Chronic and Acute Myeloid Leukemia Reviews ~ Acute myeloid leukemia (AML), which is called acute lymphocytic leukemia (ANLL), is a rapidly progressive tumor arising from hematopoietic precursors, myeloid or stem tissue, giving rise to granulocytes, monocytes, erythrocytes and platelets. There is increasing evidence that genetic events that occur in the early stem cell maturation may lead to leukemia. Second, many cases of secondary leukemia evolve from a "pre-leukemic stage" extended manifests as a hypoproduction myelodysplastic syndrome with abnormal maturation without need malignant behavior. Finally, examination of precursor cells at a stage earlier than the malignant clone extended in a planned way of leukemia may reveal genetic abnormalities such as Down syndrome or monosomy of chromosome number. In maintaining the object using general molecular neoplasia, additional genetic modifications are witnesses in the malignant clone compared with morphologically normal stem cell development above.
Myeloid acute leukemias are classified by morphology and cytochemical staining. Auer are cytoplasmic inclusion bodies crystalline characteristics, but not uniformly in all witnesses myeloid leukemia. In contrast to the mature myeloid tissue, leukemia cells have large immature nuclei with open chromatin and prominent nucleoli. M1 myeloid leukemia from early precursors only apparent maturation for all terminal myeloid cell type. M3 is a promyelocytic leukemia cancer, granulocyte precursors and M3 cells have abundant azurophil granules which are common in normal promyelocytes.
M4 leukemias are from myeloid progenitors can differentiate into granulocytes or monocytes, while derivatives M5 leukemia currently practiced precursors monocyte lineage. Therefore, M4 and M5 cells include both the kernel function and the folded gray monocyte cytoplasm, while M4 cells include granules of granulocytes standard cytochemical staining. chromosomal deletions, duplications, translocations and well balanced was observed on the leukemic tissue in some patients, before the introduction of molecular genetic techniques. leukemia M3 corresponds to a much higher frequency of the t (15; 17) which juxtaposes the PML gene with the RAR gene. RAR encodes a receptor for retinoic acid and hormonal steroid PML encodes a transcription factor which target genes are not known. Interestingly, retinoic acid can induce remission of short term M3 leukemia, supporting the importance of RAR - PML protein mixture. September chromosome monosomy can be observed in leukemias resulting preleukemic myelodysplasia syndrome leukemia or, in both cases, this finding is associated with a worse clinical outcome. As hematopoietic malignancies involving bone acute leukemia circulating cells usually appear (BLAST) and abnormal bone. Occasionally, infiltrates extramedullary leukemia chloromas recognized as can be seen in other organs and mucous surfaces. The marked improvement in the number of circulating blasts can sometimes cause vascular obstruction associated with stroke and bleeding in the brain and pulmonary vascular beds. Leukostases This results in symptoms such as stroke, retinal vein occlusion and pulmonary infarction.
In most cases of AML and other leukemias, blood counts mature granulocytes devices, erythrocytes and platelets are reduced. Susceptibility to infection and depressed amount of granulocyte function and abnormal bleeding as a result of the reduced number of platelets are common problems in people who suffer initially present with leukemia.
Myeloid leukemia (CML) is an indolent chronic leukemia manifested by an increased number of immature granulocytes in the bone marrow and peripheral blood. One of the marks may be CML Philadelphia chromosome cytogenetic function, which is due to translocation of chromosome 9:22 balanced, producing a coding of the fusion gene BCR-ABL for a kinase which phosphorylates a number of key proteins included in cell growth and apoptosis. The fusion gene can recreate a syndrome resembling CML when released in rats.
CML eventually becomes acute leukemia (blast crisis), which is associated with other cytogenetic changes and clinical course similar to acute leukemia. New drugs that block the BCR-ABL kinase course compete with the ATP binding site, induce remissions in most patients with CML in chronic phase. Furthermore, resistance to these inhibitors of BCR-ABL may include amplification of BCR-ABL breakpoint gene as well as for the development (or clonal expansion) mutations in the ATP binding pocket of BCR ABL that it allows binding inhibitors.