ABSTRACT
Occurrences of lymphoma and differentiated thyroid cancer are rare. Usually, involvement of the thyroid gland is seen as a part of extranodal involvement or as a part of radiation-induced malignant transformation in previously treated lymphoma patients. The incidence of synchronous hematological malignancy with differentiated thyroid cancer is 7%. The synchronous occurrence of differentiated thyroid cancer and lymphoma poses a significant diagnostic and treatment dilemma. Here we report a case series of four patients with lymphoma and differentiated thyroid cancer. All four patients had lymphoma treated first followed by definitive management of thyroid malignancy.
Subject(s)
Antineoplastic Agents/administration & dosage , Head and Neck Neoplasms/diagnosis , Head and Neck Neoplasms/pathology , Hodgkin Disease/diagnosis , Hodgkin Disease/pathology , Maintenance Chemotherapy/methods , Precursor Cell Lymphoblastic Leukemia-Lymphoma/complications , Adolescent , Histocytochemistry , Humans , Immunohistochemistry , Male , Neck/diagnostic imaging , Precursor Cell Lymphoblastic Leukemia-Lymphoma/drug therapy , Tomography, X-Ray ComputedSubject(s)
Jaundice, Obstructive/pathology , Parotid Neoplasms/pathology , Sarcoma, Myeloid/pathology , Stomach Neoplasms/pathology , Humans , Jaundice, Obstructive/complications , Male , Middle Aged , Parotid Gland/pathology , Parotid Neoplasms/complications , Sarcoma, Myeloid/complications , Stomach/pathology , Stomach Neoplasms/complicationsABSTRACT
The BCR-ABL1 fusion gene derived from the Philadelphia chromosome, resulting from a classical translocation event t(9;22)(q34.13;q11.23), is responsible for the pathogenesis of chronic myeloid leukemia (CML) in more than 90% of the patients. The isoderivative chromosome 22, ider(22), and relative amplification or duplication of the BCR-ABL1 gene have been considered as one of the major reasons associated with the resistance to chemotherapy with imatinib mesylate, but the data remain unclear. GTG-banding together with FISH were performed to identify the presence of the ider(22) chromosome. Reverse transcription-polymerase chain reaction (RT-PCR) for the detection of BCR-ABL1 fusion transcripts and BCR-ABL1 kinase domain mutation analysis were carried out in this study. Conventional and molecular cytogenetic analysis on metaphase chromosomes confirmed the presence of ider(22) chromosomes in both patients. Molecular characterization revealed the presence of a 210-kDa BCR-ABL1 type b3a2 and lack of mutations at the kinase domain region on the fusion product in both patients. The occurrence of the ider(22) chromosome could be considered as an important marker correlated with the aggressive progression of CML as well as the emergence of drug-resistant cell clones.
