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A. Townsend Peterson, Monica Papeş and Jorge Soberón


The suite of factors that drives where and under what conditions a species occurs has become the focus of intense research interest. Three general categories of methods have emerged by which researchers address questions in this area: mechanistic models of species’ requirements in terms of environmental conditions that are based on first principles of biophysics and physiology, correlational models based on environmental associations derived from analyses of geographic occurrences of species, and process-based simulations that estimate occupied distributional areas and associated environments from assumptions about niche dimensions and dispersal abilities. We review strengths and weaknesses of these sets of approaches, and identify significant advantages and disadvantages of each. Rather than identifying one or the other as ‘better,’ we suggest that researchers take great care to use the method best-suited to each specific research question, and be conscious of the weaknesses of any method, such that inappropriate interpretations are avoided.

Open access

Aliz-Beáta Tunyogi, I Benedek, Judit Beáta Köpeczi, Erzsébet Benedek, Enikő Kakucs, Monica Istrati and Zsuzsa Pap


Introduction: Chronic myeloid leukemia (CML) is a clonal myeloproliferative disorder; the molecular hallmark of the disease is the BCR-ABL gene rearrangement, which usually occurs as the result of a reciprocal translocation between chromosomes 9 and 22. Tyrosine kinase inhibitors (TKI) were the first drugs that targeted the constitutively active BCR-ABL kinase and it have become the standard frontline therapy for CML. Monitoring the treatment of CML patients with detection of bcr-abl transcript levels with real time qualitative polymerase chain reaction (RQ-PCR) is essential in evaluating the therapeutic response.

Material and method: At the Clinical Hematology and BMT Unit Tîrgu Mureș, between 2008-2011, we performed the molecular monitoring of bcr-abl transcript levels with RQ-PCR in 16 patients diagnosed with CML.

Results: We have 11 patients on imatinib treatment who achieved major molecular response. One patient lost the complete molecular response after 5 years of treatment. Two patients in blast crisis underwent allogeneic hematopoietic stem cell transplantation from identical sibling donors. The first patient is in complete molecular remission after 4 years of the transplant with mild chronic GVHD. The other patient had an early relapse with treatment refractory disease and died from evolution of the disease. Three patients with advanced phases of the disease present increasing transcript levels. We performed the dose escalation, and for two of them the switch to the second generation of TKI.

Conclusions: Regular molecular monitoring of individual patients with CML is clearly desirable. It allows for a reassessment of the therapeutic strategy in cases of rising levels of BCR-ABL as an early indication of loss of response.