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 effective treatment of systemic cancer began in the 1950s on two fronts, i.e., childhood leukemia and choriocarcinoma. These two diseases were successfully treated as a direct result of the use of antifolate methotrexate. The demonstration of complete durable remissions in these diseases quickly led to development of other anticancer drugs, tested using the prospective clinical trials. In the 1960s as the number of active drugs increased, combination chemotherapy was introduced. Other systemic cancers, such as Hodgkin's, large cell lymphoma, and testicular cancer, became curable in the 1970s. For the common low-growth fraction solid tumors, the curability of systemic disease remained elusive until the introduction of adjuvant therapy to treat micrometastases. The past decade of the 1980s has seen improvement in the outcomes for breast cancer, osteosarcoma, and possible colon cancer utilizing adjunctive chemotherapy. The 1980s also saw the introduction of biologic therapies that have further improved the outcomes of several leukemias and produced consistent responses in patients with renal cell and melanoma. The 1990s will undoubtedly see more improvements as the effects of current drugs will be enhanced not only by improved integration of systemic and local therapies but also by utilizing cytokines and biologic response modifiers in concert with cytotoxics. Moreover, as we understand more about the process of cancer induction, promotion, and progression, more specific anti-cancer approaches will be developed to control cancer even before clinical cancer is diagnosed. Underlying and facilitating the improvement in cancer therapy have been not only the experimental results of many laboratory scientists but also the outcomes from many controlled clinical trials, the laboratory of clinical scientists.
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PMID:Progress in the systemic treatment of cancer. Concepts, trials, drugs, and biologics. 230 52

The relationship between self-reported height and cancer risk was investigated in an integrated series of case-control studies including 273 cases of cancer of the oesophagus, 474 of the stomach, 558 of the colon, 352 of the rectum, 227 of the liver, 267 of the pancreas, 110 of the larynx, 2,388 of the breast, 545 of the cervix uteri, 563 of the endometrium, 688 of the ovary, 80 of the prostate, 263 of the bladder, 105 of the kidney, 43 Hodgkin's disease, 152 non-Hodgkin's lymphomas, 109 multiple myelomas, and a total of 5,574 controls admitted to hospital for acute, non-neoplastic conditions. No significant positive trend in risk was observed for any of the cancer sites considered, and some suggestion of elevated risks for the upper quintile of height was observed only for prostate (relative risk, RR = 1.4), kidney (RR = 2.7) and colon (RR = 1.2) in males (but not in females). For breast cancer, all the RRs for subsequent quintiles of height were close to unity. Four neoplasms showed significant inverse trends with height: oesophagus (RR = 0.7 for highest vs. lowest quintile), cervix (RR = 0.4), endometrium (RR = 0.7) and ovary (RR = 0.6). For oesophagus and cervix the trends could be explained, at least in part, in terms of social class correlates (multivariate RR 0.8 and 0.5, respectively), while for endometrium they could possibly be related to an inverse correlation between height and body mass (multivariate RR 0.9). Thus, our study did not support the hypothesis that nutrition in childhood and adolescence (which in this population is a determinant of adult height) is directly related to the subsequent risk of cancer at several major cancer sites. A number of inverse associations emerged, which may be either spurious and incidental, or suggest that poorer nutrition early in life may be an unfavourable indicator of the subsequent risk of selected neoplasms.
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PMID:Height and cancer risk in a network of case-control studies from northern Italy. 230 93

Women with malignant lymphoma, non-Hodgkin's lymphoma and Hodgkin's disease were of a significantly later age at first full-term pregnancy (AFFP) than controls without malignant disorders. The odds ratio (OR) of having the first pregnancy at 30 years of fertility was 6.4 for women with malignant lymphoma. This ratio was higher than the ratio of 3.9 in a group of breast cancer patients. A low parity in the lymphoma group enhanced the risk associated with a late AFFP.
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PMID:Late age at first full-term pregnancy as a risk factor for women with malignant lymphoma. 234 31

