Chronic Lymphocytic Leukemia, Advantages of Monoclones?Viggo Jonsson1*, Haneef Awan1, Tom Borge Johannesen2 and Geir E Tjonnfjord1
- *Corresponding Author:
- Viggo Jonsson
Department of Hematology
Rikshospital, Institute of Clinical Medicine
University of Oslo, Postbox 4950 Nydalen NO 0424 Oslo, Norway
Received date: April 29, 2014; Accepted date: July 20, 2014; Published date: July 25, 2014
Citation: Jonsson V, Awan H, Johannesen TB, Tjonnfjord GE (2014) Chronic Lymphocytic Leukemia, Advantages of Monoclones?. J Leuk (Los Angel) 2:142. doi: 10.4172/2329-6917.1000142
Copyright: © 2014 Jonsson V, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
From a basic biological point of view, genetic traits from the human genome have been selected during a long evolution in the fight for fitness. Since the susceptibility for CLL has a genotype, a theoretical question about its advantage is relevant. This is a question about mutated monoclones and whether they are an advantage to man. We suggest that the genetic capability to provide such monoclones could be explained as reminiscence from the fetal life like a “Bad for the postnates, good for the prenates” principle. Some examples are described, e.g. the fetomaternal processing of endogenous retrovirus in the production of placenta-specific transcripts of several genes in a ceasefire balance with potential infectious exogenous retrovirus. The regulation of some cytokine reactions affected lymphocytes and monocytes around the trophoblasts, which clearly has a specific clonal pattern. Feto-maternal microchimerism with longstanding implanting of clonal maternal stem cells or lymphocytes in the offspring is yet another example giving rise to later autoimmune reactions both in the mother and in the adult life of the offspring. Based on the clinical association between CLL and the other malignant hematological disorders, seen as an increased frequency of the diagnoses in affected families, a genetic linking of their susceptibility seems likely. This entity of clonal disorders may then perhaps be seen as a previous feto-maternal genetic repertoire.