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)

For people immunosuppressed by human immunodeficiency virus (HIV), we expect an increase in cancer incidence similar to that documented in transplant patients. We examined the cancer spectrum in an HIV-infected cohort, specifically malignancies not currently associated with acquired immunodeficiency syndrome (AIDS), in relation to the general population. Cancer incidence data for residents of Harris County, Texas, diagnosed between 1975 and 1994, were linked to HIV/AIDS registry data by Soundex code and date of birth to identify malignancies in an HIV-infected cohort of 14,986 persons. Incidence of cancer in this cohort was compared to the general population by standardized incidence ratio (SIR) analysis. From the HIV-infected cohort, 2289 persons (15%) were identified as having one or more malignancies, with 97% occurring in males. The linkage alone identified 29.5% of the malignancies, of which only 28.7% were diagnosed in males. Adjusting for age, HIV-infected men and women had incidences of cancer that were 16.7 [95% confidence interval (CI) 16.1-17.3] and 2.9 (95% CI 2.3-3.7) times that expected for the general population of Harris County, Texas. Besides Kaposi's sarcoma, non-Hodgkin's lymphoma, cervix cancer and brain lymphoma, non-AIDS related malignancies of Hodgkin's lymphoma, non-melanotic skin cancer in males and colon cancer in females, exhibited significant SIRs of 5.6 (95% CI 3.6-8.4), 6.9 (95% CI 4.8-9.5) and 4.0 (95% CI 1.1-10.2). Increased incidences of lung, prostate and breast malignancies were not seen in this HIV cohort. Persons infected with HIV appear to be at increased risk for the non-AIDS related malignancies, Hodgkin's lymphoma, non-melanotic skin cancer in males and colon cancer in females.
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PMID:HIV-related malignancies: community-based study using linkage of cancer registry and HIV registry data. 1063 60

A nationwide, computer-based survey of all total joint arthroplasties performed in Finland has been carried out since January 1980. From these records, a cohort of 9,444 patients, with 51,756 person-years, after primary operation with a total polyethylene-on-metal knee arthroplasty (TKA) was followed up for cancer through the Finnish Cancer Register up to December 31, 1996. During the follow-up, 706 cancers were observed. The expected number, based on national rates, was 719; therefore, the standardized incidence ratio (SIR) for all cancers was 0.98. The SIRs for non-Hodgkin's lymphoma (1.40), Hodgkin's disease (1.24) and multiple myeloma (1.54) were increased, but only that of non-Hodgkin's lymphoma was statistically significant 3-10 years after the operation. The numbers of observed cases of prostate cancer exceeded that of expected, with a SIR value of 1.49. A low SIR of lung cancer was observed among men, especially during the first 3 years (0.61), but not in women. The SIR for colon cancer was below unity in women only (SIR 0.70). The SIR for cancer of the urinary organs was close to unity (0.97). SIR relating to soft tissue and bone cancer did not differ significantly from unity, and none of the 6 sarcomas was observed at the site of a prosthesis. The overall cancer risk after TKA done for primary osteoarthrosis seems not to be increased. The increases in lymphoma and prostate cancer risk, however, are observations that could be related to TKA and justify further follow-up of the cohort.
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PMID:Cancer incidence after total knee arthroplasty: a nationwide Finnish cohort from 1980 to 1996 involving 9,444 patients. 1066 28

The CHK2 gene encodes a protein kinase that is important for the regulation of cell cycle arrest after DNA damage. CHK2 acts downstream of ataxia teleangiecstasia mutated (ATM), modulates the function of p53 and may help mediate cell cycle arrest at G2/M by phosphorylation of Cdc25C. Recently, the human homolog of the checkpoint kinase Cds1 (CHK2) has been suggested to be a tumor suppressor gene. Heterozygous germline mutations have been reported in Li-Fraumeni syndrome (LFS), a highly penetrant familial cancer phenotype, and in sporadic colon cancer. LFS is associated with the development of lymphoid malignancies, especially childhood ALL. Therefore, we analyzed the DNA from 143 lymphoid malignancies to determine whether they had mutations of the CHK2 gene. The 14 exons of CHK2 were studied by polymerase chain reaction-single strand conformational polymorphism (PCR-SSCP) and sequencing of aberrantly migrating bands. One missense mutation changing serine to phenylalanine (codon 428) in an evolutionarily highly conserved domain was found in a non-Hodgkin's aggressive lymphoma. Another point mutation in the non-coding region was identified in one of adult T-cell leukemias (ATL) samples. This result suggests that mutation of the CHK2 gene may rarely be involved in the development of selected lymphomas.
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PMID:Analysis of the CHK2 gene in lymphoid malignancies. 1169 18