Eighteen patients (6 breast cancer, 10 non-Hodgkin's lymphoma, 2 Hodgkin's disease) were treated with high-dose cyclophosphamide (7 gr/mq), while 12 (2 breast cancer, 5 non-Hodgkin's lymphoma, 5 multiple myeloma) were additionally treated with rhGM-CSF for 14 days after cyclophosphamide. During recovery, increased peak values of circulating CFU-GM were observed in 23 out of 30 patients (13 patients after cyclophosphamide, median: 5,000 CFU-GM/ml; 10 patients after cyclophosphamide + rhGM-CSF, median: 20,150 CFU-GM/ml); five of these "high releaser patients" were in 1st relapse after MACOP-B. Seven patients showed low release of CFU-GM; they had either a history of multiple exposures to chemoradiotherapeutic treatments or bone marrow replacement by neoplastic cells or both. Four out of 23 patients with high CFU-GM release were subsequently studied after administration of high-dose etoposide (2 gr/mq): increased levels of circulating progenitors were seen again, although peak values were reduced when compared to post-cyclophosphamide period. Three patients with low release and bone marrow involvement had a clear increase of circulating CFU-GM after etoposide. The results show the influence of high-dose chemotherapy, rhGM-CSF, type of previous treatment and bone marrow involvement on the degree of circulating CFU-GM release.
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PMID:Conditions influencing the expansion of the circulating hemopoietic progenitor cell compartment. 235 38

Neoadjuvant chemotherapy can be used before radiotherapy to combat microscopic metastatic loci and to facilitate irradiation. Improvement in the survival time by impeding the dissemination of metastases seems to be real for breast cancer, but has not been observed to date in randomized studies of ENT cancers. Neoadjuvant chemotherapy in Hodgkin's disease has improved survival time and tolerance to irradiation, allowing a lowering of the total doses used and the volumes irradiated. In breast and ENT cancers, it has become possible, due to tumor regression, to replace mutilating treatments with more conservative ones consisting of radiotherapy alone, without increasing the risk of local relapse. Indeed, it is in this domain that neoadjuvant chemotherapy is the most useful. Two important conditions must be met for its successful application: a) a sufficiently effective regimen must be chosen, in order to prevent tumor growth prior to irradiation (which would aggravate the prognosis); and b) an accurate identification and localization of the tumor before undertaking any treatment so as to not detract from the effectiveness of the radiotherapy.
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PMID:[Radiotherapy with neoadjuvant chemotherapy]. 251 29

Bone marrow autotransplantation involves the administration of very high doses of chemotherapy or radiation therapy, or both, followed by infusion of autologous hematopoietic stem cells. This treatment was used in the past as a salvage therapy for patients with end-stage cancers. Occasional cures in patients with chemotherapy-responsive malignancies encouraged oncologists to utilize this treatment earlier when a better result might be achieved. This has led to a substantial number of long-term disease-free survivors in non-Hodgkin's lymphoma, Hodgkin's disease, acute leukemia, and neuroblastoma. Studies are currently ongoing in the treatment of breast cancer, multiple myeloma, testicular cancer, and ovarian cancer. Important areas for future investigation include the identification of optimal criteria for patient selection and timing of the therapy, the need for infusion of hematopoietic stem cells as cloned hematopoietic growth factors become available, the identification of the most effective high-dose regimens, and the need for "purging" tumor cells from the marrow before re-infusion. Successfully addressing these issues will increasingly require large comparative trials.
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PMID:Bone marrow autotransplantation. 264 72

Age is the greatest risk factor for the development of cancer. For etiologic purposes, newly diagnosed cases of cancer among a defined population during a specified time (incidence) is the usual way of depicting cancer as it relates to age. Exposure to carcinogens in utero or perinatally can produce cancers soon after birth or years later. Cancers in older children have been related to growth factors and/or a single exposure to high doses of radiation. Hodgkin's disease occurring among young adults is different histologically, clinically, and prognostically than Hodgkin's disease among older adults. For the disease among young adults, the hypothesis is that clinical disease reflects the rare consequences of a prevalent infection of low pathogenicity; age of infection is determined by socioeconomic status. In older adults, it more closely resembles the lymphomas. This suggests dynamic trends associated with changing social environments related to etiologic factors. Among adults, the steady increase in colon cancer among both genders represents constant exposure to a carcinogen(s) starting in early life and persisting throughout older ages. Breast cancer is divided into pre- and postmenopausal phases on the basis of its age distribution. International differences in postmenopausal breast cancer suggest environmental factors in postmenopausal women and genetic and hormonal factors in premenopausal women. The age distribution of lung cancer increases linearly with the amount of cigarettes smoked and there is no indication of a threshold below which cigarette smoke is safe. The downturn among the oldest age groups results from competing causes of death or reflects a cohort effect of different exposure over time. Further, the pattern of lung cancer suggests exposure to a carcinogenic agent including substances that act principally as promoters.
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PMID:Cancer and age. 264 47

