Agnes K Hamati

East Tennessee State University, Johnson City, Tennessee, United States

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Publications (5)7.26 Total impact

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    ABSTRACT: Carcinoma of unknown primary (CUP) is not uncommon and poses both diagnostic and therapeutic challenges. Recent developments in immunohistochemical (IHS) stains in diagnostic pathology help resolve many of these clinical dilemmas. Antibodies against Thyroid Transcription Factor (TTF-1), a relatively new and organ specific marker that stains lung and thyroid malignancies, are commonly included in the first battery of stains when dealing with a CUP. The usual pattern of staining for TTF-1 is purely nuclear. However, it was recently noticed that TTF-1 stains the mitochondria of benign hepatocytes and tumor cells in hepatocellular carcinoma. We would like to report two cases where the clue to the hepatic origin of CUP was the presence of cytoplasmic staining for TTF-1. Description of both cases with pertinent literature review will be offered. Two patients were seen at the James H. Quillen Veterans Administration Medical Center (VAMC), where one had a right chest wall mass with previous history of prostatic carcinoma and the other was found to have a lytic rib lesion with a previous history of lung squamous cell carcinoma. FNA and core biopsies were performed on both lesions where the initial pathological interpretations were nonsmall cell carcinoma. IHS revealed positivity for cytokeratin-7 and granular cytoplasmic staining for TTF-1. Further workup using stains for Alpha Fetoprotein, Hepatocyte Paraffin (Hep Par 1) and CEA confirmed the diagnosis of metastatic hepatocellular carcinoma (HCC). Paying attention to cytoplasmic staining for TTF-1 in any CUP should prompt further pathological and clinical evaluation to rule out hepatocellular carcinoma.
    Tennessee medicine: journal of the Tennessee Medical Association 01/2012; 105(1):35-6, 40.
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    ABSTRACT: T regulatory (T(R)) cells suppress T-cell responses that are critical in the development of chronic viral infection and associated malignancies. Programmed death-1 (PD-1) also has a pivotal role in regulation of T-cell functions during chronic viral infection. To examine the role of PD-1 pathway in regulating T(R)-cell functions that inhibit T-cell responses during virus-associated malignancy, T(R) cells were investigated in the setting of hepatitis C virus-associated lymphoma (HCV-L), non-HCV-associated lymphoma (non-HCV-L), HCV infection alone and healthy subjects (HS). Relatively high numbers of CD4(+)CD25(+) and CD8(+)CD25(+) T(R) cells, as well as high levels of PD-1 expressions on these T(R) cells were found in the peripheral blood of subjects with HCV-L compared with those from non-HCV-L or HCV alone or HS. T(R) cells from the HCV-L subjects were capable of suppressing the autogeneic lymphocyte response, and depletion of T(R) cells in peripheral blood mononuclear cells from HCV-L improved T-cell proliferation. Additionally, the suppressed T-cell activation and proliferation in HCV-L was partially restored by blocking the PD-1 pathway ex vivo, resulting in both a reduction in T(R)-cell number and the ability of T(R) to suppress the activity of effector T cells. This study suggests that the PD-1 pathway is involved in regulating T(R) cells that suppress T-cell functions in the setting of HCV-associated B-cell lymphoma.
    Immunology and Cell Biology 10/2010; 89(4):535-9. · 3.93 Impact Factor
  • Diagnostic Cytopathology 10/2009; 38(4):310-2. · 1.49 Impact Factor
  • Southern medical journal 09/2009; 102(8):873-4. · 0.92 Impact Factor
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    ABSTRACT: Chest pain is an extremely common presenting symptom that is usually related to a cardiac cause. This case illustrates an unusual presentation of multiple myeloma as a cause of atypical chest pain. This case presentation shows the importance of having a broad differential diagnosis while evaluating patients with atypical chest pain. It also illustrates the potential role of Tc-99m sestamibi imaging as a diagnostic modality in patients with multiple myeloma.
    Southern medical journal 09/2009; 102(9):977-8. · 0.92 Impact Factor