Do you use the term "dysplasia"? If so, what do you mean by it, and if not, why not?
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Biomedical subjects
Publications and source records attributed to H A Azar.
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A human squamous cell carcinoma (SCC) of oral origin was transplanted into athymic mice that were then divided into six groups. The mice were killed at 1 to 6 weeks after tumor transplantation; the sixth group was killed 1 week after excision of SCC grafts. Plasma samples were obtained from each mouse at the time of death for the determination of SCC-associated antigen (SCCAA), a cytoskeletal protein fraction of about 48,000 daltons originally derived from SCC of the uterine cervix. The plasma SCCAA level rose gradually and proportionately to the growth of SCC xenografts from a baseline of 0.66 ng/ml [standard error (SE) + 0.12] to the preoperative peak of 8.44 ng/ml (SE + 1.86) at 5 weeks, to fall precipitously to the postoperative level of 1.05 ng/ml (SE + 0.27) at 6 weeks. No rise in plasma SCCAA level was observed in mice bearing a human malignant melanoma, and only modest rises were observed in mice bearing human adenocarcinomas and oat cell carcinoma. In this experimental model rising plasma SCCAA levels were found to be dependable indicators of SCC tumor growth. These observations and preliminary data on SCCAA levels in patients with or without SCC of the head and neck lend support to the clinical usefulness of serial plasma SCCAA determinations in monitoring patients with SCC of the oral cavity.
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The monoclonal antibody (MoAb) HMGF-1 was evaluated in the radioimmunodetection of human colonic cancer transplanted intraperitoneally (i.p.) into athymic nude mice. This antibody reacts with a component of the human milkfat globule, as well as a wide range of epithelial cells and adenocarcinomas of various origins. Purified MoAb was iodinated with 125I and administered i.p. into nu/nu mice bearing (i.p.) xenografts of human colonic adenocarcinoma (X56). Differential tissue counts of radioactivity demonstrated preferential localization of the antibody in i.p. and subcutaneous (s.c.) tumor tissue as compared to normal tissues. Maximum per cent dose per g of tumor (25.17 +/- 1.37), maximum tumor: blood ratio (4.45 +/- 0.14) and maximum tumor: tissue ratios (34.2 +/- 0.12) were obtained at the optimal labelling time of 5 days after antibody injection. Selective localization to tumor was confirmed with a control anti-hepatitis virus MoAb of the same isotype and by localization studies in non-tumor bearing athymic mice. Half lives of the persistence of the iodine 125 in the tumor bearing and non tumor bearing mice were 5 and 7 days, respectively, indicating approximate antibody half lives. Whole body scans showed distinct tumor images without the use of subtraction techniques. This pilot experimental study demonstrates the feasibility of i.p. administration of labelled antitumor MoAb in the imaging of i.p. tumors in an athymic mouse system. Whether or not these observations are applicable to the human situation remains to be carefully established.
Ten cases of "undifferentiated" large-cell tumors were ultrastructurally characterized by cells with abundant filiform cytoplasmic projections without intercellular junctions. These cases were studied by means of the avidin-biotin-peroxidase complex (ABC) technique applied to formalin-fixed, paraffin-embedded sections using antibodies against high- and low-molecular weight keratins (Ker), vimentin (Vi), epithelial membrane antigen (EMA), S-100 protein, leucocyte common antigen (LCA), kappa (K) and lambda (L) light chains, Leu-M1, lysozyme (Ly), alpha-1 antitrypsin (A1AT) and alpha-1 antichymotrypsin (A1ACT). All 10 cases were negative for Ker and EMA but positive for Vi. S-100 was present only in scattered dendritic cells. LCA was identified in seven cases. In the three LCA-negative cases, two stained for Leu-M1, and one of these also showed intracytoplasmic L; one was negative for all markers but Vi. None of the tumors showed any significant staining for Ly, A1AT, or A1ACT. Our findings indicate that these tumors are nonepithelial and nonneuroectodermal, and that they are best classified as non-Hodgkin's lymphomas. The possibility that some of the filiform large-cell lymphomas may be derived from dendritic reticular cells cannot be excluded.
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The application of immunostaining techniques to the study of sections of formalin-fixed, paraffin-embedded tissues has deeply influenced the practice of surgical pathology of tumors. We have favored in our laboratory the avidin-biotin complex immunoperoxidase method and have gradually substituted monoclonal antibodies for polyclonal sera. Better results are sometimes obtained with trypsinization prior to the application of the primary antibody. The more common primary antibodies used are directed against the following categories of cellular antigens: intermediate filaments, oncofetal products, hormones or hormone-related peptides, enzymes or enzyme-related peptides, cell- or tissue-"specific" products, lymphocyte-leukocyte antigens, and immunoglobulin chains. Controls are essential to every immunohistochemical reaction. Because of the pitfalls of immunohistochemical techniques, immunohistochemistry as applied to the study of tumors should be used with utmost care and as an extension of routine surgical pathology.
Plasma cell myeloma constitutes the commonest primary malignant tumor affecting the skeleton of the adult. It is also one of several forms of monoclonal gammopathy that include Waldenström's macroglobulinemia, the heavy chain diseases, "benign" (nonprogressive, asymptomatic) monoclonal gammopathy, and primary amyloidosis. The diagnosis of classic or advanced myeloma rests on the findings of sheets of plasmacytic cells in a bone marrow biopsy sample or aspirate; a serum monoclonal immunoglobulin usually of the IgG or IgA class or Bence Jones protein in the urine; and evidence of multiple lytic lesions in x-ray views of the skeleton. Pitfalls in the diagnosis of earlier or unusual forms of myeloma require a careful application of classic diagnostic criteria or of criteria established by clinical cooperative groups.
Our concept of the Reed-Sternberg cell has evolved considerably since the turn of the century. At the present, it is generally accepted that this cell is a polyploid lymphoreticular cell incapable of mitotic division. The two nuclei of the classic Reed-Sternberg cell probably represent the two lobes of a markedly convoluted or segmented nucleus. The Reed-Sternberg cell may be regarded as the end stage of a transformed lymphocyte that has undergone in vitro blastogenesis. It is not definitely known whether it is of the T or B cell variety. There seems to be no valid histochemical or ultrastructural evidence that it is a histiocyte. The Reed-Sternberg cell, although not 'pathognomonic,' continues to be an essential landmark for the diagnosis of Hodgkin's disease. The actively dividing cells in the neoplasm are considered to be the small lymphocytes as well as the mononucleated reticulum cells, although the triggering mechanism for cell division remains unknown.
The educational, organizational, and fiscal aspects of electron microscopy are discussed.. with emphais on the desirability of making electron microscopy an integral part of the formal training of residents in pathology and of the overall educational program of the medical staff. The rapidity of feedback of information from the pathologist to the clinician is stressed. The number of specimens processed and the variety of tissues submitted for electron microscopy can be regulated by the pathologist but should reflect the particular strength of the hospital or its department of pathology. The organization of the electron microscopy facility, its funding, and sharing of the electron microscopy program in the local community of clinical scientists are discussed
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This paper deals with the histological and ultrastructural findings in a case of the Sézary syndrome. The striking nuclear and cytoplasmic features of the Sézary cell are illustrated, and the similarities of this cell to the mycosis fungoides cell are once more stressed.
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