Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q06643 (non-Hodgkin's lymphoma)
 11,307 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Molecular characterization of neuroendocrine (Merkel cell) carcinoma of the skin. Review of the literature and report of three cases. Although neuroendocrine carcinoma of the skin (NECS) is comparatively a rare clinical-histological entity, numerous morphological and ultrastructural studies have been carried out since the tumor was identificated by Toker (1972). Recently immunocytochemistry has allowed a better molecular characterization (immunophenotype) of this tumor and a more exact diagnosis. The main problem for the pathologist is the differential diagnosis between NECS and skin neoplasms--both primitive and metastatic--which require a more aggressive treatment. Often the classical morphological criteria do not distinguish NECS from non-Hodgkin's lymphoma, amelanotic melanomas, cutaneous metastases of lung small cell carcinoma or of neuroblastoma. The co-expression of cytokeratins and neurofilaments constantly found in NECS, is surely the best differential criterion from non-neuroendocrine carcinomas. Furthermore, the typical paranuclear location of both the intermediate filaments in NECS is a distinctive peculiarity as opposed to lung microcytoma, where cytokeratins and neurofilaments, when present, show widespread perinuclear positivity. Chromogranin A is found only in a small percentage of tumor cells, whilst synthesis of calcitonin, somatostatin, gastrin, ACTH, is very rare. Finally, the lack of common leukocyte antigen (CLA), S-100 protein and vimentin in NECS rules out the diagnoses of lymphoma, melanoma and sarcoma respectively.
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PMID:[Molecular characterization of cutaneous neuroendocrine (Merkel cell) carcinoma. Review of the literature and presentation of a caseload]. 209 Oct 10

A large excess of non-Hodgkin's lymphoma has been documented in renal transplant patients and may be related to immunosuppressive therapy, persistent antigenic challenge from the graft, or both. To determine whether immuno-suppression resulting from chronic renal failure is associated with an elevated risk of certain tumors such as non-Hodgkin's lymphoma, the authors studied cancer incidence in a national cohort of 28,049 patients in the United States with chronic renal failure who received maintenance dialysis for at least six months (totaling 66,706 person-years of observation). Compared with national incidence rates, the relative risk (RR) of cancer was 0.9 (excluding nonmelanoma skin cancer, multiple myeloma, kidney cancer, and uterine cervix cancer). Moderate excesses of leukemia, non-Hodgkin's lymphoma, Hodgkin's disease, thyroid cancer, and biliary tract cancer were found, but were not statistically significant for both sexes combined. A significantly elevated risk of non-Hodgkin's lymphoma among patients with chronic glomerulonephritis (RR = 2.6) accounted for the excess observed in the total series, raising the possibility of factors specific to this disease.
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PMID:Cancer in patients receiving long-term dialysis treatment. 311 33

The Stockholm-Gotland Cancer Register was used to evaluate the clinical observation that patients with non-Hodgkin's lymphoma (NHL) had an increased risk of malignant melanoma or squamous-cell carcinoma of the skin (SCCS) and vice versa. During 1958-1992, NHL was diagnosed in a total of 6,176 patients. Of these patients, 504 developed a second primary cancer of any type except NHL, compared to 301.9 expected, giving a standardized incidence ratio (SIR) of 1.7 [95% confidence interval (CI) 1.5-1.8]. The risk of SCCS and malignant melanoma in patients with NHL was 4.8 (95% CI 3.6-6.2; n = 54) and 1.7 (95% CI 0.8-3.1; n = 10), respectively. The hazard risk for a second malignancy was relatively constant over time, whereas the skin malignancies revealed the highest risks 3-10 years after initial diagnosis. Similarly, the risk of a secondary NHL was studied in patients with malignant melanoma and SCCS during the same period and found to be 1.3 (95% CI 0.8-2.1; n = 17) and 1.8 (95% CI 1.2-2.5; n = 34), respectively. The highest risk for NHL following malignant melanoma was seen 3-10 years after first diagnosis, while the highest risk following SCCS was observed 0-2 years after initial diagnosis. One of several possible explanations or the development of NHL and a skin malignancy in the same patient is an immunological defect caused by sun exposure.
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PMID:Non-Hodgkin's lymphoma and skin malignancies--shared etiology? 766 20

