on myeloid differentiation. To explore the possibility that C/EBPdelta can promote differentiation in BCR-ABL-positive cells, we generated stable KCL22 and K562 clones that expressed an inducible C/EBPdelta gene. C/EBPdelta expression resulted in G0/G1 proliferative arrest and a moderate increase in apoptosis of the KCL22 and the K562 cells. Within 4 days of inducing expression of C/EBPdelta, myeloid differentiation of the CML blast cells occurred as shown by morphologic changes and induction of secondary granule-specific genes. We also showed that during granulocytic differentiation of KCL22 cells, the C/EBPdelta protein was detected in immunocomplexes with both Rb and E2F1. Furthermore, expression of C/EBPdelta was associated with downregulation of c-Myc and cyclin E and upregulation of the cyclin-dependent kinase inhibitor p27(Kip1) in both the KCL22 and K562 cell lines. These results show that expression of C/EBPdelta in BCR-ABL-positive leukemic cells in blast crisis is sufficient for neutrophil differentiation and point to the therapeutic potential of ectopic induction of C/EBPdelta in the acute phase of CML.Oncogene advance online publication, 10 January 2005; doi:10.1038/sj.onc.1208393.

http://www.hubmed.org/display.cgi?issn=09509232;uids=15674331

New drug for leukemia

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Reported by Susan Aldridge, PhD, medical journalist

A new drug can help patients whose leukemia is resistant to Gleevec.
Resistance to anti-cancer drugs is unfortunately a fairly common phenomenon. When Gleevec was introduced it was the most successful treatment to date for chronic myelogenous leukemia (CML) but some patients developed resistance to it.

Researchers at Temple University in the US have now found two more drugs that can help patients with Gleevec resistance. We already know that Gleevec blocks a cancer protein called BCR-ABL. But when this protein mutates, Gleevec doesn’t work. The new drugs target parts of the protein that are not susceptible to mutation. They work in cells and animal models and the researchers intend to proceed to human clinical trials in the near future. It is hoped that if given in combination with Gleevec, the drugs would provide 100 per cent response for patients with CML.

Source
Proceedings of the National Academy of Sciences early edition 24th January 2005

Pic Of The Day

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Two Russian policemen guard the desolate Red Square with St. Basil Cathedral in the background, as heavy snowfall hit the Russian capital.

Pic Of The Day

Posted by rob on January 27, 2005 under Uncategorized | Be the First to Comment

A Thai visitor looks at the descending sun on the devastated Khao Lak beach.

Proteomic analysis of nuclear matrix proteins during arsenic trioxide induced apoptosis in leukemia K562 cells.

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Chin Med J (Engl). 2005 Feb ; 118(2): 100-4
BACKGROUND: Arsenic trioxide (As2O3) has been identified as a very potent anti-acute leukemic agent. However its role in apoptosis needs to be elucidated. As2O3 interferes with the proliferation and survival of tumor cells via a variety of mechanisms. Drug-target interactions at the level of nuclear matrix (NM) may be critical events in the induction of cell death by As2O3. This study dealt with As2O3-target interactions at the level of NM in chronic myelogenous leukemia cell line K562 by proteomics. METHODS: K562 cells were cultured in MEM and treated with different concentrations of As2O3. The nuclear matrix proteins were analyzed by high-resolution two-dimensional gel electrophoresis and computer-assisted image analysis. RESULTS: As2O3 significantly inhibited the growth of chronic myelogenous leukemia cell line K562 at low concentrations. While more than 200 protein spots were shared among the nuclear matrices, about 18 distinct spots in the nuclear matrices were found characteristic for As2O3 treated cells. CONCLUSIONS: As2O3 induces apoptosis in K562 cells in a dose and time-dependent manner. Our results demonstrated that for the detection of the onset of apoptosis, the alteration in the composition of nuclear matrix proteins was a more sensitive indicator than nucleosomal DNA fragmentation test. These results indicated that As2O3 might be clinically useful in the treatment of chronic myelogenous leukemia. The changes of nuclear matrix proteins in the treated cells can be used as a useful indicator for this treatment.

http://www.hubmed.org/display.cgi?issn=03666999;uids=15667793

Selective effect of imatinib on serum IgM in a patient with CML.

