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 first National AIDS Malignancy Conference was held sixteen years after the first outbreak of Kaposi's sarcoma (KS) was noted in the medical press. The conference was devoted to the spectrum of malignancies that occur with AIDS. Researchers were divided on whether KS is tumorigenic or not. Other controversial topics included the use of standard-dose chemotherapy in patients with late-stage HIV infection, screening and aggressive treatments used for precancerous cervical changes, the management of AIDS-related malignancies in patients who are responding well to HIV treatments, and whether some AIDS-related malignancies will be classified as AIDS-defining conditions. The Centers for Disease Control and Prevention (CDC) currently considers KS, lymphoma, and cervical cancer as AIDS-defining malignancies. Specific sections of the conference dealt with pediatric cancers, squamous cell carcinoma, testicular cancer, lung cancer, and Hodgkin's disease.
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PMID:AIDS cancers: conundrums and controversies. 1136 11

As the AIDS epidemic advances, the spectrum of malignancies encountered is expanding. Several non-AIDS defining cancers, i.e. Hodgkin's disease (HD), anal and testicular cancer, are increasing in incidence in HIV-infected patients. The widespread use of highly active antiretroviral therapy (HAART) in industrialised countries has resulted in substantial improvement in the survival of HIV-infected patients. It is likely that in the future, cancers associated with long-term mild immune suppression will occur at an increased rate in long-term survivors of HIV infection. The natural history of the majority of non-AIDS defining tumours differs from that of the general population. Unusual aspects of tumour localisation, growth behaviour and therapeutical responses distinguish tumours in patients with HIV infection from those without. This paper reviews the most relevant data on the epidemiology, pathology, clinical features and treatment of the most frequently reported non-AIDS defining tumours, i.e. HD, lung, testicular and skin cancers.
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PMID:Clinical aspects and management of Hodgkin's disease and other tumours in HIV-infected individuals. 1142 62

The introduction of highly active antiretroviral therapy (HAART) has changed dramatically the landscape of HIV disease. Deaths from AIDS-related diseases have been reduced by 75% since protease inhibitor therapy and combination antiretroviral therapy came into use in late 1995. While KS is declining, the situation for non-Hodgkin's lymphoma is more complex with a reduced incidence of primary central nervous system lymphoma, but a relative stability in the number of patients developing systemic NHL. AIDS-related NHL appears not to be markedly decreased by the introduction of HAART and it is the greatest therapeutic challenge in the area of AIDS oncology. The emphasis has now shifted to cure while maintaining vigilance regarding the unique vulnerability of HIV-infected hosts. Furthermore, also for the prolongation of the survival expectancy of these patients, other non-AIDS-defining tumors, such as Hodgkin's disease, anal, head and neck, lung and testicular cancer, and melanoma have been recently reported with increased frequency in patients with HIV infection.
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PMID:AIDS-related tumors: integrating antiviral and anticancer therapy. 1188 Feb 6

The genetic and environmental components in 15 common cancers were estimated using the nationwide Swedish Family-Cancer Database. Tetrachoric correlations were used to describe similarity in cancer liability among family members. Structural equation modeling was used to derive estimates of the importance of genetic and environmental effects. Statistically significant estimates of proportion of cancer susceptibility, accounted for by genetic effects, were obtained for all studied cancers except for leukemia. The estimate was highest in thyroid cancer (53%), followed by tumors at endocrine glands (28%), testis (25%), breast (25%), cervix (22%), melanoma (21%), colon (13%), nervous system (12%), rectum (12%), non-Hodgkin lymphoma (10%), lung (8%), kidney (8%), urinary bladder (7%), stomach (1%) and leukemia (1%). The estimates of shared environmental effects ranged from 0% (cervix) to 15% (stomach). The childhood shared environmental effects were most important in testicular cancer (17%), stomach cancer (13%) and cervix in situ (13%). Our results indicate that environment has a principal causative role in cancer at all studied sites except for thyroid. The relatively large effect of heritability in cancer at some sites, on the other hand, indicates that even though susceptibility genes have been described at many cancer sites, they are likely to explain only part of the genetic effects.
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PMID:Environmental and heritable causes of cancer among 9.6 million individuals in the Swedish Family-Cancer Database. 1197 42

