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Acute Myelogenous Leukemia - TCG-small
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What You Need To Know About Acute Myelogenous Leukemia

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Acute Myelogenous Leukemia

Acute Myelogenous Leukemia - TCG

Acute Myelogenous Leukemia is the rapid, uncontrolled production of a malignant Lymphoid or Myeloid cell (ortheir precursors), leading to immune system failure, other blood cell disruption, invasion of normal body tissues by the abnormal clone, and profound metabolic disturbance.

Acute Myelogenous Leukemia happens when a hematopoietic stem cell undergoes malignant transformation into a primitive, undifferentiated cell with abnormal longevity.

These lymphocytes (acute lymphocytic leukemia [ALL], or myeloid cells (acute myelocytic leukemia [AML]) proliferate abnormally “differentiation”, replacing normal marrow tissue and hematopoieticcells and inducing anemia, thrombocytopenia, and granulocytopenia.

They are blood-borne, so can easily infiltrate various organs and sites, including the liver, spleen, lymph nodes, CNS, kidneys, and gonads.

The rapid clinical course, with death typically within one year without treatment, characteristically distinguish Acute Leukemia from the related Chronic Leukemia, who’s untreated clinical course is typically measured in years instead of months.

Ultimately,Acute Leukemia is an aggressive blood cell cancer.

There are several subtypes of acute leukemia:

Core-binding factor AML

Acute Promyelocytic Leukemia (APL)

Secondary AML

Standard AML

Core-binding factor AML and APL are distinguished by their morphological appearance under the microscope (histology) and their chromosome abnormalities (cytogenetics).

Secondary AML refers to AML developing after chemotherapy for a prior malignancy, for example breast cancer or a lymphoma such as Hodgkin’s disease.

The core-binding factor leukemias and APL have the most favorable prognosis.

Chronic Myelogenous Leukemia (CML) was the first leukemic subset for which a chromosomal marker, called the Philadelphia chromosome was discovered.

This was the first leukemia in which the molecular basis for the disease in understanding the biologic state was identified.

Much information has been collected about the genetic change generated by the Philadelphia chromosome, the P210bcr-abl protein, and the other proteins with which it interacts.

The Philadelphia chromosome was discovered in Philadelphia,Pennsylvania in 1960. This discovery was remarkable because it was the first occasion on which an abnormality in the chromosomes was linked with a malignant medical condition.

One of the major unanswered questions about CML is what accounts for the restriction of the leukemia to the myeloid cells, despite the fact that the genetic abnormality is present in the stem cell and is present in all lineages and at all levels of differentiation.

Some data have been developed suggesting that the P210 protein is present at those stages of maturation in which the expansion of myeloid precursor cells takes place.

 

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