D. Haase.
Simposio Congreso de Zaragoza 2011: Neoplasias mieloides relacionadas con la terapia.
Genetic and molecular basis in myeloid neoplasias in relation with treatment.
D. Haase.
Department of Hematology. University of Göttingen (Germany).
Conclusiones
- Therapy-induced hematologic neoplasms represent the most severe long-term complication of antineoplastic therapy with breast cancer as the leading primary malignancy. It is anticipated that the incidence will further increase in future.
- On the cytogenetic level T-HN are well characterized. They can be subdivided into at least two subgroups according to the cytogenetic profile and the antecedent therapy with distinct prognosis.
- The introduction of array CGH has enabled a more comprehensive characterization of copy number variations additive to conventional cytogenetics at a submicroscopic level displaying new critical chromosomal regions. A lot of candidate genes now have been identified which Will be promising as targets for further investigations and innovative therapeutic strategies. The same holds true for epigenetic - and gene expression analyses.
- Knowledge of the multistep pathogenesis spanning from celular damage to clonal therapy-induced malignancy now is increasing with impressive data about the rapidity of the leukemogenic process in vivo.
- A very clear picture of the genetic mechanisms behind the development of T-HN has been condensed with as yet 8 clearly distinct pathways. It has also become evident that host factors such as constitutional impairment of metabolism of foreign compounds and DNA-repair contribute substantially to the development of T-HN and provide the opportunity to define patient cohorts at risk and to develop strategies to rescue these patients from therapyassociated malignancies.
