Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0019829 (Hodgkin's disease)
 30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

CD30 (Ki-1) antigen has been considered to be expressed on hematopoietic cells including the ones of the recently described anaplastic large cell lymphoma (ALCL), the Reed-Sternberg (RS) cells of Hodgkin's disease and the scattered large parafollicular cells in normal lymphoid tissues. Since then, several reports have been published describing CD30 expression in non-hematopoietic and malignant cells, such as cultivated human macrophages, human decidual cells, histiocytic neoplastic cells, mesothelioma cells, embryonal carcinoma, and seminoma cells. In the present study, we investigated the immunohistochemical expression of CD30 antigen in 15 paraffin-embedded placentas from fetuses after spontaneous abortion in the first trimester of gestation (8th, 10th, and 12th week, respectively) using the monoclonal antibody Ber-H2. All the pregnant patients had been given hormonal medication to support gestation. In addition, a panel of monoclonal antibodies for the identification of leukocytes (CD45/LCA), B-lymphocytes (CD20/L-26), and T-lymphocytes (CD45RO/UCHLI) was performed. Our findings were correlated with those found in 15 placentas obtained from 15 fetuses at the same time, after therapeutic or voluntary abortions. This study demonstrates that, 1) decidual endometrial stromal cells are able to express the CD30 (Ki-1) antigen, 2) the expression of CD30 in decidual cells is higher in cases of hormonal administration (to support gestation), than that found in normal gestation. In the former cases (hormonal support of gestation), a mild mononuclear infiltration of the decidua by UCHLI (T marker) positive cells, accompanies the CD30 positive cells.
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PMID:Human decidual cells can express the Hodgkin's cell-associated antigen Ki-1 (CD30) in spontaneous abortions during the first trimester of gestation. 1183 44

Infectious agents, mainly viruses, are among the few known causes of cancer and contribute to a variety of malignancies worldwide. The agents and cancers considered here are human papillomaviruses (cervical carcinoma); human polyomaviruses (mesotheliomas, brain tumors); Epstein-Barr virus (B-cell lymphoproliferative diseases and nasopharyngeal carcinoma); Kaposi's Sarcoma Herpesvirus (Kaposi's Sarcoma and primary effusion lymphomas); hepatitis B and hepatitis C viruses (hepatocellular carcinoma); Human T-cell Leukemia Virus-1 (T-cell leukemias); and helicobacter pylori (gastric carcinoma), which account for up to 20% of malignancies around the globe. The criteria most often used in determining causality are consistency of the association, either epidemiologic or on the molecular level, and oncogenicity of the agent in animal models or cell cultures. However use of these generally applied criteria in deciding on causality is selective, and the criteria may be weighted differently. Whereas for most of the tumor viruses the viral genome persists in an integrated or episomal form with a subset of viral genes expressed in the tumor cells, some agents (HBV, HCV, helicobacter) are not inherently oncogenic, but infection leads to transformation of cells by indirect means. For some malignancies the viral agent appears to serve as a cofactor (Burkitt's lymphoma-EBV; mesothelioma - SV(40)). For others the association is inconsistent (Hodgkin's Disease, gastric carcinomas, breast cancer-EBV) and may either define subsets of these malignancies, or the virus may act to modify phenotype of an established tumor, contributing to tumor progression rather than causing the tumor. In these cases and for the human polyomaviruses the association with malignancy is less consistent or still emerging. In contrast despite the potent oncogenic properties of some strains of human adenovirus in tissue culture and animals the virus has not been linked with any human cancers. Finally it is likely that more agents, most likely viruses, both known and unidentified, have yet to be implicated in human cancer. In the meantime study of tumorigenic infectious agents will continue to illuminate molecular oncogenic processes.
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PMID:Infectious agents and cancer: criteria for a causal relation. 1548 39

The objective of this study was to analyse incidence and mortality cancer trends in the Italian Network of Cancer Registries (about 8,000,000 inhabitants) during the period 1986-1997. Included were 525,645 newly diagnosed cancers and 269,902 cancer deaths (subjects > 14 years). Joinpoints (points in time where trend significantly changes from linearity) were found and estimated annual percentage changes (EAPC) used to summarize tendencies. Overall cancer incidence increased in both sexes and cancer mortality significantly decreased (since 1991 among men). Lung cancer showed significantly decreasing incidence (EAPC = -1.4%) and mortality (EAPC = -1.6%) among men and increasing trends among women. In women, breast cancer incidence significantly increased (EAPC= +1.7%) and mortality decreased since 1989 (EAPC= -2.0%). Stomach cancer incidence and mortality decreased in both sexes. Prostate incidence sharply increased since 1991 and mortality decreased. Colon cancer incidence increased and rectum mortality decreased significantly in both sexes. Significant increases in incidence were also found for kidney (up to 1991 among men), urinary bladder, skin epithelioma, melanoma, liver (up to 1993 among men), pancreas, mesothelioma, Kaposi's sarcoma (up to 1995 among men), testis, thyroid, non-Hodgkin's lymphomas and multiple myeloma. Mortality significantly decreased for cancers of the oral cavity and pharynx, oesophagus, liver (women), larynx (men), bone, cervix (since 1990), central nervous system, urinary bladder, thyroid, Hodgkin's lymphomas and leukaemias (men). Non-Hodgkin's lymphoma mortality increased in both sexes. In conclusion, most of the changes seen can be explained as the effect of changes in smoking habits and of the extension of secondary prevention activities. The Italian health care system will also have to cope with growing cancer diagnostic and therapeutic needs due to population ageing.
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PMID:Population-based incidence and mortality cancer trends (1986-1997) from the network of Italian cancer registries. 1555 57