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Int J Hematol. 2004 Nov ; 80(4): 381-2

No abstract yet

http://www.hubmed.org/display.cgi?issn=09255710;uids=15615266

Pic Of The Day

Posted by rob on January 26, 2005 under Uncategorized | Be the First to Comment

Alexandra Kauc and Michal Zych of Poland perform in the Ice Dancing compulsory dance competition at the European Figure Skating Championships in Turin.

Synergistic interactions between imatinib and the novel phosphoinositide-dependent kinase-1 inhibitor OSU-03012 in overcoming imatinib resistance.

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Synergistic interactions between imatinib and the novel phosphoinositide-dependent kinase-1 inhibitor OSU-03012 in overcoming imatinib resistance.
Blood. 2005 Jan 21;
Resistance to the Abl kinase inhibitor imatinib has become a critical issue for patients in advanced phases of chronic myelogenous leukemia. Imatinib-resistant tumor cells develop, in part, as a result of point mutations within the Abl kinase domain. As Akt plays a pivotal role in Abl oncogene-mediated cell survival, we hypothesize that concurrent inhibition of Akt will sensitize resistant cells to the residual apoptotic activity of imatinib, thereby overcoming the resistance. Here, we examined the effect of OSU-03012, a celecoxib-derived phosphoinositide-dependent kinase-1 (PDK-1) inhibitor, on imatinib-induced apoptosis in two clinically relevant Bcr-Abl mutant cell lines, Ba/F3p210(E255K) and Ba/F3p210(T315I). The IC50 values of imatinib to inhibit the proliferation of Ba/F3p210(E255K) and Ba/F3p210(T315I) were 14 +/- 4 and 30 +/- 2 microM, respectively. There was no cross-resistance to OSU-03012 in these mutant cells with IC50 of 5 microM irrespective of mutations. Nevertheless, in the presence of OSU-03012, the susceptibility of these mutant cells to imatinib-induced apoptosis was significantly enhanced. This synergistic action was, at least in part, mediated through the concerted effect on phospho-Akt. Together, these data provide a novel therapeutic strategy to overcome imatinib resistance, especially with the Abl mutant T315I.

 

http://www.hubmed.org/display.cgi?issn=00064971;uids=15665113

AMN107 and BMS-354825 Trials

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Drugs for leukaemia on trial

LOH FOON FONG attended a haematology meeting in San Diego, the United States, recently and gives an update on treatment for chronic myeloid leukaemia.  

TWO drugs â?? codenamed AMN107 and BMS-354825 â?? will be moving into Phase II trials on patients who do not respond to higher doses of, or are intolerant to, imatinib mesylate (IM), the drug in current use to treat myeloid leukaemia, a type of blood cancer.  

Encouraging results of both drugs from Phase I trials were reported during the 46th Annual Meeting of the American Society of Hematology in San Diego, the United States, recently. 

Dr Francis Giles

Patients in the chronic phase of chronic myeloid leukaemia (CML) who did not react to IM were said to have responded well to the new drugs. â??We hope that the AMN107 drug has less resistance problem than the IM,â? said Dr Francis Giles, chief of developmental therapeutics from the MD Anderson Cancer Centre in Houston, Texas.  

â??We have a molecule that is more potent, binds more tightly and should be less vulnerable to mutations, and hopefully a better toxicity profile. So far what we have from the Phase 1 study is some marrow toxicity but interestingly the only marrow toxicity we have was transient to people who went on to respond to the treatment,â? he said. 

