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H Battifora

Publications and source records attributed to H Battifora.

At least 91 records · Page 5Linked to original sources
PubMed1987

Abnormalities of protooncogenes in non-small cell lung cancer. Correlations with tumor type and clinical characteristics.

Twenty-seven primary non-small cell (NSC) lung cancers were analyzed for alterations of protooncogenes by DNA hybridization techniques. Abnormalities were found in 56% of tumors including ten of 16 adenocarcinomas, three of nine squamous cell cancers and two of two larger cell cancers. Five protooncogenes were found to be commonly altered in tumors at frequencies between 12% and 60%. These were c-myc, c-myb, c-ras-Ha, c-erbB-1 and c-erb-B-2. Alterations in c-erbB-1 and c-erbB-2 correlated with histologic type of tumor and were more common in advanced cancers. Allelic deletions of c-ras-Ha or c-myb were frequently observed in primary tumors which recurred or progressed after surgery (five of six). Analysis of protooncogenes may provide insights into the pathogenesis of lung cancer and may aid in predicting clinical behavior.

Adenocarcinoma↗
PubMed1987

Association of multiple copies of the c-erbB-2 oncogene with spread of breast cancer.

Amplification of c-erbB-2 was at least three times more frequent in breast cancer than in most other types of carcinoma, and was not found in sarcomas or hematological malignancies. Amplification of c-erbB-2 was found in 15 of 86 primary breast cancers and in 3 of 12 secondary breast cancers. Amplification was more common in breast tumors of advanced stage, and in tumors which had metastasized to regional lymph nodes sites. Gene amplification was observed in 21% (4 of 19) of primary tumors which recurred within 3 years of mastectomy and in 6% (2 of 32) of nonrecurrent tumors.

Breast Neoplasms↗
PubMed1987

The cellular composition of adenoid cystic carcinoma. An immunohistochemical study.

To investigate the cellular differentiation of adenoid cystic carcinomas (ACC), a comparative immunohistochemical study of 12 normal salivary glands and eight specimens of ACC was performed. Antibodies were used against S100 protein (S), keratins (K) of various molecular weights, vimentin (V), muscle-specific actin (A), epithelial-membrane antigen, human milk fat globules, and collagen type IV. A panel of four of these antibodies (SKVA) was identified as the most helpful in characterizing cells in normal salivary glands and ACC. The immunophenotypes depended on the histologic patterns of ACC. Cells in morphologically recognizable duct structures in the cribriform and trabecular areas expressed a phenotype similar to that of the intercalated duct. Cell layers around pseudocysts and occasional cellular islands had an immunophenotype suggesting myoepithelial-cell differentiation. The most clear cut epithelial/myoepithelial bilaminar differentiation was present in areas with a trabecular pattern, in which the layers facing the stroma and the central ductal elements had SKVA phenotypes of myoepithelial and ductal differentiation, respectively. In areas with a reticular pattern, most of the cells showed ductal differentiation. Many of the cells in the cribriform and basaloid regions were immunophenotypically undifferentiated. These results indicate that ACC consists of undifferentiated cells and of cells that are differentiating toward ducts, predominantly intercalated ducts, and toward myoepithelium. These findings support previous observations by electron microscope.

Actins↗
PubMed1987

Events on different chromosomes alter the genes for the two peptides of platelet-derived growth factor in an osteogenic sarcoma.

Platelet derived growth factor consists of dimers of partially homologous peptides (A and B) encoded by separate genes on different chromosomes. A clinically aggressive osteogenic sarcoma had both an amplified A-chain gene on chromosome #7 and a reduplication of all or part of chromosome #22 containing the B-chain (c-sis) gene. Other oncogenes on chromosomes #1, #2, #5, #6, #7, #8, #11, #12, #14, and #15 were not reduplicated or amplified. These observations are consistent with the hypothesis of autocrine stimulation of growth of some sarcomas in humans, and indicate that amplification and reduplication of related genes on different chromosomes can occur in tumors in vivo.

Chromosomes, Human, Pair 22↗
PubMed1987

Protooncogene abnormalities in colon cancers and adenomatous polyps.

