Dr. Daniel  Cherry Iii Do image

Dr. Daniel Cherry Iii Do

2330 Mahan Dr 3Rd Floor
Tallahassee FL 32308
850 788-8000
Medical School: Other - Unknown
Accepts Medicare: No
Participates In eRX: No
Participates In PQRS: No
Participates In EHR: No
License #: OS 4501
NPI: 1831590710
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PAX-5: a valuable immunohistochemical marker in the differential diagnosis of lymphoid neoplasms. - Clinical medicine & research
Undifferentiated tumors and hematolymphoid neoplasms can be diagnostically challenging due to potential overlap of morphologic features and variant antigen expression. PAX-5, a transcription factor expressed throughout B-cell maturation, is detected in most B-cell neoplasms including those that lack expression of mature B-cell markers, such as classical Hodgkin lymphoma (cHL), B-lymphoblastic leukemia and B-cell lymphomas following rituximab therapy. The lack of PAX-5 expression in most CD30-positive non-hematopoietic malignancies (embryonal carcinoma and seminoma) and T-cell lymphomas, such as anaplastic large cell lymphoma (ALCL), suggests that the absence of PAX-5 may be used to confirm non-B-cell lineage. The goal of this study was to retrospectively assess PAX-5 immunoreactivity in diagnostic samples of hematolymphoid and other non-hematopoietic malignancies.Diagnostic lymph node, decalcified core bone marrow biopsies and tissue sections from 111 archived paraffin-embedded tissue blocks and a tissue lymphoma microarray were immunostained using a monoclonal antibody to PAX-5. The corresponding hematoxylin and eosin stained tissue sections and additional immunostains were simultaneously evaluated. PAX-5 immunoreactivity in neoplastic cells was scored as positive or negative. This study was exempted by the Institutional Review Board for Human Research.Nuclear PAX-5 immunoreactivity was detected in 88% (36/41) of Hodgkin lymphoma, all cases of diffuse large B-cell lymphoma (n=72), small B-cell lymphomas (n=5), B-lymphoblastic leukemia/lymphoma and mixed phenotype acute leukemia with B-cell lineage (n=5). PAX-5 was not detected in ALCL (n=22), T-cell lymphoblastic leukemia/lymphoma, mixed phenotype acute leukemia with T-cell lineage (n=5), acute myeloid leukemia (n=4), carcinoid tumors with typical morphology (n=5), melanoma (n=3), and undifferentiated/metastatic tumors (n=8). Non-neoplastic bone marrow sections showed scattered nuclear staining in small B-cell lymphocytes/hematogones. The detection of PAX-5 immunoreactivity resulted in the reclassification of two cases of ALCL to cHL.Overall, our results demonstrate that including PAX-5 in a panel with other immunomarkers helps establish B-cell lineage and increases diagnostic yield.
Identification of a patient with 7q32 deletion-associated acute myeloid leukemia and an incidental t(8;14). - Cancer genetics and cytogenetics
Constitutional activation of the MYC proto-oncogene resulting from a t(8;14) has been demonstrated in approximately 80% of Burkitt lymphoma patients, but only in one case of acute myeloid leukemia (AML). We report on a 59-year-old female diagnosed with minimally differentiated AML (M0). Chromosome analysis demonstrated both a 7q deletion and a t(8;14). Fluorescence in situ hybridization studies confirmed MYC/IGH fusion in 35% of nuclei, but the translocation was atypical due to lack of immunoglobulin heavy chain (IGH) gene disruption. Such an atypical fusion has never been reported, so the effect on MYC regulation due to proximity of IGH regulatory elements is unknown. Real-time polymerase chain reaction analysis demonstrated no increase in MYC expression (P = 0.12). These results suggest that this novel translocation does not result in dysregulation of MYC expression, so this is likely to be a coincidental, benign finding in this patient. This is yet another example of a classic cytogenetic abnormality observed on conventional chromosome analysis which has no functional significance.
Follicular lymphoma with PAS-positive amorphous material: report of two cases. - Annals of clinical and laboratory science
Extracellular, PAS-positive material has been described in various lymphoproliferative disorders, but is rare in malignant lymphomas. We report two such cases of grade 2 follicular lymphoma that were investigated by routine H&E histology, immunohistochemistry, flow cytometry, and molecular pathology. Ancillary studies confirmed the monoclonality in each case and the antigenic similarity to the neoplastic cells, with the exception of bcL-2. One possible pathogenic mechanism for this extracellular material may be the exocytosis of overproduced cell membranes.

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