There is evidence that the incidence of primary cutaneous lymphoma, like other forms of non-Hodgkin's lymphoma, is increasing, yet little is known of the pathogenetic events involved in this group of disorders. In this study we examine the frequency and spectrum of P53 gene mutations in a large series of primary cutaneous lymphomas, with particular emphasis on tumor stage mycosis fungoides, as it is in these cases that p53 overexpression has previously been reported. Sixty-six samples from 55 patients with primary cutaneous B cell and T cell lymphomas were analyzed for mutations in exons 5-9 of the P53 gene using polymerase chain reaction/single strand conformational polymorphism, and subsequent cloning and sequencing of genomic DNA. Fourteen separate P53 mutations were identified in blood, skin, and lymph node samples in 13 patients (24%). Twelve of 14 mutations occurred at dipyrimidine sites, eight resulting in C-->T transitions and one in a CC-->TT tandem base transition, a mutation spectrum strikingly similar to that reported in nonmelanoma skin cancer and characteristic of DNA damage caused by ultraviolet B radiation. In the subset of patients with mycosis fungoides, P53 mutations were identified in six of 17 patients with tumor-stage but in none of 12 patients with plaque-stage disease (Fisher's exact test p = 0.027). These data suggest a role for ultraviolet radiation in the pathogenesis of primary cutaneous lymphomas and a possible ultraviolet B-related step in the progression of mycosis fungoides from plaque to tumor-stage disease.
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PMID:Spectrum of p53 gene mutations suggests a possible role for ultraviolet radiation in the pathogenesis of advanced cutaneous lymphomas. 1008 8

Immune-suppressed populations experience higher rates of cancer than expected. The most common malignancies are non-Hodgkin's lymphoma (NHL) in those with HIV infection, in organ transplant recipients, and in those with primary immune deficiencies; Kaposi's sarcoma (KS) in those with HIV infection; and nonmelanoma skin cancer (SC) in transplant patients. These cancers are associated with infection with the Epstein-Barr virus (EBV) in NHL, human herpesvirus type 8 (HHV-8) in KS, and the human papillomaviruses (HPV) in SC. The strength of the association varies from very strong (HHV-8 in KS) to inconsistent (HPV in SC). In HIV infection, the risk of these cancers increases quite gradually (within a few years in almost all of the primary immune deficiencies), whereas this risk increases quite quickly among transplant recipients. Comparing the patterns of malignancy and immune parameters among these immune-incompetent populations and the general population may elucidate the role of host response in controlling latent oncogenic infections.
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PMID:Overview of the epidemiology of malignancy in immune deficiency. 1043 Feb 11

Little is known about the cancer risk following sarcoidosis. In a retrospective cohort study, we tested the hypothesis of an increased risk for malignant lymphomas, lung cancer as well as cancer in other organs frequently involved in sarcoidosis. Four hundred seventy-four patients from an incidence study 1966-1980 and 8,541 patients identified in the Swedish Inpatient Register (IPR) 1964-1994 were linked to the Cancer Register, the Register of Causes of Death, and the Register of Total Population. Relative risks were estimated using standardized incidence ratios (SIR). The overall relative risks for cancer were similar and elevated in both cohorts (IPR presented), SIR = 1.3; 95% confidence interval (CI) 1.2 to 1.4. For lung cancer and non-Hodgkin's lymphoma, the relative risk was doubled during the first decade of follow-up. Thereafter, the risk for lung cancer was significantly decreased whereas the risk for non-Hodgkin's lymphoma equaled unity. Throughout follow-up, elevated risks were found for melanoma (SIR = 1.6; 95% CI 1.0 to 2.3) and nonmelanoma skin cancer (SIR = 2.8; 95% CI 2.0 to 3.8). An increased risk was also found for liver cancer (SIR = 1.4; 95% CI 0.8 to 2.2). Thus, sarcoidosis appears to be associated with a significantly increased risk for cancer in affected organs. Chronic inflammation is a putative mediator of this risk.
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PMID:Increased risk for cancer following sarcoidosis. 1055 38

We studied sunlight exposure from outdoor work in relation to cancer, using data from 323,860 men participating in an occupational health service program of the Swedish construction industry. An experienced industrial hygienist assessed the exposure for 200 job tasks. We estimated relative risks (RRs) adjusted for age, smoking, and magnetic field exposure. There was an increased RR in the high-exposure group for myeloid leukemia [RR = 2.0, 95% confidence interval (95% CI) = 1.1-3.6] and lymphocytic leukemia (RR = 1.7, 95% CI = 0.9-3.2). For non-Hodgkin's lymphoma there was a 30% increase in risk in the high-exposure group (95% CI = 0.9-1.9). There was no increased risk of malignant melanoma, except for tumors of the head, face, and neck in the high-exposure group (RR = 2.0, 95% CI = 0.8-5.2), and we also found an increased risk for malignant melanoma of the eye in this group (RR = 3.4, 95% CI = 1.1-10.5). Outdoor workers had no increased risk of nonmelanoma skin cancer. Nevertheless, the RR for lip cancer (squamous cell carcinoma) among the high-exposure group was estimated at 1.8 (95% CI = 0.8-3.7). Among other sites, an increased risk of stomach cancer was suggested in this group (RR = 1.4, 95% CI = 1.0-1.9). The results for lymphoma, leukemia, and possibly also for stomach cancer might reflect a suppression of the immune system from ultraviolet light in outdoor workers.
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PMID:Occupational sunlight exposure and cancer incidence among Swedish construction workers. 1150 75