Twenty-five patients with disseminated cancer (nine with renal cell carcinoma, five with melanoma, three with Hodgkin's lymphoma and chronic myelocytic leukemia [CML], two with soft tissue sarcoma, one each with large-cell lymphoma, breast cancer, and colon cancer), 13 males and 12 females, aged 25 to 68, were treated with recombinant human interleukin-2 (rIL2) by continuous infusion and adoptive transfer of autologous lymphocytes activated in vitro with IL2. Patients underwent leukapheresis on days 1, 8, 15, and 22 of the treatment. Cells, bulk activated for 20 hours in serum-free culture medium with 1,000 U IL2/mL in transfusion transfer packs as culture vessels, were transfused the following day. The infusion of IL2 by continuous infusion for six days started immediately after each adoptive transfer for 4 weekly courses. The dose of IL2 was escalated weekly in each patient; starting doses of IL2 were also escalated in subsequent cohorts of patients until maximally tolerated doses were reached. Nine patients had objective tumor regressions (three with renal cell cancer, two with Hodgkin's lymphoma, and one each with melanoma, sarcoma, breast, and colon cancer). Six responses were partial, two were minor, and one was mixed. Responding patients were maintained with IL2 by continuous infusion for six days every 6 to 8 weeks, without adoptive cell transfer. The median duration of responses was 16 weeks (3 to 60 + weeks). Tumor regression was related to the dose of IL2 (greater than or equal to 3.4 x 10(6) U/m2/d for six days) and to the in vivo lymphoproliferative effects of the lymphokine, but not to the total number of cells adoptively transferred. Side effects of treatment were transient and quickly reversible. Renal, hepatic dysfunction, and dyspnea were directly related to the dose of IL2 and to lymphocytosis. Other toxicities were mild hypotension with mild fluid retention, oral mucositis, anemia, thrombocytopenia, fever, and fatigue.
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PMID:Recombinant interleukin-2 by continuous infusion and adoptive transfer of recombinant interleukin-2-activated cells in patients with advanced cancer. 266 33

Adjuvant chemotherapy. The frequent 6 month complete remission induction chemotherapy is not discussed here. What is under debate at present is the prolonged maintenance or adjuvant chemotherapy, which in comparative trials with 5 year follow-up does not appear to improve survival prognosis in leukemia, myeloma, non-Hodgkin lymphoma or post-menopausal breast cancer. However, it may prolong the duration of the first remission. It is suggested that the sensitivity to chemotherapy might depend on cells being induced into the G2 or M phases by growth growth promotor(s), such as estrogens in breast carcinoma. Their presence before the menopause could explain why this neoplasia in this condition is one of the few tumoral diseases transitorily sensitive to adjuvant chemotherapy. Adjuvant immunotherapy is also under debate. Immunotherapy has been reported to give a significant improvement in remission duration and/or overall survival and/or survival after relapse in several tumors and in several trials. However, for almost every trial reporting a statistically significant effect there is one (or more) which shows no significant effect. Theoretically, immunotherapy has several advantages over chemotherapy. It may be effective in minimal residual disease if tumor cells are in the G0 phase. So-called kinetic refractoriness (see separate chapter in this volume) may not apply to immunotherapy. Finally, tumor cells appear to be more sensitive than normal cells to some cytotoxic mechanisms which form a part of the biological response to tumors.
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PMID:Adjuvant treatment of minimal residual tumors. A comparison of chemotherapy and immunotherapy. 266 16

The incidence of secondary myelodysplastic syndromes (MDS) and acute leukaemias (AL) after chemotherapy and/or radiotherapy is increasing. Most cases have been described in patients with Hodgkin's disease, non-Hodgkin's lymphomas, multiple myeloma, polycythemia vera, ovarian cancer and breast cancer. We report 2 patients with secondary MDS and acute myeloblastic leukaemia after combined chemotherapy and radiotherapy for soft tissue sarcoma. Five more cases have been described in the literature. The data of all patients are summarized. The occurrence of secondary MDS/AL in patients with soft tissue sarcoma may become a problem, in particular in children, who have been cured after combined radiotherapy and chemotherapy.
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PMID:Myelodysplastic syndrome and acute leukaemia following treatment of soft tissue sarcoma. 267 58


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