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Many of the chromosomal aberrations seen in ALL dysregulate
the expression and function of transcription factors
required for normal B- and T-cell development. Most T-ALLs
have mutations in NOTCH1, a gene that is essential for
T-cell development, while a high fraction of B-ALLs have
mutations affecting genes such as PAX5, TCF3, ETV6, and
RUNX1, all of which are required for the proper differentiation
of early hematopoietic precursors. By disturbing the
expression and function of “master” regulatory factors, these
mutations promote maturation
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Acute lymphoblastic leukemia/lymphomas (ALLs) are
neoplasms composed of immature B (pre-B) or T (pre-T)
cells, which are referred to as lymphoblasts. About 85%
are B-ALLs, which typically manifest as childhood acute
leukemias. The less common T-ALLs tend to present in
adolescent males as thymic lymphomas. There is, however,
considerable overlap in the clinical behavior of B-ALL and
T-ALL; for example, B-ALL uncommonly presents as a mass
in the skin or a bone, and many T-ALLs present with or
evolve to a leukemic picture. Because of their morphologic
and clinical similarities, the various forms of ALL are discussed
here together.
ALL is the most commons cancer

• Oxygen Deprivation
• Hypoxia is a deficiency of oxygen, which causes cell injury
• by reducing aerobic oxidative respiration. Hypoxia is an
• extremely important and common cause of cell injury and
• cell death. Causes of hypoxia include reduced blood flow
• (ischemia); inadequate oxygenation of the blood due to
• cardiorespiratory failure; and decreased oxygen-carrying
• capacity of the blood, as in anemia or carbon monoxide
• poisoning and severe blood loss. Depending on the severity
• of the hypoxic state, cells may adapt, undergo injury, or
• die. For example, if an artery is narrowed, the tissue supplied
• by that vessel may initially shrink in size (atrophy), whereas
• more severe or sudden hypoxia