Hodgkin and Reed-Sternberg (H/RS) cells are characterized by chromosomal instability. Nevertheless, neither specific nor consistent chromosomal alterations could be characterized in H/RS cells. Microsatellite instability (MSI) is another form of genomic instability but its role in the pathogenesis of classical Hodgkin's disease (cHD) has not been investigated so far. We analyzed MSI and mismatch repair (MMR) protein expression in H/RS cells of cHD in order to assess genomic instability in these cells. Using a sensitive single cell approach, MSI-low was detected in a portion of single cells of the H/RS cell line L1236. Mutations of genes encoding for hMSH2 and hMLH1 were excluded by RT-PCR in L1236 cells. An analysis of pooled single H/RS cells of seven primary cases of cHD showed loss of heterozygosity for some allelic markers but absence of MSI in all 7 cases. Owing to a tight correlation between MSI-high, inactivating mutations of MMR genes and MMR protein expression in colon cancer, MMR protein expression commonly is used as a marker for MSI. In order to screen additional primary cases of cHD for MSI, we performed immunohistochemistry for hMSH2 and hMLH1 in 6 of the 7 cases analyzed by single cell PCR and 20 additional cases of cHD. H/RS cells from 25 out of 26 cases showed a nuclear staining pattern for hMSH2 and hMLH1 similar to germinal center B cells of non-malignant lymph nodes. These results indicate a proficient MMR system in most H/RS cells. It is concluded that a defect MMR system is unlikely to contribute to the malignant phenotype and genomic instability of H/RS cells in cHD.
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PMID:Proficient mismatch repair protein expression in Hodgkin and Reed Sternberg cells. 1177 65

Anemia is common in patients with cancer and is a frequent complication of myelosuppressive chemotherapy. In this study, we investigated the incidence and severity of chemotherapy-induced anemia caused by the most common chemotherapy regimens, including the new generation of chemotherapeutic agents, used in the treatment of the major nonmyeloid malignancies in adults. Five hundred fifty-two patients with histologically proven carcinoma originating from breast (n = 165), lung (n = 128), colon (n = 75), ovary (n = 84), and malignant lymphoma (n = 100) were included in this study. Hemoglobin levels for each patient were measured with an automatic counter during both pretreatment and before each chemotherapy cycle during therapy. To document the incidence of anemia, the National Cancer Institute grading system was used. Before chemotherapy, 44% of patients with breast carcinoma had anemia. There was a 16% increase in the incidence of anemia after chemotherapy. Severe anemia was observed in less than 1% of patients. No difference was found in the incidence of anemia between the fluorouracil, doxorubicin, cyclophosphamide (FAC) and cyclophosphamide, methotrexate, fluorouracil (CMF) regimens used in the adjuvant setting. However, single-agent chemotherapy with newer generation caused more anemia when compared with the FAC regimen (p < 0.005). Chemotherapy resulted in a significant decrease in hemoglobin levels when compared with pretreatment values in patients with lung cancer (p < 0.001). During treatment, the increase in the incidence of grade II anemia was associated with a parallel decrease in the incidence of grade I anemia. The incidence of severe anemia did not exceed 15%. The incidence of anemia was equivalent in both patients with small-cell lung cancer and those with non-small-cell lung cancer treated with the etoposide and cisplatin (EP) combination. Seventy-one percent of patients with colon cancer had anemia before initiation of chemotherapy. No difference was observed in posttreatment hemoglobin values compared with pretreatment values. Patients treated with irinotecan and fluorouracil and leucovorin (FUFA) combination showed similar rates of anemia. Incidence of anemia in patients with ovarian cancer at admission was 68%. Chemotherapy resulted in a prominent increase in incidence of anemia, which increased to 91.5%. There was an increase in grade II anemia, which corresponded to the decrease in grade I anemia. Less than 10% of patients developed severe anemia. No difference in the incidence of anemia was observed in patients with ovarian cancer treated with either cisplatin and cyclophosphamide or cisplatin combination. Showing a high incidence of anemia (82%) at presentation, hemoglobin levels in patients with malignant lymphoma were unaltered with chemotherapy. Severe anemia occurred in less than 3% of patients. There was a higher incidence of anemia in patients with non-Hodgkin's lymphoma receiving the cyclophosphamide, epirubicin, vincristine, prednisone (CEOP) regimen in contrast to patients with Hodgkin's lymphoma treated with the doxorubicin, bleomycin, vinblastine, dacarbazine (ABVD) combination. There was a prominent decline in the hemoglobin levels with cisplatin-based combinations in contrast to combinations including noncisplatin agents (p < 0.001). In this study, we have observed equivalent rates of treatment-related anemia when compared with previous data in patients with specific tumor types. The incidence of pretreatment anemia was high in various malignancies. The mechanisms underlying the propensity for a higher risk of pretreatment anemia in patients with malignant disorders and its influence on the outcome has to be elucidated by further population-based and molecular studies.
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PMID:Anemia in oncology practice: relation to diseases and their therapies. 1215 68