Recently, several studies have reported the detection of DNA from simian virus 40 (SV40), a macaque polyomavirus, in tumor tissues obtained from non-Hodgkin lymphoma (NHL) patients. SV40 accidentally contaminated poliovirus vaccines administered to millions of individuals in 1955-1962. A link between SV40 and NHL is biologically plausible because SV40 causes hematological malignancies in laboratory rodents. However, detection of SV40 DNA in human NHL tumors has not been confirmed by other laboratories. Casting doubt on an association between SV40 and NHL, follow-up studies of recipients of SV40-contaminated poliovirus vaccines have not revealed these individuals to be at increased risk of NHL. Furthermore, 2 recent case-control studies of NHL documented only infrequent SV40 antibody reactivity among NHL cases, and the prevalence of SV40 antibodies was similar in cases and controls. This review summarizes recent laboratory and epidemiological studies bearing on the question of whether SV40 is a cause of NHL in humans. The strengths and weaknesses of these data are discussed, and a framework for considering the collected evidence is presented. Many of the considerations raised in this review apply to the evaluation of data regarding other cancers, such as mesothelioma, brain tumors, and various sarcomas, for which an etiologic link with SV40 also has been proposed.
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PMID:Does simian virus 40 cause non-Hodgkin lymphoma? A review of the laboratory and epidemiological evidence. 1680 64

Originally, expression of the CD30 antigen was shown to be typical of the tumor cells of Hodgkin disease and of anaplastic large cell lymphomas. In reactive lymphoid tissue, CD30 is expressed only in a small population of activated lymphoid blasts. Since then, several reports have been published describing CD30 expression in non lymphoid tissues and neoplasms, such as embryonal carcinomas, seminomas, cultivated macrophages, histiocytic neoplastic cells, deciduals cells, and mesothelioma cells. In order to gain insight into the functions of CD30, given that it can mediate signals for cell proliferation and apoptosis, we studied the distribution of the antigen in different fetal archival paraffin-embedded tissues from week 8th to 16th of gestation. We investigated the immunohistochemical expression of CD30 in 30 paraffin-embedded tissue samples representing all three germ layers, using the monoclonal antibody Ber-H2 CD30 is expressed early in human fetal development (8th-10th week) in a wide variety of tissues, with the exception of the skin and thymus in which it is expressed later on. This is consistent with the observation that these organs are not fully differentiated before 10th and 13th week, respectively. No expression was observed in the cardiovascular and respiratory systems. The finding of CD30 expression in the terminal period of organogenesis, period, which is highly hormone related, implies that the antigen has an important role in cell development, maturation, and pathway to terminal differentiation in almost all fetal tissues and structures.
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PMID:Human embryonal tissues of all three germ layers can express the CD30 antigen. An immunohistochemical study of 30 fetuses coming after therapeutic abortions from week 8th to week 16th of gestation. 1650 95

An unknown proportion of formalin-inactivated poliovirus vaccine lots administered to millions of US residents between 1955 and 1963 was contaminated with small amounts of infectious simian virus 40 (SV40), a polyomavirus of the rhesus macaque. It has been reported that mesothelioma, brain tumors, osteosarcoma and non-Hodgkin lymphoma (NHL) contain SV40 DNA sequences and that SV40 infection introduced into humans by the vaccine probably contributed to the development of these cancers. The Immunization Safety Review Committee of the Institute of Medicine (IOM) reviewed this topic in 2002. The present review of recent studies showed that the earlier results describing the recovery of SV40 DNA sequences from a large proportion of the above tumors were not reproducible and that most studies were negative. Contamination with laboratory plasmids was identified as a possible source of false positive results in some previous studies. The low-level immunoreactivity of human sera to SV40 was very likely the result of cross-reactivity with antibodies to the SV40-related human polyomaviruses BKV and JCV, rather than of authentic SV40 infection. SV40 sero-reactivity in patients with the suspect tumors was no greater than that in controls. In epidemiologic studies, the increased incidence of some of the suspect tumors in the 1970s to 1980s was not related to the risk of exposure to SV40-contaminated vaccines. In summary, the most recent evidence does not support the notion that SV40 contributed to the development of human cancers.
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PMID:SV40 and human cancer: a review of recent data. 1713 33