To determine the frequency and clinical significance of oncogene abnormalities in colon cancer, deoxyribonucleic acids from 45 colon carcinomas and 15 benign adenomas were hybridized with 14 different protooncogene probes. Abnormalities of oncogenes were found in 22% of cancers at the time of resection. Amplification of c-myc or c-erbB-2 and allelic deletion of c-ras-Ha or c-myb were the most frequent abnormalities. The presence of altered oncogenes did not correlate with Dukes' stage, tumor progression, or patient survival after resection. One adenoma had an allelic deletion of the c-myb oncogene which was not seen in either the normal colon or an adjacent carcinoma. These data indicate that the spectrum of altered protooncogenes in colon carcinoma is similar to that of other adenocarcinomas, and that unstable oncogenes can be found before overt malignancy develops.

Adenocarcinoma↗
PubMed1987

Keratins versus epithelial membrane antigen in tumor diagnosis: an immunohistochemical comparison of five monoclonal antibodies.

Among the monoclonal antibodies capable of detecting epithelial lineage, some recognize keratin and others identify antigens of epithelial membranes. Of the latter, the most commonly used is directed against an antigen present in cell membranes derived from milk fat globules, epithelial membrane antigen (EMA). To determine their relative sensitivity and specificity and hence their diagnostic value, we compared four commercially available monoclonal antibodies to low-molecular-weight keratins--AE1, CAM 5.2, PKK1, and 35 beta H11--with the monoclonal antibody to EMA (anti-EMA). We studied 383 samples of human neoplasms of diverse histogenetic types and degrees of differentiation. Anti-EMA was found to be less sensitive than the monoclonal antibodies to keratin in several epithelial tumors, including tumors of the prostate (11 of 13 negative), gastrointestinal tract (13 of 34 negative), and thymus (seven of eight negative). Anti-EMA was also less sensitive in mesotheliomas (nine of 24 negative). Of the embryonal carcinomas, all stained with the monoclonal antibodies to keratin, whereas none stained with anti-EMA. False-positive staining with anti-EMA was seen in two of 14 T-cell lymphomas. We conclude that the monoclonal antibodies to low-molecular-weight keratins are more sensitive and specific for the identification of epithelial origin of neoplasms than is monoclonal anti-EMA. Anti-EMA should not be used as the sole marker of epithelial differentiation in tumor diagnosis.

Adenocarcinoma↗
PubMed1987

Rearrangement of the p53 gene in human osteogenic sarcomas.

p53 is a 53-kDa nuclear protein that is associated with malignant transformation in several tumor model systems. In a survey of 134 human carcinomas, sarcomas, leukemias, and lymphomas obtained at surgery or from peripheral blood, we found rearrangements of the p53 gene only in osteogenic sarcomas (3 of 6 osteogenic sarcomas examined). Normal tissue from one of these patients had an unrearranged gene, indicating that the genetic abnormality in the tumor was acquired. Two of the sarcomas with rearranged genes expressed levels of p53 protein that were elevated relative to other tumors. Rearranged p53 genes were also found in human osteogenic sarcoma cell lines.

Cell Line↗
PubMed1987

A monoclonal antibody against neuron-specific enolase. Immunohistochemical comparison with a polyclonal antiserum.

There is skepticism about the value of antisera to neuron-specific enolase (NSE) for immunohistochemical identification of neural and neuroendocrine differentiation in neoplasms, because of reports of detection of NSE, in a large percentage of nonneuroendocrine neoplasms. By immunohistochemical methods, the authors compared a monoclonal antibody to NSE (Mab NSE) with a heterologous antiserum to NSE (Het NSE) on 348 samples of tumors of diverse histogenesis. They studied 93 neural and neuroendocrine tumors and 255 nonneuroendocrine, nonneural tumors. The Mab NSE was slightly less sensitive but clearly more specific than the Het NSE in recognizing neural and neuroendocrine differentiation. Only 2% of the nonneuroendocrine, nonneural tumors reacted positively with Mab NSE; in contrast, 20% of the same tumors were positive with the Het NSE. Moreover, intense nonspecific staining was frequent with Het NSE, which often rendered interpretation difficult. Because of its superior specificity, the Mab NSE used in this study is more valuable than the heterologous antiserum as a diagnostic reagent in tumor diagnosis.

