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1.
Hum Pathol ; 44(4): 670-5, 2013 Apr.
Article in English | MEDLINE | ID: mdl-23313307

ABSTRACT

Composite lymphoma of T-cell and B-cell type is uncommon, and the one occurring primarily on skin is extremely rare. Herein, we report a unique case of composite lymphoma of mycosis fungoides and cutaneous small B-cell lymphoma in a 73-year-old male patient. The patient presented with multiple erythematous patches, plaques, and nodules on the upper arms, scalp, and trunk. Four punch biopsies of arm and scalp lesions demonstrated lymphoid infiltrate in superficial to deep dermis with a characteristic zone distribution of T-cell and B-cell components. T cells were distributed in papillary and perifollicular dermis and displayed a larger size with convoluted nuclei, whereas B cells were small sized, assuming nodular infiltrate in mid-deep dermis with coexpression of CD5. Molecular test detected clonal rearrangement of both TCRG and IGH/K genes with identical amplicons for each gene in all 4 biopsies. Clinical staging revealed no extracutaneous lesions. A multidisplinary approach is emphasized to establish a definitive diagnosis.


Subject(s)
Composite Lymphoma/pathology , Lymphoma, B-Cell/pathology , Mycosis Fungoides/pathology , Skin Neoplasms/pathology , Aged , B-Lymphocytes/metabolism , B-Lymphocytes/pathology , Biomarkers, Tumor/metabolism , CD5 Antigens/metabolism , Clone Cells , Combined Modality Therapy , Composite Lymphoma/genetics , Composite Lymphoma/metabolism , Composite Lymphoma/therapy , Gene Rearrangement , Genes, T-Cell Receptor gamma , Humans , Immunoglobulins/genetics , Lymphoma, B-Cell/genetics , Lymphoma, B-Cell/metabolism , Lymphoma, B-Cell/therapy , Male , Mycosis Fungoides/genetics , Mycosis Fungoides/metabolism , Mycosis Fungoides/therapy , Skin Neoplasms/genetics , Skin Neoplasms/metabolism , Skin Neoplasms/therapy , T-Lymphocytes/metabolism , T-Lymphocytes/pathology , Treatment Outcome
2.
Genes Cancer ; 3(7-8): 459-66, 2012 Jul.
Article in English | MEDLINE | ID: mdl-23264846

ABSTRACT

Activating point mutations in codons 12, 13, and 61 of the KRAS proto-oncogene are common in colorectal, non-small cell lung, pancreatic, and thyroid cancers. Constitutively activated KRAS mutations are strongly associated with a resistance to anti-epidermal growth factor receptor (EGFR) therapies, such as panitumumab and cetuximab used for treating metastatic colorectal carcinoma and EGFR tyrosine inhibitors used for advanced non-small cell lung cancers. Since anti-EGFR therapies are costly and may exert deleterious effects on individuals without activating mutations, KRAS mutation testing is recommended prior to the initiation of anti-EGFR therapy for these malignancies. The goal of this review is to summarize the KRAS mutation testing methods. Testing is now routinely requested in the clinical practice to provide data to assign the most appropriate anticancer chemotherapy for each given patient. Review of the most relevant literature was performed. Several areas were considered: ordering of the test, selection of the sample to be tested, and review of the testing methodologies. We found that several different methods are used for clinical KRAS mutation testing. Each of the methodologies is described, and information is provided about their performance, cost, turnaround times, detection limits, sensitivities, and specificities. We also provided "tips" for the appropriate selection and preparation of the sample to be tested. This is an important aspect of KRAS testing for clinical use, as the results of the test will affect clinical decisions with consequences for the patient.

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