Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We used the nationwide Swedish Family-Cancer Database to analyse the risk for testicular cancer in offspring through parental and sibling probands. Among 0 to 70-year-old offspring, 4,586 patients had testicular cancer. Standardized incidence ratios for familial risk were 3.8-fold when a father and 7.6-fold when a brother had testicular cancer. Testicular cancer was associated with leukaemia, distal colon and kidney cancer, melanoma, connective tissue tumours and lung cancer in families. Non-seminoma was associated with maternal lung cancer but the risk was highest for the late-onset cases, providing no support to the theory of the in utero effect of maternal smoking on the son's risk of testicular cancer. However, the theory cannot be excluded but should be taken up for study when further data are available on maternal smoking. The high familial risk may be the product of shared childhood environment and heritable causes.
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PMID:Familial risks in testicular cancer as aetiological clues. 1646 41

The Chemotherapy Committee of Cancer and Leukemia Group B (CALGB) was established in the mid-1970s to assemble a group of experts in cancer chemotherapy and pharmacology who could advise the CALGB disease committees about the optimal use of drugs in the fight against cancer and to provide quality assurance for the chemotherapy section of CALGB protocols. Chaired initially by Edward Henderson and then David Van Echo, the committee was also the repository of studies in diseases for which CALGB did not have a formal committee, such as testis cancer and sarcoma. In 1990, following the appointment of Richard Schilsky as Chair, the name of the committee was changed to the Pharmacology and Experimental Therapeutics (PET) Committee to reflect a more specific focus and scientific agenda (i.e., studies of chemotherapy pharmacology and development of new agents). Three PET Committee reference pharmacology laboratories (led by Merrill Egorin, Tony Miller, and Mark Ratain) were established to measure drug concentrations in biological fluids and to perform pharmacokinetic analyses. In addition, the PET Committee embarked on a number of multi-institution phase I studies. These phase I studies included studies of special populations, including the first prospective study of an anticancer agent (paclitaxel) in patients with hepatic dysfunction. In addition, the Committee studied a number of phase I combinations destined for phase II evaluation in disease-specific committees. Following Dr. Schilsky's election as CALGB Group Chair in 1994, Mark Ratain took over as Chair of the PET Committee and continued to emphasize population pharmacology as the primary theme of the Committee's research agenda. In addition, the PET Committee began to develop novel clinical trial designs, including the first completed randomized discontinuation trial of an antineoplastic agent. Most recently, the PET Committee has launched an ambitious research program in pharmacogenetics, facilitated in large part through the recruitment of Howard McLeod as Vice Chair. This area of research is a collaborative effort with the NIH Pharmacogenetics Research Network and has the potential to definitively address the hypothesis that germ line polymorphisms are a significant determinant of the toxicity and efficacy of anticancer therapy. It is anticipated that the results of the current studies will contribute significantly to the goal of individualizing cancer treatment.
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PMID:The cancer and leukemia group B pharmacology and experimental therapeutics committee: a historical perspective. 1674 Jul 94

In a population based retrospective cohort study we studied cancer risk in Danish soldiers deployed to the war in the Balkans. In particular, leukaemia, earlier linked to ammunition enforced with depleted uranium (DU) in other deployed soldiers, was a concern. Military personnel, 13,552 men and 460 women, without known cancer at first deployment to the Balkans, January 1, 1992 to December 31, 2001 were followed through December 2002. We found 96cases of cancer, 84 among men (standardised incidence ratio (SIR) 0.9) and 12 among women (SIR 1.7). Only four male bone cancers (SIR 6.0), with three during the first year of follow-up, exceeded expectations. Earlier reports on increased risk of leukaemia and testis cancer among deployed military personnel to the Balkans are not corroborated by our study. Quick and open communication about potential risks, a health check, a telephone counselling line and careful monitoring, and diminished anxiety all helped contain the 'Balkan syndrome' in Denmark.
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PMID:Depleted uranium and cancer in Danish Balkan veterans deployed 1992-2001. 1685 58