We tested for azoospermia factor (AZF) deletions 17 loci corresponding to AZF subintervals a-d in 17 cases of testicular tumors occurring in Finns. While DNA samples from 48 CEPH and 32 Finnish males showed no deletions, patients with testicular cancer displayed AZF deletion mosaicisms in various non-tumor tissues (13 cases) and specific deletion haplotypes in tumor tissues (10 cases). Two of the cases with AZF deletions were testicular non-Hodgkin lymphomas indicating that Y-microdeletions appear also in malignancies other than seminoma and non-seminoma tumors. In good agreement with this assumption, we detected one AZF deletion in normal cells from 1 of 5 HNPCC cases, heterozygous for an MLH1 mutation. We propose that AZF deletions occur in early embryogenesis due to mutations of TSPY, mismatch repair (MMR), or X-specific genes. Since fathers of testicular, tumor cases did not exhibit AZF deletions, we assumed they were not carriers of the mutation inducing AZF deletion-mosaicisms. Therefore, tumor cases should have received the MMR gene or X mutations via the maternal lineage, or for the case of TSPY and MMR genes via a sperm carrying a mutation occurred in the paternal germ-cell line. We consider AZF microdeletions in non-tumor cells to be part of a broader pattern of chromosome instability producing susceptibility to testicular tumors. Clonal transformation and expansion of one of these tumor-susceptible cell lineages give rise to testicular tumors showing genome anomalies characteristic of testicular cancers (i12p, LOH and genetic imbalance for various autosomal regions, Y- and autosomal MSI, specific AZF deletion haplotypes).
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PMID:Mosaic AZF deletions and susceptibility to testicular tumors. 1205 3

Twin studies on cancer have addressed two general questions, one about the possible carcinogenic effects of twinning and the second about heritable effects of cancer. The first question is answered by comparing the occurrence of cancer in twins to that in singletons; the second is answered in probandwise analysis of monozygotic twins compared to dizygotic twins or siblings. We used the nationwide Swedish Family-Cancer Database on 10.2 million individuals and 62,574 0-66-year-old twins to calculate standardized incidence ratios (SIRs) and 95% confidence intervals (CIs) for all main cancer compared to cancer in singletons. In probandwise analysis, the SIR was calculated for the co-twin of an affected twin. The overall risk of cancer in same or opposite sex twins was at the level of the risk for singletons. Testicular cancer was increased among same sex twins and all twins to an SIR of 1.43. Melanoma was decreased in these groups of twins to an SIR of 0.84. Some other cancer sites were increased or decreased in some groups of twins, but none in all twins. The SIR of breast cancer was 1.01 and 1.04 in same and opposite sex twins, respectively. Probandwise analysis showed increased risks for Hodgkin's disease in males and breast cancer and childhood acute lymphoid leukemia among females. The data on this unselected population of twins suggest that twinning per se is not a risk factor of cancer. However, because twins are smaller than singletons at birth, some possible effects could be masked by such differences. In utero hormonal exposures may be related to the risk of testicular cancer. The protective effects in melanoma may be due to socioeconomic factors.
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PMID:Cancer risks in twins: results from the Swedish family-cancer database. 1211 91

Use of sperm banks is indicated in young men with any type of cancer involving radiotherapy or chemotherapy, because significant amounts of the X-ray dose may reach the testes, and antimitotic drugs may affect spermatogenesis. The most common indications are seminomas, carcinomas, choriocarcinomas, or teratomas of the testicle and hematosarcomas such as Hodgkin's disease, as well as other conditions treated with antimitotics like autoimmune disease and immunosuppression before grafting. The authors were consulted by 22 patients, 8 with testicular cancer and 14 with Hodgkin's disease; only 9 were seen before treatment, and only 5 benefited by sperm bank. The protocol followed was a series of 3 sperm counts and motility readings on the 1st part of a split ejaculate, then a congelation test if indicated, each sample separated by at least 3 1/2 days of abstinence. Therefore the whole series usually took 2 weeks, requiring that chemotherapy be postponed for a while after orchidectomy, so that a period between treatments be available. If sperm preservation is considered after the beginning of treatment, there is no way of detecting the effect on spermatogenesis or on mutation. For pregnancies conceived after such treatment, amniocentesis is advised to screen for chromosoamal anomalies. Vasectomy is suggested in cases of familial cancers.
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PMID:[Sperm preservation for young cancer patients]. 1225 96

