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)

The sensitivity of 37 solid tumours of children was tested in vitro towards cytostatic agents by means of an autoradiographic short-term method. Sensitivity was measured as the magnitude of inhibition of 3 H-thymidine incorporation. The test was performed with the cytotoxic agents Cyclophosphamide, Trenimon, Bleomycin, Adriamycin, Daunomycin, Actinomycin D, and Cytosin-Arabinosid in 9 Wilms' tumours, 9 neuroblastomas, 7 non-Hodgkin-lymphomas, 5 osteogenic sarcomas, 3 soft tissue sarcomas, and 4 special tumours. None of the tumours is resistant to all cytotoxic substances. The tumours show a marked individual sensitivity pattern, and, with few exceptions, they are sensitive against 2 or more cytostatics. This behaviour is explained mainly by the usually high proliferative activity of dysontogenetic tumours, malignant lymphomas and various sarcomas. The possibilities and limits of the short-term methods for sensitivity-testing are discussed critically and in detail. For the evaluation of the results of in vitro testing and of in vivo effectiveness the close coreelations are not always taken into consideration between the type of cytostatic agent and effect on tumour metabolism, cytostatic agent and proliferation kinetics of the tumour as well as the effect of the cytostatics and the nucleic acid precursor used for the test. Despite the methodological limitations preclinical testing should be preferred in comparison with unselected chemotherapy.
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PMID:[Testing of solid tumors in childhood for sensitivity against cytostatic agents using an autoradiographic in vitro method (short-term method) (author's transl)]. 22 41

Supranormal temperatures inhibit selectively the growth of malignant cells more than that of normal cells. The autoradiographic determination of the 3H-thymidine-labelling-index (LI) in vitro is a suitable method for the examination of thermosensitivity of individual human tumours. 44 solid tumours of children (Wilms' tumours, neuroblastomas, osteogenic sarcomas, non-Hodgkin-Lymphomas and other tumours) were studied by the temperatures 37.5 and 42.5 degrees C/120 min, with this method. 90% of the histologically undifferentiated tumours showed a highly significant inhibition of the 3H-thymidine incorporation between 28.6 and 79.9% with an average of 51.1%. In 4 histologically mature tumours (carcinoma of the adrenal cortex, malignant hepatoblastoma, fibrosarcoma, hamartoblastoma) no significant decrease of the LI was present. The inhibition of incorporation with hyperthermia cannot be correlated with the primary magnitude of the LI with normothermia. In 1 neuroblastoma a 75% rise of the LI was found possibly due to exogenic caused thermotolerance. The individuality of the reaction towards heat may contribute to the biological characterization of tumours.
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PMID:The effect of hyperthermia 42.5 degrees C on the incorporation of 3H-thymidine into the DNA of solid tumours in childhood. 51 52

The authors describe a case of post radiation osteogenic osteosarcoma secondary to Hodgkin's disease. 14 similar cases were found in literature. They discuss the predisposition to the carcinogenesis due to the association of the chemotherapy and the radiotherapy for the treatment of Hodgkin's disease.
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PMID:[Post-radiation osteosarcoma following Hodgkin's disease. Apropos of a case and review of the literature]. 266 Jan 99

Fifty-nine patients with osteogenic sarcomas arising in bones following exposure to x rays and 20 patients with postradiation malignant fibrous histiocytomas of bone arising as a direct consequence of irradiation were studied. These represent 5.5% of all osteogenic sarcomas and 4.9% of all malignant fibrous histiocytomas of bones. The sarcomas may affect any skeletal site, but most commonly they arose in bones of the pelvic and shoulder girdles or the distal end of the femur. Grounds for irradiation were either nonosseous conditions or preexistent skeletal lesions. Reasons for incidental osseous irradiation included Hodgkin's disease, carcinoma of cervix, breast or lung; bilateral retinoblastoma and others, and giant cell tumor predominated among the irradiated skeletal lesions. The mean and the median radiation doses were 6,040 cGy (rad) and 5,700 cGy (rad), respectively. The period of latency between irradiation and the appearance of the bone sarcoma ranged from 3.5 to 47 y with a mean of 16.5 and median of 14.5, respectively. The cumulative disease-free survival rate for malignant fibrous histiocytoma patients at 3 y was 58%. The cumulative disease-free survival rate at 5 y for patients with osteogenic sarcoma was 17%, with a median survival estimate of 1 y. Although all patients with malignant fibrous histiocytoma who received their radiation therapy for a preexistent bone lesion survived, only 27% of the patients whose bone was normal at the time of irradiation are alive and well at the 3-y mark.
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PMID:Postradiation sarcomas of bone. 284 96

