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

Intensive chemotherapy and radiotherapy of Hodgkin's Disease has resulted in improved survival rates. With long-term follow-up, however, a risk of secondary malignancy in these individuals is now appreciated. The authors of this report have encountered five patients who developed bone or soft tissue sarcomata more than 5 years after treatment of Hodgkin's Disease. The four males and one female ranged in age from 14 to 74 years at the time of diagnosis of Hodgkin's disease. Two had received radiotherapy alone for treatment of Hodgkin's disease, two were treated with radiation and chemotherapy, and one received only chemotherapy. The latent period prior to diagnosis of sarcoma ranged from 6 to 11 years. There was one case each of neurofibrosarcoma, fibrosarcoma, osteosarcoma, liposarcoma and leiomyosarcoma. Four patients died within 1 year of the diagnosis of sarcoma. One is alive with no evidence of disease 2 years following diagnosis and surgical excision of the sarcoma. On the basis of the Massachusetts General Hospital experience in the treatment of Hodgkin's Disease, the authors calculate a risk of 0.9% of sarcoma occurring in five year survivors of Hodgkin's disease. Previously reported cases of sarcoma following treatment of Hodgkin's disease are summarized. The pertinent literature is reviewed.
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PMID:Sarcoma of bone and soft tissue following treatment of Hodgkin's disease. 636 Mar 33

We report a case of leiomyosarcoma in the bladder 8 years after completion of 45 months of cyclophosphamide chemotherapy for Hodgkin's disease. One year after cystoprostatectomy a large fibroblastic tumor arose in the soft tissues of the pelvis.
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PMID:Bladder leiomyosarcoma and pelvic fibroblastic tumor following cyclophosphamide therapy. 687 88

Methyl-GAG was given to 71 patients with advanced malignancies as a weekly brief infusion (30-120 minutes) or as a biweekly 24- or 120-hour infusion. Mucositis (stomatitis, pharyngitis, esophagitis, and, rarely, inflammation of other mucous membranes) was dose-limiting in all three schedules. Generalized fatigue, malaise, myalgia, dysesthesias, nausea, and vomiting were more frequent in the brief-infusion schedule. Myelosuppression was mild and not dose-related. Fever, ventricular arrhythmias, skin rash, tender swelling of the palms, neuropathy, and paralytic ileus were rare. Toxicity was increased in patients with renal insufficiency or "third-space" fluid but was not increased by hepatic dysfunction. Cumulative and overlapping toxicity was evident only in the weekly schedule. Higher doses of methyl-GAG were tolerated when the duration of infusion was increased. The recommended doses for phase II trials are 700 mg/m2 weekly as a 1-2 hour infusion, 850 mg/m2/24 hours biweekly, and 1500 mg/m2/120 hours biweekly. Therapeutic effects were seen in all schedules and included objective responses in colon carcinoma (one of 13 patients), renal cell carcinoma (one of nine), and Hodgkin's lymphoma (one of two) and objective improvements in esophageal carcinoma (one of three), endometrial carcinoma (two of two), and leiomyosarcoma (one of three).
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PMID:Methyl-GAG in patients with malignant neoplasms: a phase I re-evaluation. 705 68

Only about 2% of the urinary tract are not of urothelial origin. Our knowledge of their morphology and biology is mainly based on single case reports, and therefore apart from a few exceptions very poor. Generally, the most often affected site is the urinary bladder (79.2%), followed by the urethra (12.7%), pelvis (4.9%) and ureter (3.2%). The urinary bladder also is the only organ in which all different histological types of these tumors were described. According to their histogenesis non-urothelial tumors (NUT) can be classified by the following main groups: soft tissue tumors, mixed epithelial and non epithelial tumors (carcinosarcomas), neuroendocrine carcinomas, carcinoids, malignant lymphomas, malignant melanomas and extragonadal germ cell tumors. Moreover some very interesting tumor-like lesions, like malakoplakia and inflammatory pseudosarcoma, mainly occur in this region. About 75% of all NUT of the urinary tract belong to the soft tissue tumors. Rhabdomyosarcomas in children and leiomyomas and -myosarcomas in adults are the more frequent histological types. Leiomyosarcomas can easily be confused with other tumor types or even with inflammatory pseudotumors. The use of immunohistochemistry to achieve a correct diagnosis is mandatory but not always successful. A relatively frequent tumor occurring in the bladder of young adults is the paraganglioma (pheochromocytoma), which usually produces typical symptoms of catecholamine excess. Carcinosarcomas of the urinary bladder contain both epithelial and mesenchymal components. They have to be distinguished from collision tumors (coexistent but separate carcinoma and sarcoma), spindle cell transitional carcinomas as well as from carcinomas with osseous or cartilaginous metaplasia. Carcinoids and neuroendocrine carcinomas developed from the neuroendocrine cells scattered all over the transitional epithelium of the bladder. Neuroendocrine carcinomas of the bladder are also called "oat cell carcinomas" since they show the same histological features and immunoreactivity as the oat cell carcinomas of the lung. They share also the same poor prognosis. The affection of the urinary tract in generalized malignant lymphomas and leukemias occur in more than 30% of cases. Lymphomas, primarily localised in the urinary bladder are, however, extremely rare. The most frequent ones are low grade non Hodgkin lymphomas, although 3 cases of Hodgkin disease and a few cases of primary extramedullary plasmacytoma of the bladder have been reported, too.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Non-urothelial tumors of the urinary tract]. 751 Dec 78

