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Lymphocytic Cells (lymphocytic + cell)

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Medical Sciences	100%

Selected Abstracts

Case of combined adrenal cortical adenoma and myelolipoma

PATHOLOGY INTERNATIONAL, Issue 9 2004
Takaharu Matsuda
We report a case of myelolipoma 10 mm in size within a functional cortical adenoma that was 33 × 22 × 17 mm in size. A 29-year-old woman was referred to hospital for transient hypertension. A right adrenal tumor was detected by computed tomography (CT) scan and magnetic resonance imaging (MRI). Her cortisol levels indicated a loss of the normal diurnal pattern, and urinary 17-hydroxycorticosteroids was elevated. She underwent a right adrenalectomy under the diagnosis of adrenal adenoma with Cushing's syndrome. The tumor was fairly well encapsulated by a thin layer of connective tissue. The major tumor portion was composed of two distinct cell types, clear cells and eosinophilic cells, arranged in an alveolar structure. These findings were representative of cortical adenoma. The adrenal cortical adenoma centrally included well-demarcated adipose tissue admixed with scattered islands of myelopoietic elements: erythroblasts, myeloid cell series and lymphocytic cells, which was eventually recognized as myelolipoma. Recently, adrenal myelolipoma has commonly been found because of the ease of detecting it as an incidentaloma by CT scan or MRI. However, the present adrenal myelolipoma case is uncommon because it is combined with a functioning cortical adenoma. Only six similar cases have previously been reported in English and Japanese publications. Furthermore, in the present case, the myelolipoma formed a tumor nodule, and to our knowledge, this is the first reported case of a radiographically recognizable tumor nodule. We discuss the etiology of myelolipoma and suggest that myelolipoma can develop in the course of endocrine hyperfunction. [source]

Two Cases of Lymphomatoid Papulosis in Children

PEDIATRIC DERMATOLOGY, Issue 2 2003
Eri Aoki
Histologically there was an infiltration of small lymphocytic cells with scattered large atypical cells expressing CD30. Characterization of T-cell receptor gene rearrangement showed monoclonality of the infiltrating cells. The second patient, a 15-year-old Japanese girl, had a 2-week history of self-healing papulovesicular eruptions on her face and limbs. Large CD30+ atypical cells were also noted in the perivascular lymphocytic infiltration. Immunohistochemical studies revealed CD8 expression on almost all CD30+ cells in the second case. In the literature, there have been two reports of children with large CD30+ atypical cells expressing CD8 and two cases expressing CD4, whereas all adult cases reported have had cells expressing only CD4. [source]

Distribution of Foxp3-, CD4- and CD8-positive lymphocytic cells in benign and malignant prostate tissue

APMIS, Issue 5 2010
ALEXANDER VALDMAN
Valdman A, Jaraj SJ, Compérat E, Charlotte F, Roupret M, Pisa P, Egevad L. Distribution of Foxp3-, CD4- and CD8-positive lymphocytic cells in benign and malignant prostate tissue. APMIS 2010; 118: 360,5. Foxp3 is a transcription factor that inhibits antitumor immune response and is expressed in regulatory T cells (Tregs). High levels of Tregs have been reported in several human cancers. This study investigates the distribution of cells positive for Foxp3, CD4 and CD8 in benign prostatic tissues and prostatic carcinoma. Tissue microarrays were constructed from radical prostatectomy specimens of 36 patients. From each patient, six cores were taken: two cores from cancer, one from benign tissue of each of the peripheral (PZ), transition (TZ) and central zones (CZ) and one from atrophy. Foxp3-, CD4- and CD8-positive cells were more common in cancer than in non-atrophic benign tissue (p < 0.01) and more common in atrophy than in non-atrophic PZ, but did not differ significantly between cancer and atrophy. Cells positive for Foxp3 and CD4 were less prevalent in CZ than in PZ and TZ. Tregs infiltrate more in prostate cancer (PC) than in benign tissue. Their presence in atrophy may have relevance for the hypothesis on atrophy as a potential precursor lesion of PC. CZ has the lowest Treg levels, and a possible role for the low rate of cancer in this zone remains to be investigated. [source]

BPDE-induced lymphocytic 3p21.3 aberrations may predict head and neck carcinoma risk

CANCER, Issue 3 2002
Yong Zhu Ph.D.
Abstract BACKGROUND Tobacco exposure is an established risk factor for head and neck squamous cell carcinoma (HNSCC). Benzo[,]pyrene diol expoxide (BPDE), a main metabolic product of the tobacco smoke constituent benzo[,]pyrene, induces chromosomal aberrations at specific loci. Chromosomal aberrations in peripheral blood lymphocytes (PBLs) induced by BPDE may reflect individuals' genetic susceptibility to tobacco carcinogens. METHODS This study was designed to detect BPDE-induced aberrations in PBLs at locus 3p21.3 in cultured lymphocytic cells. Our hypothesis is that the presence of BPDE-induced 3p21.3 aberrations is a biomarker of an individual's genetic susceptibility and that individuals with these aberrations are at an increased risk for HNSCC. PBL cultures from 52 cases and 54 controls were treated with 2 ,M BPDE for 24 hours before the 3p21.3 aberrations were assessed by flourescence in situ hybridization. One thousand lymphocyte interphases were scored for each sample. RESULTS We found that BPDE-induced chromosome 3p21.3 aberrations occurred more frequently in cases (mean: 31.4 per 1000 cells) than in controls (mean: 22.1 per 1000 cells; P < 0.001). However, when 6q27 was selected as a control locus, no such difference was observed (P = 0.545). When the 75th percentile value of induced aberrations in the controls was used as a cutoff point to classify 3p21.3 BPDE-induced sensitivity, 30 of the 52 cases (57.69%) and only 14 of the 54 controls (25.93%) were sensitive to BPDE exposure. This approach resulted in an odds ratio of 4.8 (95% confidence interval: 1.87,12.28) for HNSCC risk associated with BPDE-induced 3p21.3 aberrations. There was also a dose-response relationship between the number of BPDE-induced aberrations at 3p21.3 and risk for HNSCC. CONCLUSIONS The results from this study demonstrated that 3p21.3 may be a specific molecular target of tobacco carcinogens and that BPDE sensitivity at this locus may reflect an individual's genetic susceptibility to HNSCC. Cancer 2002;95:563,8. © 2002 American Cancer Society. DOI 10.1002/cncr.10689 [source]