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T Lymphoblastic Leukemia / Lymphoma

Acute lymphocytic leukemia (ALL) is a clonal stem cell malignancy of excessive lymphoblast proliferation. It is now understood that ALL and lymphoblastic lymphoma are the same disease entities at the morphologic and immunophenotypic levels and classified as either B- and T-cell lymphoblastic leukemia/lymphoma (B-ALL and T-ALL). T-ALL comprises 15% of paediatric and 25% of adult ALL cases. T cell transformation is a multi-step process in which different genetic alterations cooperate to alter the normal mechanisms that control cell growth, proliferation, survival, and differentiation during thymocyte development. In this context, constitutive activation of NOTCH1 signaling is the most prominent oncogenic pathway in T cell transformation. In addition, T-ALLs characteristically show the translocation and aberrant expression of transcription factor oncogenes. These oncogenic transcription factors include T-cell leukaemia homeobox protein 1 (TLX1 also known as HOX11), TLX3 (HOX11L2), LYL1, TAL1 and MLL.

Carcinogen

*Thorium-232 and its decay products, administered intravenously as a colloidal dispersion of thorium232 dioxide

*: Although this is a risk factor for ALL in general, the strength of association with different histological tumor types is not well understood.

Drug

Vincristine

Prednisone

Daunorubicin

Asparaginase

Methotrexate

Cyclophosphamide

Vincristine

Doxorubicin

Dexamethasone

Cytarabine

6-mercaptopurine

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