Expression of KP1/CD68 macrophage-associated antigen in a series of 840 selected malignant neoplasms, including immunomorphologically characterized cases of non-Hodgkin's lymphoma (NHL) (434), Hodgkin's disease (HD) (115), soft tissue sarcoma (147), carcinoma (49), and other tumors (95), was examined. KP1 expression was detected in a significant number of NHLs (107 of 434; 24.7%), most of them (65 of 107; 60.7%) of the diffuse small cell subtype. Only 14 of the 155 large cell lymphomas, compared to 10 of the 51 Ki-1/CD30+ anaplastic large cell (ALC) lymphomas examined, were KP1 positive. Conversely, none of the T-lineage NHL--other than Ki-1/CD30+ ALC lymphomas--or the HD cases tested was labeled by KP1 antibody. Among the other neoplasms tested, KP1 was reactive with a variable proportion of cases of malignant fibrous histiocytoma (19 of 24; 79.2%), malignant schwannoma (8 of 22; 36.4%), liposarcoma (3 of 9; 33.3%), leiomyosarcoma (8 of 37; 21.6%), cutaneous or metastatic melanoma (51 of 73; 69.9%), and renal cell carcinoma (3 of 5; 60%). These results indicate that KP1 shows a relatively wide spectrum of immunoreactivity with malignant neoplasms of presumed non-histiocyte origin, thus arguing against its expected specificity and high value in diagnostic pathology. Although the significance of KP1 expression by some subsets of NHLs remains to be elucidated, its close association with B-cell NHLs, mostly of the diffuse small cell type, should stimulate further pathologic and clinical investigations.
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PMID:KP1/CD68 expression in malignant neoplasms including lymphomas, sarcomas, and carcinomas. 772 38

Extrahepatic portal vein obstruction has been reported to be associated with tumors of liver, bile ducts and pancreas. We report two cases, one with gastric leiomyosarcoma and another with Non Hodgkin's lymphoma, complicated by portal vein block and presenting with gastric variceal bleeding. Portal vein block in both cases was due to direct vascular infiltration. Development of portal hypertension posed difficulties in management.
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PMID:Unusual tumors causing extrahepatic portal venous obstruction. 872 58

The magnitude for and risk factors of the two most important AIDS neoplasm, Kaposi's sarcoma and non-Hodgkin's lymphoma, are reviewed in detail. The association between AIDS and other cancers is mostly speculative because surveillance biases tend to favor detecting associations that may be spurious. The overall relative risk of other cancers appears, however, to be only twofold above that in the general population, with associations being most convincing for anal (but not cervical) cancer and leiomyosarcoma and possible also for Hodgkin's disease, testicular cancer, and conjunctival cancers.
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PMID:The epidemiology of AIDS--related neoplasms. 888 Jan 92

The Epstein-Barr virus (EBV) was isolated 40 years ago from cultures of Burkitt lymphoma cells (BL). The tumor was encountered in Africa and exhibited characteristical geographical, clinical and pathological features. Serological studies revealed that the virus is ubiquitous in humans. The primary infection is often accompanied by the syndrome of acute infectious mononucleosis (IM). It can induce malignant proliferation of B lymphocytes in conditions of immunodeficiency. EBV can immortalize B lymphocytes in culture. These cells carry the virus as episomes and express 9 virally encoded proteins. Their immunological recognition constitutes the surveillance which is responsible for the healthy virus carrier state. The main virus reservoir is represented by a low number of resting B lymphocyte which contain the viral genome but do not express its transformation proteins. The viral genome is detectable in all African BLs, in variable proportions of nasopharyngeal carcinoma, Hodgkin's disease, T cell lymphoma, lymphoepithelial like carcinoma, gastric carcinoma and leiomyosarcoma cases. The role of EBV in the genesis of these tumors is unknown.
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PMID:The complexity of the Epstein-Barr virus infection in humans. 955 13

