Precursor B-cell lymphoblastic leukemia

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| image = Acute lymphoblastic leukemia.jpg

| caption = A Wright's stained bone marrow aspirate smear from a person with precursor B-cell acute lymphoblastic leukemia.|

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Precursor B-cell lymphoblastic leukemia is a form of lymphoid leukemia in which too many B-cell lymphoblasts (immature white blood cells) are found in the blood and bone marrow. It is the most common type of acute lymphoblastic leukemia (ALL). It is sometimes additionally classified as a lymphoma, as designated leukemia/lymphoma. ALL is the most prevalent childhood malignancy, with precursor B-cell ALL (B-ALL) accounting for approximately 75–80% of newly diagnosed pediatric ALL cases.

Subtypes

It consists of the following subtypes:{{cite journal |author=Randolph TR |title=Advances in acute lymphoblastic leukemia |journal=Clin Lab Sci |volume=17 |issue=4 |pages=235–45 |year=2004 |pmid=15559730 |url=http://findarticles.com/p/articles/mi_qa3890/is_200410/ai_n9429273/pg_2}}

  • t(9;22)-BCR/ ABL
  • t(v;11q23)-MLL rearrangement
  • t(1;19)-E2A/PBX1
  • t(12;21)-ETV/ CBFα
  • [http://atlasgeneticsoncology.org/Anomalies/t1719ID1078.html t(17;19)-E2A-HLF]

Molecular mechanisms

One interesting model of precursor B ALL shows aberrant function of a single gene, namely Pax5, as capable to change phenotype of B cells toward precursor cells.{{cite journal |vauthors=Carotta S, Nutt SL |title=Losing B cell identity |journal=BioEssays |volume=30 |issue=3 |pages=203–7 |date=March 2008 |pmid=18293359 |doi=10.1002/bies.20725 }}{{cite journal |vauthors=Den Boer ML, van Slegtenhorst M, De Menezes RX, etal |title=A subtype of childhood acute lymphoblastic leukaemia with poor treatment outcome: a genome-wide classification study |journal=Lancet Oncol. |volume=10 |issue=2 |pages=125–34 |date=February 2009 |pmid=19138562 |pmc=2707020 |doi=10.1016/S1470-2045(08)70339-5 }} In approximately two-thirds of pediatric B-ALL patients, specific chromosomal translocations and their fusion genes are detectable, and these fusion genes play crucial roles as risk factors for strategic treatment. More than 200 fusion genes or mutated genes have been identified in ALL patients to date.

Diagnosis

t(12;21)-ETV/ CBFα has a better prognosis as compared to other subtypes.

Treatment

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References

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