Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06126 (CD1a)
 2,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Effective presentation of tumor antigens is fundamental to strategies aimed at enrolling the immune system in eradication of residual disease after conventional treatments. Myeloid malignancies provide a unique opportunity to derive dendritic cells (DCs), functioning antigen-presenting cells, from the malignant cells themselves. These may then co-express leukemic antigens together with appropriate secondary signals and be used to generate a specific, antileukemic immune response. In this study, blasts from 40 patients with acute myeloid leukemia (AML) were cultured with combinations of granulocyte-macrophage colony-stimulating factor, interleukin 4, and tumor necrosis factor alpha, and development to DCs was assessed. After culture, cells from 24 samples exhibited morphological and immunophenotypic features of DCs, including expression of major histocompatibility complex class II, CD1a, CD83, and CD86, and were potent stimulators in an allogeneic mixed lymphocyte reaction (MLR). Stimulation of autologous T-cell responses was assessed by the proliferative response of autologous T cells to the leukemic DCs and by demonstration of the induction of specific, autologous, antileukemic cytotoxicity. Of 17 samples, 11 were effective stimulators in the autologous MLR, and low, but consistent, autologous, antileukemic cytotoxicity was induced in 8 of 11 cases (mean, 27%; range, 17%-37%). This study indicates that cells with enhanced antigen-presenting ability can be generated from AML blasts, that these cells can effectively prime autologous cytotoxic T cells in vitro, and that they may be used as potential vaccines in the immunotherapy of AML.
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PMID:Stimulation of autologous proliferative and cytotoxic T-cell responses by "leukemic dendritic cells" derived from blast cells in acute myeloid leukemia. 1131 69

A 49-year-old Hispanic woman with a T4N1M0 infiltrating duct carcinoma of the left breast underwent four courses of FAC (doxorubicin 86 mg, 5-fluorouracil 860 mg, cyclophosphamide 86 mg, and dexamethasone 10 mg) adjuvant chemotherapy plus four courses of paclitaxel (Taxol; Bristol-Myers Squibb Oncology, Princeton, NJ) and subsequent mastectomy. The tumor shrunk from 6.5 cm to 2.5 cm after the treatment. The residual tumor in the surgical specimen measured 1.5 cm with eight positive out of 24 axillary lymph nodes. The tumor showed typical chemotherapy changes and a massive proliferation of histiocytes that mimicked a neoplasm. A nodular proliferation of the same cells in one axillary node raised the impression of a second malignant tumor in the breast spreading to the node. The histiocytic cells contained lamellar and coarse periodic acid-Schiff-positive material distending their cytoplasm and they were strongly positive for CD68 and negative for CD1a, pan keratin, and S-100. These findings ruled out histiocytoid carcinoma, granular cell tumor, and Erdheim-Chester disease. The proliferating histiocytes had ultrastructural findings of paclitaxel-induced cytotoxicity with disorganized stacks of intermediate filaments positive for vimentin by immunostains and fewer masses of tubulin. The treated breast carcinoma cells were tubulin-positive but the proliferating histiocytes were tubulin-negative.
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PMID:Pseudoneoplastic proliferation of histiocytes with paclitaxel-induced ultrastructural changes in a mastectomy specimen. 1549 38

Juvenile xanthogranulomas (JXG) are uncommon non-Langerhans cell histiocytic proliferations which arise most often in children. While most cases present as solitary cutaneous lesions, occasional cases involve extracutaneous sites. Rare examples of JXGs have been reported involving all levels of the neuroaxis. We present two cases of JXGs involving the nervous system, and review the literature. The first patient was a 14-year-old female with headaches and a mass involving the left trigeminal nerve; pathologic examination showed a JXG. At 11 months follow-up, after administration of systemic chemotherapy, the patient remained stable with residual tumor. The second patient was a 15-year-old female with leg weakness and numbness, who underwent complete surgical resection of a dural JXG. At eight months follow-up, she showed no evidence of tumor, and was able to walk without difficulty. Review of the literature revealed 38 previously published reports of JXGs involving the nervous system. The CNS was involved in the majority (75%) of cases. The clinical characteristics of JXGs arising in the CNS varied significantly from cases in the peripheral nervous system (PNS); CNS tumors occurred in younger patients, more often males, and were more likely to be associated with concurrent cutaneous and extra-nervous systemic lesions. The clinical outcomes were similar for CNS and PNS lesions, with the caveat that all three lethal JXGs occurred in the CNS. The clinical and radiologic presentation of JXGs is nonspecific, thus necessitating biopsy and pathologic examination to arrive at the diagnosis. The pathologic differential diagnosis includes a heterogeneous group of histiocytic proliferations; immunostaining for histiocytic markers CD68, factor XIIIa, and Fascin, and the absence of Birbeck granules and CD1a immunoexpression suggests the diagnosis of JXG. In many cases, total surgical resection is curative. However, some cases will require additional chemotherapy and/or radiotherapy.
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PMID:Juvenile xanthogranulomas of the nervous system: A report of two cases and review of the literature. 2264 Jan 64