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)

Presented are the case histories of monozygotic male twins concordant for Hodgkin disease. This is believed to be the third such case report in the world literature. Its significance as it relates to the role of heredity in carcinogenesis is discussed.
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PMID:Hodgkin disease in monozygotic twins: a case report. 57 77

Contemporary clinical research is actively engaged at the conquest of residual neoplastic disease. The preliminary results of combined treatment modalities for osteogenic sarcoma, Ewing's sarcoma, rhabdomyosarcoma, breast cancer, malignant melanoma and Hodgkin's disease have shown a significant decrease in the incidence of distant metastases. In some neoplasias the decreased relapse rate was associated to improved survival. Since the problem of long-term carcinogenesis does exist, the use of prolonged adjuvant chemotherapy, at present moment, is best limited to patients at high risk of early relapse when treated only with local or local-regional modalities.
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PMID:Treatment of residual neoplastic disease in solid tumours. 106 17

We report about two cases of cancer of the testis occurring 2 and 7 years after Hodgkin's disease treated with combined chemotherapy and radiation therapy. From an etiopathogenic point of view, this association may, of course, be accidental, but it may also have an iatrogenic origin or be caused by contiguous carcinogenesis, or even by an immune deficiency. In addition to orchidectomy, the therapeutic history of these patients requires an adaptation of the treatment of their tumors of the testes.
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PMID:[Cancer of the testis after Hodgkin's disease. Apropos of 2 cases]. 128 22

Urinary bladder cancers following prolonged cyclophosphamide therapy are being increasingly reported. We report a case of transitional cell carcinoma of the urinary bladder occurring 12 years after pulse intravenous therapy with cyclophosphamide for Hodgkin's disease. The mechanism of bladder carcinogenesis and the possible role of the uroprotector MESNA in preventing cyclophosphamide induced bladder cancer are discussed.
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PMID:Urinary bladder cancer following cyclophosphamide therapy for Hodgkin's disease. 129 84

Tumor registry data indicate a two- to fourfold increased incidence of breast cancer following mantle irradiation, but cumulative risk is unknown. Radiation exposure to the breasts underlying the mantle block ranges from 4 to 40 Gy and is dependent on relative positions of the breasts and mantle block. Unshielded outer breast quadrants near axillary nodal regions receive 36 to 40 Gy, while central breast quadrants under the lung blocks receive approximately 4 Gy as determined by dose volume histogram analysis. Relative dose risk analysis for breast cancer following mantle irradiation was performed and indicated an overall excess risk of 1.5 for the upper outer quadrant (total dose 40 Gy), 1.3 for the upper and lower inner, and central quadrants (total dose 15 to 20 Gy), and 1.2 for the lower outer quadrant (total dose 4 Gy). Linear and cell-kill carcinogenesis models demonstrated similar relative risk assessments in the low-dose regions, defined as < 15 Gy. Predicted risk for breast cancer in the high-dose regions (> or = 15 Gy) varied considerably according to the model evaluated. The linear model predicted a three to ten times greater risk above baseline breast cancer incidence for the high-dose regions. In contrast, the cell-kill model predicted no excess cases of breast cancer, assuming cell death at these higher dose levels. The greatest relative predicted risk is observed in women < 20 years of age at the time of irradiation; however, women older than 20 years continue to have a 50% higher than baseline risk for subsequent breast cancer development. All women treated for Hodgkin's lymphoma should undergo dose volume histogram evaluation. Prospective clinical and mammographic evaluations should be performed in all female patients following mantle irradiation to better define the risk for secondary breast carcinogenesis.
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PMID:Calculated risk of breast cancer following mantle irradiation determined by measured dose. 147 17

The frequency of chromosome aberrations in the peripheral blood of patients successfully treated for Hodgkin's disease (HD) and non-Hodgkin's lymphoma is compared with that seen in age-matched haematologically normal subjects. Findings are considered in relation to risk factors associated with the development of secondary myelodysplastic syndrome (MDS) or acute myeloid leukaemia (AML). Overall aberration frequencies were not significantly increased in patients compared with normal subjects. However, there were differences in aberration type. The frequency of exchanges was significantly higher among patients (P less than 0.01) and the frequency of gaps lower (P less than 0.0005). The mean frequency of exchanges was also greater in patients receiving multiple compared to single courses of therapy (P less than 0.0005) and in patients receiving radiotherapy or combined modality therapy compared to chemotherapy alone (P less than 0.005 and P less than 0.0005). Four patients had aberration frequencies greater than 2 SD above the patient mean. One of these was also found to have a mutation of the ras oncogene. None of the patients has yet developed secondary MDS/AML.
Carcinogenesis 1992 Jul
PMID:Chromosome aberrations following cytotoxic therapy in patients in complete remission from lymphoma. 163 73

