By A. Hagemeijer, H. J. Adriaansen, C. R. Bartram (auth.), Anton Hagenbeek MD, PhD, Bob Löwenberg MD, PhD (eds.)
Relapse of leukemia following profitable remission-induction remedy is still a tremendous challenge within the therapy of sufferers with acute leukemia. Leukemia recurs most often in sufferers with acute myeloblastic leukemia (AML) and excessive hazard acute lymphoblastic leukemia (ALL) following chemotherapy and not more frequently in sufferers with low probability ALL and especially in sufferer teams> submitted to allogeneic marrow transplantation. ' it truly is most likely that the nice majority of those recurrences originate from residual leukemic cells that live to tell the tale preliminary remission-induction chemotherapy. this day, numerous study teams in the course of the international position emphasis on stories interested by the detection and remedy of 'minimal residual disorder' (MRD). those investigations are carried out with the typical target to take on the rest cells. 'Minimal Residual ailment in Acute Leukemia: 1986' summarizes the short developments during this zone. a number of disciplines are fascinated by the research of leukemic cells. The views of cytogenetic and molecular genetic ways for applica tion within the detection of MRD are reviewed. during this appreciate, glossy cyto genetics supply hugely particular tumor markers. The answer of cyto genetic equipment will be really enhanced whilst mixed with different strategies which pick out correct subpopulations of cells. Characterization of oncogenes and gene rearrangements, together with these of immunoglobulin and T-cell receptor genes, and the size of gene items, were verified. thoughts in accordance with those techniques provide fascinating instruments for the detection of MRD. New probabilities of making use of monoclonal anti our bodies also are presented.
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Extra resources for Minimal Residual Disease in Acute Leukemia 1986
Since each Hu-ets subclone recognized a distinct human fragment, it was possible that chromosoma lly separate DNA segment s, each homo 1ogou s to di ffe rent port ions of the v-ets oncogene, existed in the human genome. To explore this possibility, we prepared multiple samples of DNA from a panel of hamster x human somatic cell hybrids each of which segregrate human chromosomes in different combinations (11, 18, 19) these samples were examined with our separate Hu-ets clones. 83 kb Eco R1 fragment, both of which werehomo 1ogous to the 5' port i on of v-ets ,Were concordantly associ ated in these hybrids containing the human chromosome 11.
And Moore, K. L. (1984) Cytogenet. Cell Genet. 37, 312-339. Shows, T. B. (1984) Cytogenet. Cell Genet. 37, 340-397. Kozak, C. A. (1984) in Genetic Maps (Cold Spring Harbor Press, New York) (In press) O'Brien, S. J. (1984) Genetic Maps, Vol. 3. (Cold Spring Harbor Press, New York), pp. 385-387. Nadeau, J. H. and Taylor, B. A. (1984) Proc. Natl. Acad. Sci. A. 81, 814-818. O'Brien, S. , Bonner, T. , O'Connell, C. and Nash, W. G. (1983b) Nature 303, 74-77. , Simonson, J. M. and Eichelberger, M. A. (1982) in Techniques in Somatic Cell Genetics.
In an analysis of 89 metaphase spreads from normal human peripheral blood cells, 37 grai ns were found situated on chromosome 21; 34 of these were located on the terminal portion of chromosome 21. These labeled sites, each consisting of one to three grains, represented 20% of all labeled sites distributed throughout the 89 metaphase spread. Compilation of grain positions from multiple (N=50) labeled No. 3. 3 region. 2 11. q11. _11 ... 3 21 FIGURE 4. 2. situ hybridization of ets-2; demonstrates the distribution of 37 grains which fell on human chromosome 21 in 89 metaphase spreads after in situ hybridization using the Hu-ets-2 as a probe (H33).