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#1
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2013 MDS Conference
Hi All,
Now the abstracts from the MDS Conference in Berlin are available. http://www.sciencedirect.com/science...126/37/supp/S1 Kind regards Birgitta-A |
#2
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One conference paper I find particularly interesting is Did the prognosis of MDS patients improve during the last 30 years? by J. Neukirchen et al.
They did a large survey to see how median survival times for MDS patients changed over the decades. The most significant trend they found was that for patients with more than 5% blasts in the bone marrow who did not have an allogeneic transplant, median survival times was 50% higher in the last decade compared with the preceding two decades. This improvement applied to all age groups. The difference can be explained by the availability of new treatments and perhaps the increased success of transplants. They found that the prognosis for MDS patients with at less than 5% blasts did not change significantly over the same time period, presumably because treatment approaches such as supportive care for patients with low-risk MDS haven't changed as much over the years. |
#3
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Quote:
They did a large survey to see how median survival times for MDS patients changed over the decades. The most significant trend they found was that for patients with more than 5% blasts in the bone marrow who did not have an allogeneic transplant, median survival times was 50% higher in the last decade compared with the preceding two decades. This improvement applied to all age groups. The difference can be explained by the availability of new treatments and perhaps the increased success of transplants. Can you tell us what treatments increased survival times by 50 %? They found that the prognosis for MDS patients with at less than 5% blasts did not change significantly over the same time period, presumably because treatment approaches such as supportive care for patients with low-risk MDS haven't changed as much over the years it became obvious to me that a lot of scientists have become frustrated by the lack of progress they've made in the last 30 years. This is further supported by the accuracy of the prognostic scoring technique developed 20 years ago. Its still quite accurate but doesn't account for demethylators that might add a few months. Perhaps that's why SCT gets a lot more attention, a bit more progress and more encompassing then a cure for the rare MDS. Rare diseases not much $$ to be made by big pharma. |
#4
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Not from this study. They studied overall survival and attributed the increase to overall improvements in treatment. Actually, earlier diagnosis and better care (which is more general that just treatment) probably contributed as well.
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#5
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Berlin 2013
Hi sbk007,
As far as I understand the suppl of Leukemia Research with the abstracts is free. Here is another interesting abstact about hypocellularity: Hypoplastic myelodysplastic syndromes are not a specific clinical entity J. Schemenau, S.E. Baldus, M. Anlauf et al Department of Hematology and Oncology, Heinrich-Heine-Universität Düsseldorf, Düsseldorf, Germany Background: About 10-15% of all Myelodysplastic syndromes (MDS) present with hypocelluar bone marrow, but data on haematological characteristics and clinicial outcome are sparse. Introduction: Recently, Tong et al proposed a special prognostic scoring system for patients with MDS and hypocellular marrow. Purpose: The aim of our study was to describe haematological, cytogenetic, clinical, and prognostic characteristics of patients with hypocellular MDS using the data base of the Düsseldorf registry. Materials and Methods: We analysed data of 3742 patients, in which cellularity was assessed by means of central cytology and/or histology. Patients characteristics at the time of diagnosis were compared between hypercellular (N=1686), normocellular (n=1580) and hypocellular (n=476) cases. Prognostic parameters used in the IPSS as well as in the prognostic score for hypoplastic MDS were analysed. Patients were followed up until December 31th 2012. Results: There were no significant differences with regard to age, gender, haematological features, such as haemoglobin between hyper-, normo- and hypocellular cases (p=n.s.), whereas a significant difference in platelet levels between hypo- and normocellular MDS (p=0,005) and ANC levels between hypocellular compared to normo and hypercellular MDS (p=0,001) could be found. Differences with regard to cytogenetic risk groups, LDH, IPSS-,WPSS and IPSS-R risk groups, bonemarrow blasts and general health condition could not be described (all p values n. s.), except for WHO Types (p=0,005). Median survival of the hypercellular cases was 20 months, as compared to 32 months in the normo-, and 29 months in the hypocellular cases (p=0,0005). The cumulative risk of AML evolution 2 and 5 years after diagnosis was comparable 29%, 20%, 25% after 2 years, 44%, 37%, 45% after 5 years (p=0,003). The risk groups defined by the recently published hypocellular prognostic score (Tong et al, Cancer 2012) differed in terms of prognosis, but the capacity of the score to subdivide the patients was even higher when applied to normo- and hypercellular cases. The low risk group of hypercellular patients had a worse prognosis as compared to normo- and hypocellular patients. Conclusions: Patients with hypocellular MDS did not differ significantly from hyper- and normocellular types with regard to haematopoietic insufficiency and prognosis and therefore should not define a separate MDS type. As the prognostic parameters did not differ, the hypocellular score is working fine, but is not specific. These cases can be prognosticated using the IPSS with the same results as compared to other MDS cases. Kind regards Birgitta-A |
#6
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Thank you Birgitta
The link took me to the article but registration required to read it and so 31.00. The study you posted seems to support the current system in use. All I was saying is that you could spend many hours combing papers from1980 till now and it all brings you back to the same place we were 20 years ago. Aside from Vidaza, Dacogen, and some experimental hypomethylating drugs that might buy 9 months there has been little progress. What progress that has been is recognizing this and going to SCT. Now the game becomes how do we increase survival curves with SCT. There you get action because SCT can cure a lot of different diseases broadening interest and therefore money. As sad is may seem, w/a/disease that affects 6/100,000 people per year 80% over the age of 70 you can see there's not much in it to warrant investment in research. However if you can treat MDS AND some other disease not as rare then its more attractive. I think this is why all of the clinical trials I have come across lump mdsers w/ AML,CML, or something not as rare. Thanks again P.S. Vidaza, dacogen,SGI110, these are used because they demethylate dna. The researchers believe DNA gets over methylated and as such chromosomes get whacked and genes cant express(make proteins) so by demehylating you get gene expression and hopefully remission for a while. Last edited by sbk007 : Fri May 10, 2013 at 08:22 PM. |
#7
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Day one summary available at MDS Beacon
The Day One Summary at MDS Beacon has been posted. As usual, a well-written update for all who missed their flight connection to Berlin.
http://www.mdsbeacon.com/news/2013/0...pdate-day-one/
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Ric: Low-risk MDS (blasts <4%); 4 cycles Revlimid no positive response; PRBC transfusion dependent; so far, 392'units' over 8 3/4 years; BMB #4 (15/04/01) shows evolution to AML (blasts 20-30%) 47,XY,del(5) (q22q35),+21[24][cp24]/46,XY(1). |
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