Antibodies, Monoclonal↗
PubMed1987

The distribution of vimentin and keratin in epithelial and nonepithelial neoplasms. A comprehensive immunohistochemical study on formalin- and alcohol-fixed tumors.

Vimentin has been regarded as the intermediate filament characteristic of normal and neoplastic mesenchymal cells and keratins as typical of epithelial cells and the neoplasms derived from them. However, many epithelial cells in tissue culture or in effusion, as well as cells in some solid epithelial neoplasms such as renal, endometrial, ovarian, pulmonary, and thyroid adenocarcinomas, have been shown to coexpress vimentin and keratin. The recent availability of monoclonal antibodies that work reasonably well in paraffin-embedded tissue led us to carry out a comprehensive immunohistochemical study on formalin- and alcohol-fixed specimens of neoplasms in which we used monoclonal antibodies against vimentin. These results were compared with our previous study in which the same tumor tissues were investigated using antibodies against keratin. The antigenicity of vimentin was found to be preserved in all alcohol-fixed specimens and in 63% of formalin-fixed tissues. Vimentin was the sole intermediate filament present in virtually all sarcomas, meningiomas, schwannomas, and melanomas. In addition, variable percentages (10-57%) of carcinomas, neuroendocrine carcinomas, neuroblastomas, thymomas, and mesotheliomas were positive for vimentin, which, except in the neuroblastomas, was coexpressed with keratins. Among the adenocarcinomas, more than 50% of papillary carcinomas of the thyroid, as well as renal, endometrial, ovarian, and lung carcinomas, coexpressed keratins and vimentin. A distinctive paranuclear and basal localization of vimentin was observed in the cells of many of these tumors, in contrast to the predominantly apical distribution of the keratins. The authors conclude that coexpression of vimentin and keratin is more widespread than previously reported and that antibodies to vimentin, by themselves, are of limited value for the differentiation of epithelial from mesenchymal neoplasms.

Antibodies, Monoclonal↗
PubMed1987

Immunohistochemical evaluation of pleural mesothelioma and pulmonary adenocarcinoma. A bi-institutional study of 47 cases.

Pleural mesotheliomas and peripheral pulmonary adenocarcinomas were evaluated by immunohistochemistry at two institutions (Yale University School of Medicine and the City of Hope National Medical Center). Twenty-three mesotheliomas, 11 with ultrastructural verification, and 24 pulmonary adenocarcinomas were studied. Antikeratin, anticarcinoembryonic antigen, anti-human milk fat globule related antigen, MC-1, B72.3, and Leu M-1 antibodies were employed. The immunohistochemistry of each case prepared at one institution was reviewed at the other. As groups, the two tumor types were distinguishable using this antibody panel. Essentially, mesotheliomas were keratin positive only. The adenocarcinomas were positive for CEA, MFG, B72.3, and Leu M-1. However, there were some ambiguities presented by the immunohistochemistry. The higher molecular weight keratins were found in most but not all mesotheliomas and in only a few adenocarcinomas. Lower molecular weight keratins were positive not only in all the mesotheliomas, but also in nearly all the adenocarcinomas, but also in a tumor determined by electron microscopy to be mesothelioma. Preabsorption of CEA decreased the sensitivity for adenocarcinoma, but did not change the positivity of the putative mesothelioma. B72.3 and Leu M-1 were specific for adenocarcinoma, but were found in only half of them. The MFG was apparently specific for adenocarcinoma, but the findings were difficult to interpret. At the level of individual cases, greater sensitivity of separation can be achieved by combining the results of two or more antibodies, but the lack of a detectable specific antigen in mesothelioma continues to make some cases difficult to evaluate by immunohistochemistry alone.

Adenocarcinoma↗
PubMed1987

Distinction between undifferentiated (small noncleaved) and lymphoblastic lymphoma. An immunohistologic study on paraffin-embedded, fixed tissue sections.

