Detection of BCR-ABL1 kinase domain mutations causing imatinib resistance in chronic myelogenous leukemia.

The reciprocal translocation between chromosomes 9 and 22 [t(9;22)(q34;q11), Philadelphia chromosome] creates a BCR-ABL1 fusion protein that occurs in approximately 95% of cases of chronic myelogenous leukemia (CML), 15% of cases of adult acute lymphoblastic leukemia, and 5% of adult cases of acute myeloid leukemia. The BCR-ABL1 protein is a constitutively activated tyrosine kinase that induces and maintains the neoplastic phenotype in these leukemias. PCR-based methods to identify and quantitate the tumor-specific BCR-ABL1 RNA have been shown to be an ultrasensitive diagnostic, prognostic, and monitoring tool for Philadelphia-positive leukemias.

Quantitative BCR-ABL1 RQ-PCR fusion transcript monitoring in chronic myelogenous leukemia.

The reciprocal Philadelphia translocation between chromosomes 9 and 22 [t(9;22)(q34;q11)] creates a BCR-ABL1 fusion protein that occurs in approximately 95% of cases of chronic myelogenous leukemia (CML), 15% of cases of adult acute lymphoblastic leukemia, and 5% of adult cases of acute myeloid leukemia. The BCR-ABL1 protein is a constitutively activated tyrosine kinase that induces and maintains the neoplastic phenotype in these leukemias. PCR-based methods to identify and quantitate the tumor-specific BCR-ABL1 RNA have been shown to be an ultrasensitive diagnostic/prognostic tool for Philadelphia-positive leukemias.

Metastatic hepatocellular carcinoma mimicking acinic cell carcinoma of the parotid gland: a case report.

Background: Fine needle aspiration (FNA) is becoming increasingly important in the diagnosis of salivary gland lesions. One of the diagnostic difficulties that arise from FNAs is the distinction between primary and metastatic tumors. We describe a case where a right cheek/parotid mass was originally diagnosed as acinic cell carcinoma (ACC) upon biopsy.