Abstract
T-cell acute lymphoblastic leukemia (T-ALL) comprises 15% of childhood leukemia. Although multiagent pulse chemotherapy has improved event-free survival in recent decades, the lack of reliable prognosticators and high rate of relapse remain a challenge. Described is a novel discovery of tumor-derived hyperprolactinemia in childhood T-ALL through a case associated with paraneoplastic galactorrhea. Prolactin production by tumor cells, although a rare phenomenon, is previously demonstrated in several adult cancers and 2 pediatric malignancies with unknown implications. This is the first report demonstrating tumor-derived prolactin in pediatric T-ALL and offers potential as a disease marker and therapeutic drug target.
MeSH terms
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Adolescent
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Antineoplastic Combined Chemotherapy Protocols / therapeutic use
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Arthralgia / etiology
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Asparaginase / administration & dosage
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Chromosome Deletion
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Doxorubicin / administration & dosage
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ETS Translocation Variant 6 Protein
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Fatigue / etiology
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Female
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Galactorrhea / blood
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Galactorrhea / etiology*
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Gene Deletion
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Humans
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Paraneoplastic Endocrine Syndromes / blood
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Paraneoplastic Endocrine Syndromes / etiology*
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Polyethylene Glycols / administration & dosage
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Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / complications*
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Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / diagnosis
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Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
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Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics
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Prednisone / administration & dosage
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Prolactin / blood*
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Proto-Oncogene Proteins c-ets / genetics
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Remission Induction
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Repressor Proteins / genetics
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Vincristine / administration & dosage
Substances
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Proto-Oncogene Proteins c-ets
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Repressor Proteins
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Polyethylene Glycols
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Vincristine
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pegaspargase
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Doxorubicin
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Prolactin
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Asparaginase
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Prednisone