Update on myelodysplastic syndromes: new approaches to classification and therapy.

@article{Langston2004UpdateOM,
  title={Update on myelodysplastic syndromes: new approaches to classification and therapy.},
  author={Amelia A Langston and Radhika Walling and Elliott F. Winton},
  journal={Seminars in oncology},
  year={2004},
  volume={31 2 Suppl 4},
  pages={
          72-9
        },
  url={https://api.semanticscholar.org/CorpusID:35556655}
}
Improvements in understanding of hematopoiesis, immunology, and genetics have led to a better understanding of the natural history of these disorders and have facilitated development of more rational and targeted treatment approaches.
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73 References

Evolving concepts in myelodysplastic syndromes.

Clearly, MDS represent a heterogeneous group of disorders, and no uniform etiology or treatment can be prescribed for all patients, and the need for patients to be seen at specialized centers and placed on experimental protocols if they need treatment.

A hypothesis for the pathogenesis of myelodysplastic syndromes: implications for new therapies

A multistep pathogenesis of MDS is proposed, where targeted injury or mutation within hemopoietic stem cells may be followed by an immunologic response adversely affecting progenitor survival and disease progression associated with loss of tumor suppressor activity.

Important features of myelodysplastic syndrome

Primary MDS is a multistep alteration to the hematopoietic stem cells that include genes involved in cell cycle control, mitotic checkpoints as well as growth factor receptors, secondary signal proteins and transcription factors which gives the cell a growth advantage over its normal counterpart.

Nonmyeloablative preparative regimens for allogeneic hematopoietic transplantation. Biology and current indications.

The use of relatively nontoxic, nonmyeloablative, or reduced-intensity preparative regimens still allows engraftment and the generation of graft-vs-malignancy effects, is potentially curative for susceptible malignancies, and reduces the risk of treatment-related morbidity.

Opportunities for TrisenoxĀ® (arsenic trioxide) in the treatment of myelodysplastic syndromes

Biologic features of MDS, which include accelerated apoptotic potential, limited maturation capacity, and medullary neovascularity, create a strong scientific rationale for the investigation of ATO in MDS.

Pentoxifylline, Ciprofloxacin and Dexamethasone Improve the Ineffective Hematopoiesis in Myelodysplastic Syndrome Patients

It is concluded that hematologic improvement in response to PCD therapy supports the validity of this unique anti-cytokine approach and future trials should combinePCD therapy with established approaches (growth factors/chemotherapy) and also should focus on identifying more effective ways of suppressing the pro-apoptotic cytokines in MDS.

Poor response rate to a continuous schedule of Amifostine therapy for ā€˜low/intermediate riskā€™ myelodysplastic patients

It is concluded that therapeutic response to Amifostine in MDS may be schedule dependent and no patients satisfied response criteria on study but two patients showed minor responses.

Molecular pathogenesis of MDS

Evidence suggests that as yet unidentified tumor suppressor genes should have important roles in the molecular mechanisms of MDS, which is considered to be a family of clonal disorders of hematopoietic stem cells that are characterized by ineffective hematoiesis and susceptibility to acute myelogenous leukemias.

Maintenance treatment of patients with myelodysplastic syndromes using recombinant human granulocyte colony-stimulating factor.

G-CSF administered to MDS patients by daily subcutaneous administration was well-tolerated and effective in causing persistent improvement of the neutrophil levels and marrow myeloid maturation, associated with a decreased risk of infection and, in some patients, with decreased red blood cell transfusion requirements.

Effects of treatment with 5-azacytidine on the in vivo and in vitro hematopoiesis in patients with myelodysplastic syndromes.

5-azacytidine, a cell-cycle specific ring analog of the pyrimidine nucleoside cytosine, as a continuous intravenous infusion, led to normalization of the number of CFU-e derived colonies as well as an increase in theNumber of BFU- e derived colonies, correlated with the spontaneous rise in hemoglobin levels and red cell transfusion independence.
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