Hereditary non-polyposis colon cancer (HNPCC) is an autosomal dominant disorder featuring familial clustering of colorectal and/or endometrial cancer, and other malignancies. Except for a rare case report, Hodgkin's disease (HD) and non-Hodgkin's lymphoma (NHL) have not been considered part of HNPCC. Recent murine models for HNPCC have shown an increased incidence of B- and T-cell lymphoma, as well as tumors of the gastrointestinal tract and other organ systems, involving defects in genes resulting in faulty mismatch repair (MMR) of DNA. These MMR genes include MLH1, MSH2, MSH3, MSH6, PMS1 and PMS2. We sought to analyze the occurrence of NHL and HD in families with clusters of colorectal cancers (CRC). Probands from 21 kindreds were classified as HNPCC (3), HNPCC-like (5), and HNPCC-variant (13); seen and followed by Clinical Genetics at Memorial Hospital the kindreds were assessed for the occurrence of NHL or HD. Of the 21 pedigrees, a total of 37 patients were identified who were diagnosed with leukemia, lymphoma, or HD. Fourteen of the 37 patients with a diagnosis of NHL or HD were further classified and showed varying histologies ranging from chronic lymphocytic leukemia/small lymphocytic lymphoma (2), mycosis fungoides (1), follicular lymphoma (1), extranodal marginal zone lymphoma of MALT type (2), diffuse large B-cell lymphoma (4), nodular sclerosis HD (3), and mixed cellularity HD (1). Microsatellite instability studies were performed on 6 cases but none showed evidence of replication error repair defects. Immunohistochemical stains performed on paraffin sections from these 6 representative cases showed differential protein expression of MLH1, MSH2, MSH6, and PMS2 when compared to normal reactive tissues from the same patient but showed no significant differences when compared to controls of non-familial, sporadic lymphomas. These results suggest that lymphomas arising in the setting of familial CRC do not bear the molecular hallmarks of HNPCC. Further studies are needed to explain the differential patterns of expression of RER-associated proteins in lymphomas, as well as the association of lymphomas and possibly renal cell cancers in a subset of kindreds in which CRC clustering is evident.
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PMID:Analysis of mismatch repair defects in the familial occurrence of lymphoma and colorectal cancer. 1240 Jun 5

In the first part our intention was, essentially, to present the particularities of glucose tumoral cells metabolism, PET components, the synthesis of 18F FDG and the detection of unknown cancers. This second part makes reference about mainly types of tumors who benefit by FDG-PET indications. Clinical PET has a rapid growth because of its use in cancer diagnosis and management. According with published studies all over the world, the sensibility and specificity of FDG-PET, noninvasive method, is higher than that of the conventional methods like CT, IRM, ultrasonography. PET is en excellent detection method of most of common cancer types and depends not on the histological neoplasm type; the more aggressive is the tumor, more it will uptake the radiotracer. The cost is significant, so the indications must be very precise: evaluating the malignity of solitary pulmonary nodules, evaluating the recurrences of melanoma, colon cancer diagnosis, differentiation between recurrent brain tumor and radiation injury, differential diagnosis of the benign lymph and malign lymph nodes, staging of Hodgkin's and non-Hodgkin's lymphoma, evaluation the response to therapy. Because the PET images are difficult to interpret, appears the necessity of correlation with anatomic images: this was the fusion images beginnings (the PET and CT images combination); now the physiologic information has precise anatomic localization. The growing of this method is very probably, both using 18F FDG -thanks to its highly favorable physical characteristics- and other new radiopharmaceuticals. The clinical cases that illustrate the applications are investigated at CERMEP, Lyon, France.
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PMID:[18F FDG PET-Applications in Oncology]. 1263 54