There were also some skin rashes that did not go away with any drug and some changes in the liver which went away even when patients continued the drug at the same dosage, he said. The researchers are working on defining the dosage toxic limit, he said. 

When IM was discovered five years ago, it was a major breakthrough in leukaemia treatment because it targeted specific proteins in cancer cells and stopped them from growing without killing the normal cells like traditional treatment did. 

The results from IM, or also commonly called Imatinib, were so significant that the drug was quickly introduced to the world. IM is now recognised as the main standard treatment for CML patients and offers more than 90% survival in newly-diagnosed patients. Interferon alpha was previously considered the standard treatment for this group of patients. 

CML is a cancer that starts in the bone marrow and invades the blood. The incidence of CML is 1.6 per 100,000 per year. The American Cancer Society estimates that 4,600 cases will be diagnosed in the United States this year. It usually occurs among middle-aged adults, mostly among 50-year-olds. 

Dr Jorges Cortes

About 95% of CML patients have a genetic abnormality called the Philadelphia (Ph+) chromosome. The chromosome produces an abnormal enzyme Bcr-Abl tyrosine kinase that blocks the normal signal that tells the body to stop producing white blood cells. As such, there is a proliferation of white blood cells. IM is a relatively selective inhibitor of the abnormal enzyme. 

Despite the breakthrough, the disease in a small number of chronic phase CML patients continues to deteriorate and patients in worse stages, accelerated and blast phases of CML, have a poorer prognosis and higher IM resistance rates. 

Close to 80% of patients who are treated with IM as the first line therapy on the standard 400gm dose achieve a complete cytogenic response (the disease is no longer detected in the genes), said Dr Jorge Cortes, the scientist from the MD Anderson Cancer Centre in a press briefing on Five years of Imatinib: Lessons Learned in CML Treatment Strategy organised by Novartis Corporation (Malaysia).  

After three years, over 90% of them are still sustaining the cytogenic response and the molecular response rate continues to improve, he said. 

â??It clearly changed the way we manage patients. We have gone from an era of trying to control the manifestation of the disease to trying to achieve cytogenic responses, which we had learned from the use of interferon. Now we are trying to achieve molecular responses,â? he said. 

In CML, improvement in molecular response means the reduction in quantities of Bcr-Abl while a complete molecular response means the Bcr-Abl levels are undetectable. 

Australian data has indicated that more patients are getting into complete molecular response after four years. If they achieve a good response, especially if it is cytogenic within 12 months and molecular by 12 months, their survival rate is good, said Dr Cortes. 

â??But what happens after 10 years, we donâ??t know. Four or five years is remarkable considering anything we had in the past,â? he said. 

Dr Oliver Ottmann.

â??There is a new method our (American) group and the Australian team are looking at â?? higher doses of IM and trying to improve on the early responses to get more durable responses. We are seeing more early responses,â? he said. 

Dr Oliver Ottmann, study coordinator and head of the Experimental Haematology at the Johann Wolfgang Goethe University, Frankfurt, Germany, said combination therapy would be the future direction of leukaemia treatment: IM can be combined with non-targeted conventional therapy or two intelligent agents can be combined together.  

Since IM was introduced, transplantation has taken a back seat. What is the role of transplantation today? 

Although it can cure patients, the number of transplants carried out on CML patients has decreased, said Dr Cortes. 

â??Patients are reluctant to go for a transplant because of the mortality risk. But for young patients, transplant will still be an option,â? he said. 

The problem with transplantation is that patients can have a relapse 10-15 years after the transplant, he said. â??Since medical treatment has become more defined, hopefully, we will develop transplantation into a more defined therapy,â? he said.  

Dr Ottmann said the transplant method when combined with IM has worked in some elderly patients, who usually cannot tolerate the method. 

The greatest challenge with mutations for IM and the two new drugs being researched is with one particular mutation known as T315I. 