Forty-four patients with relapsed or resistant Hodgkin's disease were treated with adriamycin 40 mg m-2 i.v. on day 1, vincristine 1.4 mg m-2 i.v. on days 1 and 8, prednisolone 40 mg m-2 orally daily for 8 days, etoposide 200 mg m-2 orally daily for 4 days according to the nadir white cell count, and bleomycin 10 mg m-2 i.v. days 1 and 8 (HOPE-Bleo). Median age was 27 (range 12-71). When stage was considered according to all sites currently or previously involved by Hodgkin's disease (cumulative stage) 26 patients (59%) had stage IV, 13 (29%) stage III and five (11%) stage II disease; 33 (75%) had B symptoms. All patients had received previous chemotherapy and 18 (41%) had received two or more regimens. Twenty-six patients (59%) achieved CR and 10 (23%) PR; the median duration of CR was 22 months and median survival for all patients was 48 months. Eight patients remain in continuous CR; none of these had received extensive previous chemotherapy. Among the 19 patients who had relapsed from CR achieved by a single previous chemotherapy regimen, six (32%) achieved long CR on HOPE-Bleo. The regimen was generally well tolerated but the principal toxicity was myelosuppression. There were two toxic deaths, one due to neutropenic sepsis and the other due to acute peritonitis. The HOPE-Bleo regimen is an effective treatment for relapsed or resistant Hodgkin's disease, with a low probability of carcinogenesis and infertility. These factors suggest that HOPE-Bleo deserves further evaluation as primary treatment for Hodgkin's disease and very careful selection of relapsed patients for high dose salvage chemotherapy with bone marrow transplants must be exercised.
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PMID:Etoposide and adriamycin containing combination chemotherapy (HOPE-Bleo) for relapsed Hodgkin's disease. 169 23

Blood leukocyte DNA obtained from 11 Hodgkin's disease patients undergoing ABVD chemotherapy was analysed for the presence of the precarcinogenic adduct O6-methylguanine (O6-meG) at various times (1-2 h up to 49 h) after i.v. treatment with the methylating drug dacarbazine. Adduct formation was detected in all but one of the patients examined at levels ranging up to 0.45 fmol/micrograms DNA (7.2 x 10(-7) mol/mol guanine). The levels of the adduct decreased by approximately 30% over the 24 h following exposure and were usually not detectable 49 h after exposure. In five out of seven individuals examined after more than one treatment, consistent methylation responses were noted, while in the remaining two cases the responses were mixed. No correlation between the extent of adduct formation and lymphocyte levels of the repair enzyme O6-alkylguanine-DNA alkyltransferase was observed. The average extent of O6-meG formation 1 h after dacarbazine treatment was (4.3 +/- 3.1) x 10(-2) fmol/micrograms DNA per mg/kg dose [( 1.2 +/- 0.8) x 10(-3) fmol/micrograms DNA per mg/m2 dose)]. Following exposure of rats to similar doses of dacarbazine, the corresponding levels of adduct in blood leukocyte DNA were 1.1 x 10(-2) fmol/micrograms DNA per mg/kg dose (2.6 x 10(-3) fmol/micrograms DNA per mg/m2 dose).
Carcinogenesis 1991 Feb
PMID:In vivo formation and repair of O6-methylguanine in human leukocyte DNA after intravenous exposure to dacarbazine. 170 22

The frequency of sister chromatid exchanges (SCEs) was determined in Hodgkin's disease (HD) patients prior to therapy, following radiotherapy, and following combined radiotherapy and chemotherapy. The frequency of hprt- mutants in these patients has been reported previously. The frequency of SCEs and hprt- mutants in the same individuals were compared. In non-HD controls the mean SCE frequency and the mean of high SCE frequency cells (HFCs) were significantly increased by smoking, while mutant frequency (MF) showed no effect. Untreated HD patients had mean SCEs, mean HFCs and mean MFs that were higher than non-MD controls. In treated patients, mean SCE and HFC frequencies were lower than untreated patients and non-HD controls, while their MFs were significantly elevated. Overall, SCE frequency was not correlated with MF in control or HD patient groups, suggesting that these biomarkers may reflect, in this case, fundamental biological differences between these processes.
Carcinogenesis 1991 Nov
PMID:Sister chromatid exchange frequency in Hodgkin's disease patients with elevated in vivo hprt mutant frequencies. 193 1

Development of secondary malignancies following treatment of Hodgkin's disease with radiation (central axis midline dose of 3600-4500 cGy) is a recognized risk, and the incidence in breast cancer has been reported to increase by a factor of 4.3 (95% confidence level 2.0 to 8.4) for patients treated with mantle irradiation. Increased incidence of breast cancer has also been shown in atomic bomb survivors, women who underwent multiple fluoroscopic examinations, and women treated for postpartum mastitis. The dose response, however, for radiation dose above 1000 cGy is virtually unknown. Quantitative analysis of carcinogenesis after radiation is exacerbated by the large dose gradient across the breast (300-4200 cGy for midline doses of 4000 cGy), large individual variation in breast size and treatment field position. We have developed differential dose volume histograms calculated using a 3-dimensional (Eg TAR) algorithm as a potential tool for retrospective and prospective epidemiological evaluation. The breast volume forms a bimodal distribution with respect to dose and with further analysis other quantities, such as mean dose and integral dose, can be calculated from the histograms. Using the mean dose, the linear model for carcinogenesis predicts an increased incidence of secondary breast cancer by a factor of 11.6 and 9.6 for the left and right breast, respectively. The dose calculations has been corrected for inhomonogenities 3-dimensionally and test of the accuracy has been included.
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PMID:Dosimetry of the breast for determining carcinogenic risk in mantle irradiation. 193 34


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