The male reproductive system is especially sensitive to the deleterious effects of many natural environmental agents, the workplace, and medical agents. Immunosuppressants and anticancer agents, which improve the prognosis of survival or the quality of life of patients, induce temporary sterility in all treated patients and complete sterility in 50% of treated patients. These agents affect spermatogenesis. Quantitative effects include oligo- and azoospermia. Qualitative effects involve spermatozoa changes, which inhibit implantation and their ability to fertilize the ovum and adversely affect embryonic development. Research is and has been underway to identify possible ways to preserve spermatogenesis. The Centers for the Study and Conservation of Human Sperm (CECOS) in France receives sperm every year from many men with cancer, especially Hodgkin's disease or testicular cancer, who wish CECOS to preserve their sperm through cryopreservation before they undergo chemotherapy or radiotherapy. Using less deleterious agents instead of cytotoxic drugs is a possible means to protect spermatogenesis. Agents which have been tested include antioxidants, gonadotropin-releasing hormone analogs, follicle stimulating hormone, and steroids. Of these agents, medroxyprogesterone acetate and testosterone together (MPA + T) have been examined the most in rats (contraception and protection) and in men (contraception). The rat studies show that MPA + T can indeed protect spermatogenesis. Clinical trials in men are needed to support these findings. INSERM supports a multidisciplinary group examining spermatogenesis preservation called Prosperm, which will likely be the impetus for the start-up of such clinical trials. Prosperm members include researchers and physicians who network to keep each other up-to-date on spermatogenesis protection. Their collaboration is especially needed, since recent epidemiological studies indicate that diverse environment factors adversely affect spermatogenesis.
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PMID:[Spermatogenesis protection: myth or reality?]. 1228 96

Since the advent of HAART, the natural history of HIV disease has been changing, with decreased risk of life-threatening opportunistic infections and prolonged survival. Concurrently, a variety of non-AIDS-defining cancers have been reported with increased incidence in HIV-infected adults, including anal cancer, Hodgkin's disease, head and neck cancer, testicular cancer, lung cancer, colon cancer, basal cell cancer, squamous cell cancer of the skin, and melanoma. It appears that these tumors may have a more aggressive clinical course in HIV-infected people. Available data, however, suggest that antitumor response and survival in HIV-infected people with malignancy are improved in people with higher CD4 counts. The possible mechanisms for the increased incidence and altered clinical course of these malignancies in HIV-infected people remain unclear.
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PMID:Non-AIDS-defining cancer in HIV-infected people. 1285 61

The introduction of highly active antiretroviral therapy (HAART) has changed dramatically the landscape of HIV disease. Deaths from AIDS-related diseases have been reduced by 75% since protease inhibitor therapy and combination antiretroviral therapy came into use in late 1995. While KS is declining, the situation for non-Hodgkin's lymphoma is more complex with a reduced incidence of primary central nervous system lymphoma, but a relatively stability in the number of patients developing systemic NHL. AIDS related NHL appears not to be markedly decreased by the introduction of HAART and it is the greatest therapeutic challenge in the area of AIDS oncology. The emphasis has now shifted to cure while maintaining vigilance regarding the unique vulnerability of HIV-infected hosts. Furthermore, also for the prolongation of the survival expectancy of these patients, other non AIDS-defining tumors, such as Hodgkin's disease, anal and head and neck, lung and testicular cancer, and melanoma have been recently reported with increased frequency in patients with HIV infection.
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PMID:Therapeutic approaches to AIDS-related malignancies. 1452 90


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