The morphologic differentiation between malignant lymphoma of the small noncleaved cell (SNC) type and lymphoblastic lymphoma (LBL) is at times difficult, particularly when fresh tissue is not available for immunologic studies. We have examined the reactivities of a panel of monoclonal and polyclonal antibodies, including LN-1, LN-2, and antibodies to immunoglobulin light chains, leukocyte common antigen (LCA), Leu-M1, vimentin, S-100 protein, lysozyme, and alpha-1-antitrypsin, in paraffin-embedded, B5- and formalin-fixed tissue involved by SNC or LBL. The immunophenotypes in all of the cases included in this study had been characterized previously in fresh-frozen sections or cell suspensions. Among 21 samples of B5-fixed SNC, LN-1 was reactive in 17 and LN-2 in 18 cases. Among 13 B5-fixed LBL, LN-1 was reactive in two cases and LN-2 was reactive in two cases. Each of 20 B5-fixed samples of SNC was reactive with at least one of the antibodies, whereas 10 of the 13 B5-fixed samples of LBL were negative for both antibodies. Lesser reactivity was evident in formalin-fixed tissues, with only nine of 27 SNC specimens positive for LN-1 and 16 of 27 positive for LN-2. Most or all of the SNC and LBL samples were negative for immunoglobulin light chains, Leu-M1, vimentin, S-100 protein, lysozyme, and alpha-1-antitrypsin. The majority of both SNC and LBL were positive for LCA. We conclude that LN-1, preferably in combination with LN-2, can be used for distinguishing between SNC and LBL in paraffin-embedded, B5-fixed tissue when fresh tissue is not available.

Adolescent↗
PubMed1987

Proto-oncogene abnormalities in human breast cancer: correlations with anatomic features and clinical course of disease.

DNAs from fifty-three primary breast cancers were hybridized with 16 different proto-oncogene or oncogene probes. Abnormalities of one or more of five proto-oncogenes were found in fifty-eight percent of tumors at the time of mastectomy. Amplification of c-myc and c-erbB-2, and allelic deletions of c-ras-Ha and c-myb were the most common abnormalities. The presence of altered proto-oncogenes correlated with clinical stage of the cancers. Fifteen of 43 evaluable tumors of stages I to III recurred, and four of five evaluable stage IV tumors progressed within 16 to 24 months of surgery. All but one of the cancers that recurred or progressed had detectably altered proto-oncogenes (P less than .001). Analysis of proto-oncogenes may have prognostic value in breast cancer.

Adult↗
PubMed1987

Specificity of proto-oncogene amplification in human malignant diseases.

DNAs from 253 fresh human tumors of 38 different types were hybridized with 17 different oncogene probes. The analysis demonstrated unique associations between amplification of specific oncogenes and specific types of tumors. In a large number of cases it was determined that amplified oncogenes occurred in 10 to 20% of tumors with the following specific associations: c-myc in adenocarcinomas, squamous carcinomas and sarcomas but not hematologic malignancies; c-erbB2 in adenocarcinomas, particularly breast cancers; c-erbB1 in squamous carcinomas; N-myc in neuroblastomas. A small number of cases suggested other specific associations: amplified c-myb in breast cancers; amplified c-ras-Ha and c-ras-Ki in ovarian carcinomas. In addition, there was a correlation between amplification of c-myc and the clinical stage of adenocarcinomas, and amplification of c-erbB2 and the clinical stage and lymph node involvement of breast cancers.

Carcinoma↗
PubMed1986

The use of antikeratin antibodies in the immunohistochemical distinction between neuroendocrine (Merkel cell) carcinoma of the skin, lymphoma, and oat cell carcinoma.

Paraffin sections of formalin-fixed tumor samples from 26 patients with neuroendocrine (Merkel cell) carcinoma of the skin (NECS) were studied immunohistochemically with three monoclonal antibodies to low molecular weight keratin (MAB-K) and with antibodies to leukocyte common antigen (LCA), neurofilament (NF), neuron-specific enolase (NSE), S100 protein (S100), and chromogranin (CGN), to investigate the relative diagnostic value of these antibodies. Samples from 20 lymphomas, 10 non-oat cell undifferentiated carcinomas, 10 oat cell carcinomas, and 10 melanomas served as controls. Keratin was found in 25 of the 26 NECS and in all undifferentiated and oat cell carcinomas. A ball-like immunostaining for keratins, resembling an inclusion body was seen only in cases of NECS and some carcinoids. Neurofilament, NSE, and CGN were expressed by fewer NECS than was keratin and all NECS were negative for LCA and S100. None of the lymphomas and melanomas contained detectable keratin, NF, NSE, or CGN. Only the lymphomas stained with LCA. Only the melanomas were S100-positive. It is concluded that keratin is the most useful single discriminating marker in the separation of neuroendocrine (Merkel cell) carcinoma of the skin from lymphoma, melanoma and, when the characteristic inclusion-like pattern is seen, from metastatic oat cell carcinoma.