We investigated the risk of second malignancies among 29,511 survivors of germ-cell testicular cancer recorded in 13 cancer registries. Standardized incidence ratios (SIRs) were estimated comparing the observed numbers of second malignancies with the expected numbers obtained from sex-, age-, period- and population-specific incidence rates. Seminomas and nonseminomas, the 2 main histological groups of testicular cancer, were analyzed separately. During a median follow-up period of 8.3 years (0-35 years), we observed 1,811 second tumors, with a corresponding SIR of 1.65 (95% confidence interval (CI): 1.57-1.73). Statistically significant increased risks were found for fifteen cancer types, including SIRs of 2.0 or higher for cancers of the stomach, gallbladder and bile ducts, pancreas, bladder, kidney, thyroid, and for soft-tissue sarcoma, nonmelanoma skin cancer and myeloid leukemia. The SIR for myeloid leukemia was 2.39 (95% CI: 1.41-3.77) after seminomas, and 6.77 (95% CI: 4.14-10.5) after nonseminomas. It increased to 37.9 (95% CI: 18.9-67.8; based on 11 observed cases of leukemia) among nonseminoma patients diagnosed since 1990. SIRs for most solid cancers increased with follow-up duration, whereas they did not change with year of testicular cancer diagnosis. Among subjects diagnosed before 1980, 20 year survivors of seminoma had a cumulative risk of solid cancer of 9.6% (95% CI: 8.7-10.5%) vs. 6.5% expected, whereas 20 years survivors of nonseminoma had a risk of 5.0% (95% CI: 4.2-6.0%) vs. 3.1% expected. In conclusion, survivors of testicular cancers have an increased risk of several second primaries, where the effect of the treatment seems to play a major role.
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PMID:Second malignancies among survivors of germ-cell testicular cancer: a pooled analysis between 13 cancer registries. 1709 41

Offering sperm cryopreservation to preserve the fertility of male cancer patients is a relatively recent service in Asia. This study analyzed the types of cancer, timing of collection, sperm quality, and utilization for reproductive services by patients during a 10-year period at a medical center in Taiwan. A total of 75 oncology patients elected to freeze sperm for fertility preservation at our medical center during the initial 10 years of the availability of this service. The mean age of the patients was 25.7 years. Storage was discontinued in 13 (17%) patients and their survival duration was 13.1 +/- 11.1 months. The utilization rate of sperm cryopreservation was 2.8% (75/2642). The types of cancer varied, with leukemia (35%), lymphoma (25%), and testicular cancer (13%) comprising the largest groups. A significantly lower sperm count was found in patients with chronic myelogenous leukemia, suggesting the need for earlier sperm collection after initiation of cancer treatment. Only three (4%) patients utilized their specimens for reproductive purposes. There was no clinical pregnancy during the study period, although one biochemical pregnancy was achieved. The low rates of sperm cryostorage for fertility preservation in cancer patients in this study suggest that there is a need for greater emphasis of this option for male oncology patients whose fertility is likely to be affected by chemotherapeutic treatment.
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PMID:Initial 10-year experience of sperm cryopreservation services for cancer patients. 1718 46

We studied 5555 seminoma patients and 3733 patients with nonseminomatous testicular cancers diagnosed in Southeast England between 1960 and 2004. For both groups survival improved over time: 10-year relative survival increased from 78% in 1960-1969 to 99% in 1990-2004 for seminomas, and from 55 to 95% for nonseminomas. In the early period mortality was still significantly increased more than 15 years after diagnosis in both groups, whereas in more recent periods the excess deaths mainly occurred in the first 5 years after diagnosis. For seminomas, there was a significant excess of cancers of the colon (standardised incidence ratio (SIR) 2.36; 95% confidence interval (CI) 1.13-4.35), soft tissue (SIR 13.64; CI 1.65-49.28) and bladder (SIR 4.28; CI 2.28-7.31) in the long term (20+ years after diagnosis), of pancreatic cancer in both the medium (10-19 years) (SIR 2.91; CI 1.26-5.73) and long term (SIR 5.48; CI 2.37-10.80), of leukaemia in both the short (0-9 years) (SIR 3.01; CI 1.44-5.54) and long term (SIR 4.48; CI 1.64-9.75), and of testis cancer in both the short (SIR 6.69; CI 4.28-9.95) and medium term (SIR 3.96; CI 1.08-10.14). For nonseminomas, significant excesses were found in the long term for cancers of the stomach (SIR 5.13; CI 1.40-13.13), rectum (SIR 4.49; CI 1.22-11.51) and pancreas (SIR 10.17: CI 3.73-22.13), and for testis cancer in the medium term (SIR 5.94; CI 2.18-12.93). Leukaemia was significantly increased in the short term (SIR 6.78; CI 2.93-13.36). The better survival observed is largely attributable to improved treatment, and the trend in reducing the toxicity of therapy should continue to reduce future health risks in testicular cancer survivors.
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PMID:Mortality and incidence of second cancers following treatment for testicular cancer. 1726 80

The pathogenesis of male infertility can be reflected in alterations of spermatogenesis caused by testicular cancer, aplasia of the germinal cells, varicocele, environmental factors or defect in the transport of the sperms, among others. In general, 48% of men suffer unexplained infertility. During a long time, the masculine reproductive tract and the immune system have been studied as different and independent systems. However, in the last two decades a particular interest has arisen in the interaction of both systems on masculine infertility, in particular in the evaluation of antisperm antibodies as a common cause of infertility. Also, the inflammation due to genital or systemic infections can cause alterations in the testicular function. The recognition of intratesticular antigens provokes the production of antibodies by B lymphocytes. Then, the immune system induces a cellular response, by cytokines secretion, activation of complement and T lymphocytes activation. In this review the components and the immune system response mechanism, the organization of the testicle as a reproductive organ and the mediators of the immunologic response will be examined: interleukin-1 (IL-1), IL-6, leukaemia Inhibitory factor, tumor necrosis factor-alpha, the molecule FasL (CD95L) and Fas (CD95), macrophage migration-inhibitory factor, mononuclear phagocyte colony stimulating factor, Granulocyte/macrophage colony stimulating factor, as well as stem cell factor, interferon, transforming growth factor B and activins.
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PMID:[Immune-testicular regulation and cytokines]. 1743 49