Fourteen patients with malignant tumors of bone (ten osteogenic sarcomas, one Ewing's tumor, one giant-cell tumor, two non-Hodgkin's lymphomas), plus one patient with a synovial cell sarcoma, who had been treated by standard extremity-conserving chemotherapy regimens, were examined before treatment by means of localized phosphorus 31 magnetic resonance spectroscopy. Thirteen (86%) of 15 examinations were successful, and 100% of successful examinations showed metabolic abnormality in the tumor. Tumors contained excess adenosine triphosphate and inorganic phosphate, an unusual peak of phosphomonoester, consistent with excessive glycolysis in tumors. The intratumor pH was normal in the 12 bone tumors, but acidic in the single soft-tissue sarcoma (pH 6.8). Metabolic response was observed in all seven patients monitored during chemotherapy, with the earliest examinations being performed two days after first treatment. An increase in the inorganic phosphate level, loss of adenosine triphosphate, and loss of phosphomonoester indicated tumor response; loss of all abnormal metabolites (two of seven patients) indicated regression of the tumor. Tumor relapse was accompanied by reappearance of abnormalities in the magnetic resonance spectrum. Phosphorus 31 magnetic resonance spectroscopy offers a unique means of determining the early response of these malignant tumors to therapy as well as predicting their relapse.
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PMID:Osteosarcoma and other neoplasms of bone. Magnetic resonance spectroscopy to monitor therapy. 347 51

Supranormal temperatures between 40 and 43 degrees C are not necessarily lethal to tumor cells, but lead to characteristic changes of the cell cycle. The parameters of the proliferation kinetics were studied in 35 solid tumors of children at a temperature of 42.5 degrees C with an autoradiographic in vitro method, in comparison to normothermia: 9 Wilms' tumors, 10 neuroblastomas, 8 osteogenic and soft tissue sarcomas, 6 non-Hodgkin-lymphomas, and 3 other tumors. 28 tumors showed significant prolongation of DNA synthesis times by an average factor of 1.27 (1.10--3.12). Mitosis times undergo an average prolongation by the factor 2.75 (1.07--8.87). Together with significant decrease of the 3H-thymidine labeling index the prolongation of the cell cycle time amounts to an average of 2.67 (1.05--8.30). The cause of the changes of the cell cycle are discussed. Probably, the heat sensitivity of tumors is correlated with the proliferation rate and with the degree of histological differentiation; but this cannot be confirmed statistically due to the small number of cases. 2 cases responded with a decrease of the duration of the cell cycle; in one case this was probably due to an exogenic thermotolerance. The changes of the cell cycle are of a particular importance for the therapeutic combination with radio- or chemotherapy. These relations are discussed.
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PMID:Autoradiographic study on the effect of hyperthermia (42.5 degrees C) on the proliferation kinetics of solid tumors in children. 737 57

More aggressiveness in treatment of childhood malignancies has had an evident impact on survival and rate of cure but, it has also allowed us to discover long-term effects of these treatments, and second malignant tumors of them. Between 1970 and 1993, 472 cases of malignant tumors in childhood were diagnosed in our department. Six of them (1.27%) developed a second tumor (five malignant and one benign). Relationship between first and second tumors are: seven years old boy, cervical lymphosarcoma-thyroid carcinoma; eleven years old boy, osteogenic sarcoma-vesical carcinoma: two years and six months old boy, cerebellar astrocytoma-soft tissue osteogenic sarcoma; five years old girl. Wilm's tumor-scapular osteogenic chondroma; one year and a half old girl, abdominal neuroblastoma-granulocytic sarcoma (chloroma); twelve years old boy. Hodgkin's disease-acute myeloblastic leukemia. All of them were clearly related to concogenic effect of radiation or chemotherapy.
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PMID:[Second tumors in childhood]. 776 70