A substantial excess risk of lymphomas and nonmelanoma skin cancer has been demonstrated following organ transplantation. Large sample size and long follow-up time may, however, allow more accurate risk estimates and detailed understanding of long-term cancer risk. The objective of the study was to assess the risk of cancer following organ transplantation. A nationwide cohort study comprising 5931 patients who underwent transplantation of kidney, liver or other organs during 1970-1997 in Sweden was conducted. Complete follow-up was accomplished through linkage to nationwide databases. We used comparisons with the entire Swedish population to calculate standardised incidence ratios (SIRs), and Poisson regression for multivariate internal analyses of relative risks (RRs) with 95% confidence intervals (CI). Overall, we observed 692 incident first cancers vs 171 expected (SIR 4.0; 95% CI 3.7-4.4). We confirmed marked excesses of nonmelanoma skin cancer (SIR 56.2; 95% CI 49.8-63.2), lip cancer (SIR 53.3; 95% CI 38.0-72.5) and of non-Hodgkin's lymphoma (NHL) (SIR 6.0; 95% CI 4.4-8.0). Compared with patients who underwent kidney transplantation, those who received other organs were at substantially higher risk of NHL (RR 8.4; 95% CI 4.3-16). Besides, we found, significantly, about 20-fold excess risk of cancer of the vulva and vagina, 10-fold of anal cancer, and five-fold of oral cavity and kidney cancer, as well as two- to four-fold excesses of cancer in the oesophagus, stomach, large bowel, urinary bladder, lung and thyroid gland. In conclusion, organ transplantation entails a persistent, about four-fold increased overall cancer risk. The complex pattern of excess risk at many sites challenges current understanding of oncogenic infections that might become activated by immunologic alterations.
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PMID:Cancer risk following organ transplantation: a nationwide cohort study in Sweden. 1526 36

The aim of this study was to investigate variations in the length of time that patients with cancer wait from diagnosis to treatment with radiotherapy. A total of 57,426 men and 71,018 women diagnosed with cancer between 1992 and 2001 and receiving radiotherapy within 6 months of diagnosis were identified from the Thames Cancer Registry database. In total, 12 sites were identified for which a substantial number or proportion of patients received radiotherapy: head and neck, oesophagus, colon, rectum, lung, nonmelanoma skin cancer, breast, uterus, prostate, bladder, brain and non-Hodgkin's lymphoma. Median waiting times from diagnosis to radiotherapy were calculated, together with the proportion of patients who received radiotherapy within 60 days of diagnosis, and analysed by year of diagnosis, cancer site, deprivation quintile, age at diagnosis, sex and cancer network of either residence or treatment. Logistic regression was used to adjust the proportion receiving treatment within 60 days for the effects of the other factors. There were significant differences in the proportions receiving radiotherapy within 60 days between different networks and different cancer sites, which remained after adjustment. Median waiting times varied from 42 to 65 days across networks of residence, with the adjusted proportion treated within 60 days ranging from 44 to 71%. There was no difference between male and female patients after adjustment for the other factors, particularly site. There was a highly significant trend over time: the median wait increased from 45 days in 1992 to 76 days in 2001, while the adjusted proportion being treated within 60 days declined by almost a half, from 64 to 35%, over the same period.
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PMID:Waiting times for radiotherapy: variation over time and between cancer networks in southeast England. 1578 52

There is increasing evidence that vitamin D reduces the risk of many types of cancer. Geographic variations in cancer mortality rates in Spain are apparently linked to variations in solar ultraviolet (UV) irradiances and other factors. Cancer mortality rates for 48 continental Spanish provinces for 1978-1992 were used in linear regression analyses with respect to mortality rates for latitude (an index of solar UVB levels), skin cancer (an index of high cumulative UVB irradiance), melanoma (an index related to solar UV irradiance and several other factors) and lung cancer (an index of cumulative effects of smoking). The 9 cancers with mortality rates significantly correlated with latitude for 1 or both sexes were brain, gastric, melanoma, nonmelanoma skin cancer (NMSC), non-Hodgkin's lymphoma (NHL), pancreatic, pleural, rectal and thyroid cancer. Inverse correlations with latitude were found for laryngeal, lung and uterine corpus cancer. The 17 cancers inversely correlated with NMSC are bladder, brain, breast, colon, esophageal, gallbladder, Hodgkin's lymphoma, lung, melanoma, multiple myeloma, NHL, ovarian, pancreatic, pleural, rectal, thyroid and uterine corpus cancer. The 16 correlated with melanoma are bladder, brain, breast, colon, gallbladder, leukemia, lung, multiple myeloma, NHL, ovarian, pancreatic, pleural, prostate, rectal, renal and uterine corpus cancer. The results for lung cancer were in accordance with the literature. These results provide more support for the UVB/vitamin D/cancer hypothesis and indicate a new way to investigate the role of solar UV irradiance on cancer risk. They also provide more evidence that melanoma and NMSC have different etiologies.
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PMID:An ecologic study of cancer mortality rates in Spain with respect to indices of solar UVB irradiance and smoking. 1714 99


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