We retrospectively analyzed 163 patients who had been cryopreservating their sperm one year or more. They consisted of 72, 76 and 15 patients with a germ cell tumor, hematologic cancer and other diseases, respectively. Forty-eight patients (29.4%) were still cryoperservating their sperm, and the average period of cryoperservation was 4.7 +/- 3.0 years (1-13.1 years). Only 6 patients (3.7%) had used their cryopreserved sperm and the average preserved period was 6.0 years (1.3-12 years). In 115 of the 163 cases, the cryopreserved sperm was abandoned, and the main reason was the recovery of spermatogenesis. Of the cases that underwent semen analysis after treatment, 20.9% of the patients with testicular cancer and 57.9% of the patients with hematologic cancer, have not recovered spermatogenesis. Because chemotherapy to the testicular tumor and leukemia risk injuring testiclar function, cryopreservation of the sperm before treatment should be recommended. Because the preservation period tends to be prolonged, development of a system for long-time preservation is awaited.
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PMID:[Semen cryopreservation for patients with malignant or non-malignant disease: our 14-year experience]. 1787 44

Etoposide is routinely used in combination-based chemotherapy for testicular cancer and small-cell lung cancer; however, myelosuppression, therapy-related leukemia and neurotoxicity limit its utility. To determine the genetic contribution to cellular sensitivity to etoposide, we evaluated cell growth inhibition in Centre d' Etude du Polymorphisme Humain lymphoblastoid cell lines from 24 multi-generational pedigrees (321 samples) following treatment with 0.02-2.5 microM etoposide for 72 h. Heritability analysis showed that genetic variation contributes significantly to the cytotoxic phenotypes (h (2) = 0.17-0.25, P = 4.9 x 10(-5)-7.3 x 10(-3)). Whole genome linkage scans uncovered 8 regions with peak LOD scores ranging from 1.57 to 2.55, with the most significant signals being found on chromosome 5 (LOD = 2.55) and chromosome 6 (LOD = 2.52). Linkage-directed association was performed on a subset of HapMap samples within the pedigrees to find 22 SNPs significantly associated with etoposide cytotoxicity at one or more treatment concentrations. UVRAG, a DNA repair gene, SEMA5A, SLC7A6 and PRMT7 are implicated from these unbiased studies. Our findings suggest that susceptibility to etoposide-induced cytotoxicity is heritable and using an integrated genomics approach we identified both genomic regions and SNPs associated with the cytotoxic phenotypes.
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PMID:Identification of genomic regions contributing to etoposide-induced cytotoxicity. 1908 52

Despite fertility-preserving initiatives, postcancer reproduction is expected to be lower than that of the general population. Using data from the Cancer Registry and the Medical Birth Registry of Norway, postcancer pregnancy rates were analyzed in 27,556 survivors and compared to those from a matched comparison group ("controls") from the general population. All were born after 1950, diagnosed from 1967 to 2004 at age of 16-45, and had an observation time from the date of diagnosis (assigned date for controls), until pregnancy, death, age 46, or December 31, 2006. Cox regression was used to estimate pregnancy rates, after adjusting for educational level, parity and diagnostic period. Overall, cancer survivors had a lower pregnancy rate than the controls, but the rate for survivors was higher in males than in females [hazard rate (HR)=0.74 (95% confidence interval (CI) 0.71-0.78) and HR=0.61 (95% CI 0.58-0.64), respectively]. However, the rates did not differ between controls and survivors of malignant melanoma or thyroid cancer. By contrast, the lowest HRs for pregnancy occurred in survivors of leukemia, cervical or breast cancer. Increased pregnancy rates during the study period were detected for ovarian cancer [HR=0.2 (95% CI 0.1-0.3) to HR=0.7 (95% CI 0.5-0.9)], testicular cancer [HR=0.6 (95% CI 0.4-0.9) to HR=0.8 (95% CI 0.7-0.8)], and Hodgkin lymphoma diagnosed in men [HR=0.7 (95% CI 0.5-0.9) to HR=0.9 (95% CI 0.7-1.0)]. In summary, fertility-preserving attempts have succeeded in patients with ovarian or testicular cancer and in males with Hodgkin lymphoma. Male survivors initiated pregnancies in a higher degree than female survivors.
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PMID:Pregnancy after adolescent and adult cancer: a population-based matched cohort study. 2138 11


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