â??In IM-treated patients, all of the common mutations except T315I appear to be highly sensitive to IM,â? said Dr Giles. â??At this stage, we are highly suspicious based on the pre-clinical data that the T3151 may be particularly resistant. We canâ??t say it clinically yet although I suspect it would be true,â? he said adding that less than 10% of patients have the mutations. 

â??However, we do not have to worry about mutations if there is no disease. These mutations need time to develop. If we can eliminate them, it will not be a long-term issue,â? he said. 

Dr Nicholas Choong, oncologist and haematologist at the University of Chicago, said the challenge with IM, ANM107 and BMS-354825 is that they might block the signal of the receptors on normal cells, and stop the receptors from conveying messages to the chromosomes for certain genes to be expressed. The implications are that normal blood cells with the receptors can be affected and platelets level can fall and patients become anaemic or have their white blood count wiped out and patients become susceptible to infections, he said. As such, doctors will have to find the right dosage for each patient so that the normal cells are not affected, he said. 

Dr Choong added that the AMN and BMS are promising drugs for a difficult disease but further studies need to be done for the toxicity. â??In the first phase BMS study, patients had irregular heart beats. They may or may not be related to the toxicity. Itâ??s too early to say. They are better defined in larger clinical trials,â? he said. 

IM is also being tested for treating other cancers. Now more than 150 clinical trials are evaluating IM in certain forms of prostate, lung and brain cancers, and blood diseases. 

 

http://thestar.com.my/lifestyle/story.asp?file=/2005/1/26/features/9648305&sec=features

Program Introduces New Tool That Helps Identify Older Patients’ Capacity To Benefit From, Tolerate Cancer Treatment

Posted by rob on January 25, 2005 under Uncategorized | Be the First to Comment

Program Introduces New Tool That Helps Identify Older Patients’ Capacity
                  To Benefit From, Tolerate Cancer Treatment

    WHITE PLAINS, N.Y., Jan. 25 /PRNewswire/ — The Leukemia & Lymphoma
Society announced today the launch of a pilot program, “Breaking Through the
Age Barrier.”  The launch coincides with the Society’s release of a toolkit
for older patients and their caregivers.  The pilot program, for patients and
healthcare professionals, aims to encourage older blood cancer patients to get
the best possible care and equip their medical team with tools to make
treatment decisions.  At the core of the project is the Geriatric Assessment
which helps providers recognize who will benefit from treatment who may have
special needs that need to be addressed during treatment.  A Comprehensive
Geriatric Assessment checklist, which evaluates an individual’s physical and
emotional capacity to undergo and tolerate cancer treatment and its side
effects, includes simple forms to fill out as well as physical and laboratory
tests.
    “Older patients may need special attention when it comes to cancer
treatment,” says Robin Kornhaber, the Society’s Senior Vice President of
Patient Services.  “But the concept of being too old for cancer treatment is
outdated.”  More than half of all cancers occur in people older than 65 years
and they appear to benefit from treatment to the same extent as younger
individuals.

    Six-Chapter Pilot Program Introduces Geriatric Assessment
    The Society’s pilot program will be introduced this spring in Detroit,
Mich., Palm Beach, Fla., Northern New Jersey, Upstate New York, Baltimore,
Md., and Orange, Riverside, San Bernardino, Calif.  Next year, the Society
expects the program to be offered at each of its 63 chapter sites across the
U.S.  At the pilot sites this year, the Society will hold workshops for older
patients to familiarize them with advocacy, communication and emotional
aspects of battling blood cancer.
    The Society will also introduce the Comprehensive Geriatric Assessment
checklist (CGA) to elderly patients.  Health care professionals review CGA
criteria with patients to assess how much an older adult might benefit from
cancer treatment and how well he or she would be likely to tolerate it.  The
CGA is also useful in identifying problems that can be remedied (such as poor
nutrition), making cancer treatment safer for the individual.
    By familiarizing elderly patients with this tool, the Society hopes
patients will fully participate in this evaluation and even ask for such an
assessment if one is not offered.  This provides patients the opportunity to
proactively engage in treatment decisions and also helps patients recognize
the impact their general health, independence and emotional well-being may
have on the success of their cancer treatment.
    The CGA looks at a person’s ability to carry out day-to-day activities
independently (called functional status), the presence of other illnesses,
living conditions and support, thinking and mood, other medications taken,
nutrition and so-called geriatric syndromes.

