Potential misdiagnosis of angioimmunoblastic T-cell lymphoma with Hodgkin's lymphoma: a case report.

BACKGROUND: Angioimmunoblastic T-cell lymphoma (AITL) is an aggressive neoplasm. We investigated the potential utility of touch imprints evaluated in conjunction with the histology of lymph nodes in the diagnosis of AITL. CASE A 58-year-old man presented with generalized lymphadenopathy, splenomegaly, and autoimmune phenomena, which complicated the diagnosis. Touch imprints were obtained from the lymph node biopsy, which were valuable in making the correct diagnosis. The cytologic and microscopic features of these imprints and lymph node samples showed a heterogeneous population of hematolymphoid cells, including small to intermediate lymphoid cells, immunoblasts, plasma cells, dendritic cells, and eosinophils, as well as small vessels that were surrounded by some of the abnormal cells. Neoplastic cells stained positive for CD3, CD4, and CD5. Isolated immunoblasts stained with CD20 and CD30. CONCLUSION: We draw attention to this neoplastic diagnosis and correlate the cytomorphologic and immunohistochemical findings with the adequate clinical setting in order to avoid misdiagnosis, primarily with Hodgkin's lymphoma and reactive hyperplasia. Touch imprints are useful in the diagnosis of AITL if the broad population of proliferating cells is distinguished. However, some cases display binucleated or mononucleated cells with prominent nucleoli and many eosinophils, which may induce a potential misdiagnosis with Hodgkin's lymphoma.

The dual kinase complex FAK-Src as a promising therapeutic target in cancer.

Focal adhesion kinase (FAK) and steroid receptor coactivator (Src) are intracellular (nonreceptor) tyrosine kinases that physically and functionally interact to promote a variety of cellular responses. Plenty of reports have already suggested an additional central role for this complex in cancer through its ability to promote proliferation and anoikis resistance in tumor cells. An important role for the FAK/Src complex in tumor angiogenesis has also been established. Furthermore, FAK and Src have been associated with solid tumor metastasis through their ability to promote the epithelial mesenchymal transition. In fact, a strong correlation between increased FAK/Src expression/phosphorylation and the invasive phenotype in human tumors has been found. Additionally, an association for FAK/Src with resistances to the current anticancer therapies has already been established. Currently, novel anticancer agents that target FAK or Src are under development in a broad variety of solid tumors. In this article we will review the normal cellular functions of the FAK/Src complex as an effector of integrin and/or tyrosine kinase receptor signaling. We will also collect data about their role in cancer and we will summarize the most recent data from the FAK and Src inhibitors under clinical and preclinical development. Furthermore, the association of both these proteins with chemotherapy and hormonal therapy resistances, as a rationale for new combined therapeutic approaches with these novel agents, to abrogate treatment associated resistances, will also be reviewed.