Along with a brief review of the literature, we report the clinicopathologic features of 12 cases of extramammary malignancies metastatic to the breast. Histological diagnoses of the primary tumor were as follows: non-Hodgkin diffuse large B-cell lymphoma (3 patients), acute mycloid leukemia (3 patients), serous papillary adenocarcinoma, well-differentiated adenocarcinoma, squamous cell carcinoma, undifferentiated neoplasm, mesothelioma, and melanoma. The most common mammographic finding was a well-circumscribed mass with increased density but without speculation, calcifications or other signs that characterize the majority of primary carcinomas. Ultrasound revealed well-circumscribed masses without retrotumor acoustic shadowing. The interval between diagnosis of primary cancer and the appearance of breast metastasis ranged from 0 to 108 months (mean: 17, median: 1). Survival after the detection of the breast metastases ranged from 0.2 to 144 months (mean: 23, median: 9.5). In conclusion, metastasis can mimic either benign disease or primary malignancy and is often an unexpected diagnosis in a patient presenting with a breast mass. Thus, an accurate diagnosis is important to avoid unnecessary mutilating surgery. These masses generally indicate disseminated metastatic disease, with a very poor survival rate.
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PMID:Metastases to the breast from extramammary malignancies: a clinicopathologic study of 12 cases. 1721 43

As the number of long-term cancer survivors increases, secondary malignancies are becoming a greater clinical issue. Although some of these malignancies may be related to common environmental exposures, a significant number are considered to be therapy-related. Pleural malignant mesothelioma is a neoplasm that may be related to asbestos exposure or radiation exposure. Previous reports of pleural mesothelioma as a second malignancy have tended to follow radiotherapy for extra-thoracic malignancies such as Hodgkin's disease, breast cancer and Wilms' tumor. We report the case of a 66-year-old woman with no prior asbestos exposure who developed pleural mesothelioma 17 years after pneumonectomy and adjuvant radiation therapy for non-small cell lung cancer. Opacification of the lung field from prior therapy made determination of the diagnosis more challenging. Secondary malignancies such as mesothelioma should be considered in patients who develop unexplained symptoms even long after treatment of a primary tumor.
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PMID:Malignant mesothelioma following thoracic radiotherapy for lung cancer. 1747 64

Malignant mesothelioma is a relatively uncommon malignancy. Although the pathogenesis is primarily related to asbestos, the disease may be associated with radiation exposure. Recently, increased risks for second primary mesothelioma after radiation for lymphoma have been reported. Because these findings are based on small numbers of patients, they need to be confirmed. We examined mesothelioma risk in 2567 5-year survivors of Hodgkin lymphoma. The risk was almost 30-fold increased in Hodgkin lymphoma patients treated with irradiation compared with the general population. Although histology and survival of the mesothelioma cases were comparable with cases from the general population, asbestos exposure and the proportion of males were lower than expected. The evidence for radiotherapy as cause for mesothelioma independent of exposure to asbestos is expanding, and the diagnosis of mesothelioma should be kept in mind whenever related symptoms arise in patients who had previous irradiation.
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PMID:Malignant mesothelioma after radiation treatment for Hodgkin lymphoma. 1971 83

We previously reported a strong IL4I1 gene expression in primary mediastinal B-cell lymphoma (PMBL) and recently identified the protein as a secreted L-phenylalanine oxidase, physiologically expressed by myeloid cells, which inhibits T-cell proliferation in vitro. Here, we analyzed the pattern of IL4I1 protein expression in 315 human lymphoid and non-lymphoid malignancies. Besides PMBL, IL4I1 expression in tumors was very frequent. IL4I1 was detected in tumor-associated macrophages from most of the tumors and in neoplastic cells from follicular lymphoma, classic and nodular lymphocyte predominant Hodgkin lymphomas and small lymphocytic lymphoma, three of which are germinal center derived. IL4I1-positive tumor cells were also detected in rare cases of solid cancers, mainly mesothelioma. The enzymatic activity paralleled protein expression, suggesting that IL4I1 is functional in vivo. Depending on the tumor type, IL4I1 may impact on different infiltrating lymphocyte populations with consequences on tumor evolution. In the particular case of follicular lymphoma cells, which are susceptible to antitumor cytotoxic T cells killing but depend on interactions with local T helper cells for survival, a high level of IL4I1 expression seems associated with the absence of bone marrow involvement and a better outcome. These findings plead for an evaluation of IL4I1 as a prognosis factor.
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PMID:The novel immunosuppressive enzyme IL4I1 is expressed by neoplastic cells of several B-cell lymphomas and by tumor-associated macrophages. 1943 10


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