The osteogenic consequences of bone marrow ablation followed by bone marrow transplantation for Hodgkin's and non-Hodgkin's lymphoma were examined. Pre- and post-transplantation iliac crest bone biopsies were reviewed for all patients undergoing transplantation at the Johns Hopkins Oncology Center between January 1981 and December 1989. Histomorphometric measurements included percentage of filled trabecular lacunae to estimate osteocyte viability, marrow cellularity and marrow fibrosis. A total of 37 non-Hodgkin's and 32 Hodgkin's patients had adequate biopsies for study inclusion. Twenty-seven received chemotherapy alone, while the remaining 42 had lethal total body irradiation plus chemotherapy. Twelve transplants were allogeneic. Estimated osteocyte viability was decreased for over 4 weeks after bone marrow transplantation. Continuing osteocyte dropout in the central regions of trabeculae was seen in conjunction with active new osteocyte formation along the periphery. Marrow fibrosis was significantly increased and marrow cellularity decreased. There were no major distinctions based on lymphoma type, pretransplant treatment regimen or type of bone marrow transplant. The results indicate that disruption of marrow hematopoiesis causes a diminution in osteocyte viability. Although there is an early appearance of new osteogenesis, the source of progenitor cells cannot be determined from this study.
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PMID:Bone morphology after bone marrow transplantation for Hodgkin's and non-Hodgkin's lymphoma. 844 Mar 46

In three new approved indications (non Hodgkin's lymphoma, Hodgkin's lymphoma and acute lymphoblastic leukaemia) and in three previously existing indications (ovarian cancer, soft tissue sarcomas and osteogenic sarcomas), non comparative trials show that ifosfamide can induce tumour regression in patients who relapse after a first course of chemotherapy (sometimes containing cyclophosphamide). But clinical assessment has not yet formally demonstrated that this leads to a significant increase in survival time and/or quality of life, mainly because of toxicity. In cervical cancer, a new indication, a comparative trial shows higher tumour response rates with the ifosfamide + cisplatin combination than with cisplatin alone. However, the greater toxicity of the combination and the lack of any increase in survival must both be taken into account. In breast cancer and lung cancer comparative trials show no difference in efficacy between cyclophosphamide and ifosfamide, while toxicity may be worse with ifosfamide. Ifosfamide has no specific value in these approved indications. The same applied to ENT cancer, against which ifosfamide seems to have little activity.
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PMID:Ifosfamide: new idications-new dose strength. Limited evidence of effectiveness. 1018 82

This article reviews the potential clinical uses of antagonists of growth-hormone-releasing hormone (GHRH) for tumor therapy. GHRH antagonists suppress the growth of various human cancer lines xenografted into nude mice; such tumors include breast, ovarian, endometrial and prostate cancers, lung cancers (small-cell lung carcinomas and non-small-cell lung carcinomas), renal, pancreatic, gastric and colorectal carcinomas, brain tumors (malignant gliomas), osteogenic sarcomas and non-Hodgkin's lymphomas. The antitumor effects of GHRH antagonists are exerted in part indirectly through the inhibition of the secretion of GH from the pituitary and the resulting reduction in the levels of hepatic insulin-like growth factor I (IGF-I). The main effects of the GHRH antagonists are, however, exerted directly on tumors. GHRH ligand is present in various human cancers and might function as an autocrine and/or paracrine growth factor. Pituitary-type GHRH receptors and their splice variants are also found in many human cancers. The inhibitory effects of GHRH antagonists seem to be due to the blockade of action of tumoral GHRH. Antagonists of GHRH can also suppress cancer growth by blocking production of IGF-I and/or IGF-II by the tumor. Further development of GHRH antagonists that are still-more potent should lead to potential therapeutic agents for various cancers.
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PMID:Antagonists of growth-hormone-releasing hormone: an emerging new therapy for cancer. 1808 44


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