Kaposi's sarcoma and non-Hodgkin's lymphoma were among the earliest recognized manifestations of the acquired immunodeficiency syndrome (AIDS) epidemic. Excluding these two tumors, the overall risk of all other cancers in human immunodeficiency virus (HIV)-infected individuals is similar to that of the general population. However, varying levels of evidence link several additional neoplasms to HIV infection. The evidence is strongest for an association with Hodgkin's disease, with lower relative and absolute risks than for non-Hodgkin's lymphoma. Anogenital intraepithelial neoplasia also appears to be HIV associated, but increases of invasive disease are still uncertain for both cervical and anal cancers. Various studies have suggested associations with testicular seminoma, multiple myeloma, oral cancer, and melanoma, but the data are inconsistent. Leiomyosarcoma and benign leiomyomas have increased in incidence in HIV-infected children but are unusual in HIV-infected adults. Conjunctival carcinoma is seen in HIV-infected individuals in sub-Saharan Africa but it is uncommon in Western countries. Most other cancers do not seem to have increased incidences in HIV infection. The etiologic mechanisms of HIV-related cancer likely differ among these diverse cancers and do not globally increase cancer risk.
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PMID:Association of non-acquired immunodeficiency syndrome-defining cancers with human immunodeficiency virus infection. 970 98

Apoptosis is a physiological process wherein the cell initiates a sequence of events culminating in the fragmentation of its DNA, nuclear collapse, and finally disintegration of the cell into small, membrane-bound apoptotic bodies. Expression of Fas (APO-1, CD95) Receptor (FasR) and programmed or active cell (PCD) death was studied in childhood astrocytomas (ASTRs) with varying stages of malignancy, including pilocytic ASTR, low grade ASTR, anaplastic ASTR, and glioblastoma multiforme (GBM). The great majority of childhood glial tumors, particularly ASTRs express FasR whereas normal cells in the central nervous system (CNS) do not. FasR represents a transmembrane glycoprotein which belongs to the nerve growth factor/tumor necrosis factor (NGF/TNF) receptor superfamily. Apoptosis within ASTRs is triggered by the binding of FasR to its natural ligand (FasL) or by cross-linking with antibodies developed against FasR. Presence of FasL was also detected in childhood glial tumors. The expression of both FasR and FasL was also observed within the same ASTRs. Therefore, spontaneous, IP regulatory, intratumoral apoptotic cell death (autocrine suicide) is possible in childhood glial tumors. During a systematic, immunocytochemical screening of 42 childhood ASTRs tissues divided according to WHO classification: 6 WHO grade I or pilocytic ASTRs; 14 WHO grade II or low grade ASTRs; 16 WHO grade III or anaplastic ASTRs and 6 WHO grade IV or glioblastoma multiforme (GBM), we detected strong expression (intensity of staining: "A"--the highest possible; number of stained cells: +2 to +4, between 20% to 90%) of FasR, employing 4 microns thick, formalin fixed, paraffin-wax embedded tissue slides. FasR was present on 70% to 90% of tumor cells in pilocytic ASTRs, in 50% to 60% of the tumor cells in low grade ASTRs, in between 30% and 40% of the tumor cells in anaplastic ASTRs, and in between 20% to 35% of GBM cells. The panel of normal tissues employed as positive and negative tissue controls demonstrated presence of FasR in the prenatal thymus, mature tonsils and colonic epithelium. The use of a sensitive, indirect, six step immunoperoxidase or alkaline phosphatase conjugated streptavidin-biotin antigen detection technique provided excellent immunocytochemical results. A broad spectrum of neoplastic cells have been identified to express FasR: 1) carcinomas of epithelial origin, such as breast (ductal invasive, lobular invasive, mucinous), renal cell, gastric, colorectal, endometrial, prostate, pancreas, hepatocellular and large cell and squamous cell lung carcinomas: 2) non-epithelial neoplasms such as B cell mediastinal B cell and nodal non-Hodgkin's lymphomas large granular lymphocytic leukemia of T or NK cell origin malignant fibrous histiocytoma, malignant mesothelioma, leiomyosarcoma, epitheloid sarcoma and alveolar soft part sarcoma, as well as melanomas. Flow cytometry studies have also detected FasR expression on cells of adult T cell, and hairy cell leukemias, as well as in chronic B cell lymphocytic leukemia (BCLL). The coexpression of both FasR and FasL on several malignant cell types may represent an effective mechanism of tumor escape from the cellular immunological response of the host. It has been well established that brain tumors and melanomas produce their autocrine FasL, and even become capable of switching the signal transduction associated with FasL-FasR coupling from the PCD pathway to a tumor growth, proliferative pathway. It seems that the therapeutical use of FasR-FasL (main apoptotic pathway) may represent a new and exciting type of immunotherapy in the treatment of primary childhood glial tumors.
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PMID:Fas (Apo-1, CD95) receptor expression in childhood astrocytomas. Is it a marker of the major apoptotic pathway or a signaling receptor for immune escape of neoplastic cells? 1058 78


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