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

Non-steroidal anti-inflammatory drugs (NSAIDs), including aspirin, seem to have chemopreventive properties against several types of cancer, particularly colon cancer. Persons with rheumatoid arthritis, an autoimmune disease for which NSAIDs are used commonly, have been reported to be at lower risk of colon cancer but at elevated risk of non-Hodgkin lymphoma (NHL), raising the possibility that NSAIDs may be a risk factor for NHL. We evaluated the association of use of NSAIDs, arthritis history, and risk of NHL in a prospective cohort of 27,290 postmenopausal women from the state of Iowa. The frequency of use of aspirin and of other NSAIDs excluding aspirin (e.g., ibuprofen), as well as a physician diagnosis of rheumatoid arthritis (RA) or osteoarthritis (OA), were self-reported on a questionnaire mailed in 1992. The incidence of NHL was ascertained through annual linkages to the Iowa SEER Cancer Registry. Relative risks (RR) and 95% confidence intervals (CI) were estimated using Cox proportional hazards regression. Through 7 years of follow-up, 131 cases of NHL were identified. Compared to women who did not use either aspirin or other non-aspirin NSAIDs, women using aspirin exclusively (RR = 1.71; 95% CI = 0.94-3.13), non-aspirin NSAIDs exclusively (RR = 2.39; 95% CI = 1.18-4.83), or both types of drugs (RR = 1.97; 95% CI = 1.06-3.68) were at increased risk of NHL. A diagnosis of RA (RR = 1.75; 95% CI = 1.09-2.79), but not OA (RR = 1.06; 95% CI = 0.67-1.68), was associated with risk of NHL, but the positive association of use of aspirin and other NSAIDs with NHL was independent of RA history. Multivariate adjustment for other NHL risk factors only attenuated slightly these associations, whereas exclusion of cases occurring during the first 2 years of follow-up strengthened the associations. These data suggest that use of NSAIDs, either aspirin or other non-aspirin NSAIDs, are associated positively with risk of NHL, and that this association is independent of RA history.
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PMID:Association of aspirin and other non-steroidal anti-inflammatory drug use with incidence of non-Hodgkin lymphoma. 1505 81

Survival of patients aged 15-24 years, diagnosed with cancer during the period of 1990-1994, is described within Europe. Data on 15101 patients, extracted from the files of the 56 adult cancer registries included in the EUROCARE-3 database, representing 20 European countries, were analysed and compared. Five-year survival for 'all cancers combined' was 75% in males (ranging from 59% in Estonia to 89% in Iceland), and 78% in females (ranging from 59% in Estonia to 89% in Norway). The Northern European countries (except Denmark) and Austria had the highest survival figures, while survival in the Eastern European countries was lower than the European average. Denmark, UK, and the pool of the central European countries, had intermediate survival figures. Haemopoietic tumours were the most common malignancies: 5-year survival was high for Hodgkin's disease (89%), intermediate for non-Hodgkin's lymphoma (68%) and lower for acute lymphoblastic leukaemia (ALL) (47%) and acute myeloblastic leukaemia (AML) (39%). Five-year survival for gonadal germ cell cancers, the second most common malignancy in young adults, was 90%. Five-year survival for the other cancers under consideration was as follows: 89% for skin melanoma, 66% for all Central Nervous System (CNS) tumours, 57% for bone tumours, 58% for osteosarcoma, 42% for Ewing's sarcoma, 57% for soft-tissue sarcomas, 99% for thyroid carcinoma, 82% for uterine cervical carcinoma, and 83% for ovarian carcinoma. For more 'adult-specific tumours', 5-year survival was good for colon (77%) and lung (60%) cancers, and less favourable, compared with adults, for breast cancer (68%). Adolescents (15-19 years) had significantly worse survival than young adults (20-24 years) for all malignancies combined. Survival for Hodgkin's lymphoma, CNS tumours, melanoma and colon cancer showed marked regional variability. Since many of the tumours occurring in young adults are curable, these results should encourage, without delay, efforts to identify obstacles to improving outcome and reducing geographical inequalities in survival for this group of patients.
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PMID:Cancer survival in European adolescents and young adults. 1464 22


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