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)

In the present study the occurrence of estrogen and progestin receptors in the lymphoid tissue of 20 canine non-Hodgkin's Lymphoma patients was investigated. Lesions in all dogs were histologically classified according to criteria used in human patients. No progestin receptors could be demonstrated. Estrogen receptors were found only in the cytosol of two canine lymphomas. Antiestrogen binding sites were present in all 18 cases examined (range 37-356, median 110 fmol/mg protein). No correlation with age, sex or histological classification was found. A pilot study was carried out in five of these dogs that were negative for estrogen receptors and positive for antiestrogen binding sites. These dogs were treated with the antiestrogen tamoxifen (20-30 mg/day) for 2-3 weeks, but the treatment had no apparent effect. It was concluded that if antiestrogens do play a role in the treatment of non-Hodgkin's lymphoma in the dog, it is most likely not by means of antiestrogen binding sites.
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PMID:The occurrence of estrogen and progestin receptors and anti-estrogen binding sites (AEBS) in canine non-Hodgkin's lymphomas. 367 74

Estrogen receptors (ER) and androgen receptors (AR) were determined in a series of 23 leukemia or lymphoma cell lines including 8 T-cell lines, 12 B-cell lines, and 3 non lymphoid cell lines. The phenotypic characterization of these cells by currently available immunological markers provides an estimate of their stage of differentiation. The result indicate that none of the investigated cell lines bear simultaneously ER and AR. Four were found to bear ER: U266, RPMI 8226, HL60, IARC/310/LT2, and four to express AR: RAJI, IARC/301/LTI, U937, REH6. The presence of cytosolic receptors was always associated with that of nuclear receptors. The expression of either ER or AR is restricted to discrete maturation stages of different haemopoietic cell lineages. Thus AR were found among the most immature lines of the T, B or monocytic lineage but they could be detected neither in the promyelocytic line HL60, nor in the pluripotential K562. The present results are in keeping with the demonstration of AR in some leukaemic blasts or in non Hodgkin's lymphomas. In contrast with AR, ER are present in two myeloma cell lines, in the promyelocytic cell line, HL60 and in a T-cell line bearing the phenotype of mature suppressor/cytotoxic T cells.
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PMID:Distribution of androgen and estrogen receptors among lymphoid and haemopoietic cell lines. 407 52

Ovarian function has been studied in 44 adult females who previously received quadruple chemotherapy (MVPP) for Hodgkin's disease. The median age at treatment was 23 years, and the length of time between completion of treatment and study ranged from 6 months to 10 years (median, 30 months). Seventeen women maintained regular menses, 10 developed oligomenorrhea, and 17 developed amenorrhea. At treatment, the 17 women who subsequently developed amenorrhea were significantly older (median, 30 years) than those who maintained regular menses (median, 22 years) or developed oligomenorrhea (median, 23 years). All patients older than 36 years at the start of treatment stopped menstruating during chemotherapy. The cause of the menstrual disturbance in these patients was chemotherapy-induced ovarian damage characterized by high serum gonadotrophin and low serum estradiol concentrations. After completion of treatment there were 17 pregnancies, which resulted in 9 normal infants, 3 terminations, and 4 spontaneous abortions. Nine patients took the combination oral contraceptive pill throughout chemotherapy; however, subsequently 4 developed amenorrhea and 3 oligomenorrhea, suggesting that these patients had not been protected from chemotherapy-induced ovarian damage. Estrogen replacement therapy was of definite benefit in the symptomatic patients with premature ovarian failure.
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PMID:The effect of combination chemotherapy on ovarian function in women treated for Hodgkin's disease. 641 21

Breast cancer (BC) is the first female cancer in France, accounting for 49,240 new cases in 2004. Approximately 80% of those tumors have positive hormone receptors (HR). Tamoxifen was used in four chemoprevention randomized trials, as well as another SERM (Selective Estrogen Receptor Modulation), raloxifen. This review analyses the updated results of these trials. All trials have shown that the risk of developing HR positive BC was reduced by tamoxifen or raloxifen, but without impact on HR negative BC and overall survival. Moreover, several unfavorable side effects (thrombo-embolic accidents and uterine cancers) have been observed. A new assessment of BC risk factors seems necessary, including not only family history and some histopathological abnormalities (e.g. atypical hyperplasia), but also new elements such as high bone and breast density and thoracic irradiation at young age (Hodgkin's disease). Indeed, tamoxifen efficacy seems optimal in very "high-risk" women. Therefore, the creation of a new and most comprehensive "risk model" is necessary as well as a tailored SERM use (maybe with other compounds), in order to optimize results and reduce potential side effects.
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PMID:[Breast cancer chemoprevention. Rational, trials results and future]. 1946 83

A variety of evidence suggests that estrogens may induce non-Hodgkin lymphoma (NHL). The reaction of catechol estrogen quinones with DNA to form depurinating estrogen-DNA adducts is hypothesized to initiate this process. These adducts are released from DNA, shed from cells into the bloodstream and excreted in urine. The aim of this study was to determine whether or not the depurinating estrogen-DNA adducts might be involved in the aetiology of human NHL. Estrogen metabolites, conjugates and depurinating DNA adducts were identified and quantified in spot urine samples from 15 men with NHL and 30 healthy control men by using ultraperformance liquid chromatography/tandem mass spectrometry. The levels of estrogen-DNA adducts were significantly higher in the men with NHL than in the healthy control men. Thus, formation of estrogen-DNA adducts may play a critical role in the aetiology of NHL, and these adducts could be potential biomarkers of NHL risk.
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PMID:Urinary biomarkers suggest that estrogen-DNA adducts may play a role in the aetiology of non-Hodgkin lymphoma. 1986 89

The treatment and prevention of solid tumors have proved to be a major challenge for medical science. The paradigms for success in the treatment of childhood leukemia, Hodgkin's disease, Burkett's lymphoma, and testicular carcinoma with cytotoxic chemotherapy did not translate to success in solid tumors--the majority of cancers that kill. In contrast, significant success has accrued for patients with breast cancer with antihormone treatments (tamoxifen or aromatase inhibitors) that are proved to enhance survivorship, and remarkably, there are now two approved prevention strategies using either tamoxifen or raloxifene. This was considered impossible 40 years ago. We describe the major clinical advances with nonsteroidal antiestrogens that evolved into selective estrogen receptor modulators (SERMs) which successfully exploited the ER target selectively inside a woman's body. The standard paradigm that estrogen stimulates breast cancer growth has been successfully exploited for over 4 decades with therapeutic strategies that block (tamoxifen, raloxifene) or reduce (aromatase inhibitors) circulating estrogens in patients to stop breast tumor growth. But this did not explain why high-dose estrogen treatment that was the standard of care to treat postmenopausal breast cancer for 3 decades before tamoxifen caused tumor regression. This paradox was resolved with the discovery that breast cancer resistance to long-term estrogen deprivation causes tumor regression with physiologic estrogen through apoptosis. The new biology of estrogen action has been utilized to explain the findings in the Women's Health Initiative that conjugated equine estrogen alone given to postmenopausal women, average age 68, will produce a reduction of breast cancer incidence and mortality compared to no treatment. Estrogen is killing nascent breast cancer cells in the ducts of healthy postmenopausal women. The modulation of the ER using multifunctional medicines called SERMs has provided not only significant improvements in women's health and survivorship not anticipated 40 years ago but also has been the catalyst to enhance our knowledge of estrogen's apoptotic action that can be further exploited in the future.
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PMID:Estrogen-mediated mechanisms to control the growth and apoptosis of breast cancer cells: a translational research success story. 2381 2