    Age Not a Barrier to Treatment
    “Age alone is not enough to identify a patient’s chances to benefit from
cancer treatment,” said Lodovico Balducci, M.D., program leader of the Senior
Adult Oncology Program at the H. Lee Moffitt Cancer Center and Research
Institute in Tampa.  “One 75-year-old can be perfectly healthy with no other
illnesses and be very independent and capable, while another may be struggling
with other ailments and be completely dependent.  Health care professionals
who conduct a CGA with patients will get a more complete picture, and
patients, in turn, when educated about the value of the CGA will find it more
palatable and will likely be more engaged in their health care.”

    Without such an assessment, it is not unusual for an older patient to be
turned away from a clinical trial (a controlled test of a new drug or medical
device in humans) based on age or for a clinician to take a less-aggressive
treatment tact with an elderly patient.  When John Rowe of Washington, D.C.,
was diagnosed with chronic myelogenous leukemia in 2000, he was initially
rattled, but quickly optimistic.  He was 62 and in good health when the
diagnosis came.  He had heard about a new experimental drug (now marketed as
Gleevec) in clinical trials and was going to see a 35-yr-old ‘whiz kid’
oncologist.  The ‘whiz kid,’ however, consulted a statistical table, told Rowe
that, at 62, he probably had between one and four years left, should get his
affairs in order and the doctor would keep him comfortable until the end came.
Rowe quickly collected his own patient records, ceased his relationship with
the whiz kid, investigated the clinical trials on his own and was enrolled.
He’s been on Gleevec for four years and was in remission six months after
starting on the drug.

    Toolkit for Older Adults and Their Caregivers
    In addition, The Leukemia & Lymphoma Society has published “A Toolkit for
Older Adults with Cancer, and Their Caregivers.”  The brochure series includes
pamphlets on choosing a healthcare team, understanding treatment options and
clinical trials, money matters and a caregiver’s guide.  The brochure series,
which is available free, can be obtained by calling The Leukemia & Lymphoma
Society’s Information Resource Center (IRC) at 1-800-955-4572.  For
information about the Breaking Through the Age Barrier pilot program and when
it will be offered, patients are encouraged to call their local chapters.

    About The Leukemia & Lymphoma Society
    The Society, headquartered in White Plains, NY, with 63 chapters in the
United States and additional branches in Canada, is the world’s largest
voluntary health organization dedicated to funding blood cancer research and
providing education and patient services. The Society’s mission: Cure
leukemia, lymphoma, Hodgkin’s disease and myeloma, and improve the quality of
life of patients and their families. Since its founding in 1949, the Society
has invested more than $360 million in research specifically targeting
leukemia, lymphoma and myeloma. Last year alone, the Society made more than
812,000 contacts with patients, caregivers and healthcare professionals.

    For more information about blood cancer, visit http://www.LLS.org or call
the Society’s Information Resource Center (IRC), a call center staffed by
master’s level social workers, nurses and health educators who provide
information, support and resources to patients and their families and
caregivers. IRC information specialists are available at (800) 955-4572,
Monday through Friday, 9 a.m. to 6 p.m. ET.

SOURCE The Leukemia & Lymphoma Society
Web Site: http://www.LLS.org

http://www.prnewswire.com/cgi-bin/stories.pl?ACCT=109&STORY=/www/story/01-25-2005/0002901885&EDATE=

Pic Of The Day

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An Indian family of tsunami survivors are sillhouetted against the setting sun as they return to their shelter with their belongings in Nagapattinam District