Adult↗
PubMed1986

Further evidence that "malignant angioendotheliomatosis" is an angiotropic large-cell lymphoma.

Malignant angioendotheliomatosis is a rare, generally fatal disease characterized by a multifocal proliferation of neoplastic mononuclear cells within the lumens of small blood vessels. Although the disease primarily involves the vasculature of the skin and central nervous system, vascular involvement of other organs may occur and may produce a variety of clinical findings. Some early investigators concluded that malignant angioendotheliomatosis was a neoplasm of endothelial cells, but recently others have suggested that it is of hematopoietic origin. We have studied three patients with the disease and have characterized the immunophenotype of the neoplasm on cryostat-cut fresh-frozen tissues. A detailed antigenic phenotyping of neoplastic lymphoid cells showed that one patient had the immunophenotype T11+, Leu-1+, Leu-3+, Leu-2+, B1-, B2-, SIg-, LN1-, LN2-, the predominant phenotype for peripheral T-cell lymphoma; the others had T11-, Leu-1-, Leu-3-, Leu-2-, B1+, B2+, SIg+, LN1+, LN2+, consistent with a B-cell-derived lymphoma. On the basis of our results, we suggest that angiotropic (intravascular) large-cell lymphoma would be more appropriate than malignant angioendotheliomatosis as a name for this disease.

Adult↗
PubMed1986

Amplification of c-erbB-2 oncogene in human adenocarcinomas in vivo.

There are two genes related to the viral erbB gene in the human genome. c-erbB-1 is the same as the gene for the epithelial-growth-factor (EGF) receptor, and c-erbB-2 encodes a receptor-like protein very similar to, but distinct from, the EGF receptor. Hybridisation analysis of DNA from 101 fresh human malignant tumours showed that the c-erbB-2 gene was amplified in 5 of 63 adenocarcinomas and none of 38 other types of tumours, whereas the c-erbB-1/EGF-receptor gene was amplified only in 1 of 8 squamous-cell carcinomas. Thus, the protein products of the amplified c-erbB-2 gene may have a role in the evolution of adenocarcinomas, as does the EGF receptor in some squamous-cell carcinomas.

Adenocarcinoma↗
PubMed1986

Leu-M1 antigen in human neoplasms. An immunohistologic study of 400 cases.

Several studies have shown that the Leu-M1 antigen, a monocyte/granulocyte-related marker, is consistently expressed by the neoplastic cells of patients with Hodgkin's disease (HD). It has been suggested that reactivity of Reed-Sternberg cells with Leu-M1 can be used in support of a morphologic interpretation of HD, and that it is helpful in the differential diagnosis of HD from morphologically similar lesions. To evaluate the significance of the Leu-M1 positivity of Reed-Sternberg cells in the diagnosis of HD, we investigated the distribution of Leu-M1 antigen in a series of patients with HD, non-Hodgkin's lymphomas, and nonhematopoietic neoplasms. We were able to demonstrate the presence of Leu-M1 antigen not only in the majority of patients with HD, but also in 12 of 18 (67%) peripheral T-cell lymphomas, as well as in a variety of nonhematopoietic neoplasms, which included 113 of 199 carcinomas, most of them (58%) adenocarcinomas. Only one of 34 sarcomas showed a focal positive reaction. Leu-M1-related antigen was not detected in any of 18 mesotheliomas, 15 germ cell tumors, 13 melanomas, three schwannomas, or three astrocytomas. Our study indicates that Leu-M1 positivity has no value in supporting the diagnosis of HD in situations where the histologic diagnosis of HD is doubtful. However, since anti-Leu-M1 reacted positively in the majority of adenocarcinomas but was absent in mesotheliomas, melanomas, and most sarcomas, this antigen could serve as a new marker that may be helpful in situations in which carcinoma is a part of the differential diagnosis.

Adenocarcinoma↗