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Specific Death (specific + death)
Selected AbstractsMismatch repair expression in testicular cancer predicts recurrence and survivalINTERNATIONAL JOURNAL OF CANCER, Issue 8 2008Alfredo Velasco Abstract We investigated mismatch repair (MMR) gene expression in testicular cancer as a molecular marker for clinical outcome (recurrence, response to chemotherapy and death) using protein expression and specific genetic alterations associated with the presence or absence of MMR activity. One hundred sixty-two cases of paraffin-embedded testis cancer specimens were subjected to immunohistochemical analysis using monoclonal antibody for MLH1 and MSH2 MMR proteins and genetic analysis using specific polymorphic markers. The degree of MMR immunoreactivity and genetic instability in the form of loss of heterozygosity (LOH) and/or microsatellite instability (MSI) were determined by comparing matched normal and tumor tissue. The degree of immunohistochemical staining for MMR expression was associated with a shorter time to tumor recurrence, resistance to chemotherapy and death. Furthermore, clinical relapse and cancer specific death was also associated with tumors exhibiting a high degree of MSI, p = 0.01 and 0.04, respectively. In contrast, LOH was not associated with recurrence, resistance to chemotherapy or death. Therefore, MMR expression defines testis cancers with distinct molecular properties and clinical behavior, such that tumors with decreased MMR immunostaining and/or increased frequency of MSI have a shorter time to recurrence and death despite chemotherapy. © 2007 Wiley-Liss, Inc. [source] Genetic and plasma variation of insulin-like growth factor binding proteins in relation to prostate cancer incidence and survivalTHE PROSTATE, Issue 12 2009Mattias Johansson Abstract BACKGROUND Binding proteins regulate bioavailability of insulin-like growth factor-I (IGF-I) in the circulation and affect apoptosis of tumor cells in the prostate. We analyzed genetic variation within genes coding for IGF binding proteins in relation to prostate cancer incidence and survival. We also investigated if circulating IGFBP3 affects prostate cancer-specific survival. MATERIALS AND METHODS Eleven haplotype tagging SNPs and two single SNPs in the IGFBP1, IGFBP3, and IGFALS genes were genotyped within the CAncer Prostate in Sweden (CAPS) study including 2,774 cases and 1,736 controls. Plasma samples for analyses of total- and intact IGFBP3 levels were available for 1,521 cases and 909 controls. Complete follow-up of vital status was achieved by linkage to the Swedish Cause of Death Register. RESULTS We found no clear association between the genetic variants and prostate cancer incidence or survival. The rare allele of the IGFBP3 SNP rs2854744 was associated with elevated plasma levels of total IGFBP3 (Ptrend,=,9,×,10,8), but not intact IGFBP3 (Ptrend,=,0.16). Elevated levels of total- (Ptrend,=,0.03) and intact IGFBP3 (Ptrend,=,6,×,10,14) were associated with increased risk of prostate cancer specific death. Treatment and tumor characteristics accounted for the association with total IGFBP3, whereas the association with intact IGFBP3 was attenuated, but still statistically significant in adjusted analysis (Ptrend-adjusted,=,0.0004). Elevated intact IGFBP3 was also significantly associated with increased risk of prostate cancer-specific death among patients who were chemically or surgically castrated (Ptrend-adjusted,=,0.0003), and among patients who had not been treated (Ptrend-adjusted,=,0.02). CONCLUSIONS Circulating levels of intact IGFBP3 measured after diagnosis is associated with increased risk of prostate cancer-specific death. Prostate 69:1281,1291, 2009. © 2009 Wiley-Liss, Inc. [source] Advanced age at diagnosis is an independent predictor of time to death from prostate carcinoma for patients undergoing external beam radiation therapy for clinically localized prostate carcinomaCANCER, Issue 1 2003Anthony V. D'Amico M.D., Ph.D. Abstract BACKGROUND Whether age at diagnosis is predictive of time to prostate carcinoma specific death after external beam radiation therapy (RT) for patients who are diagnosed with clinically localized prostate carcinoma during the prostate specific antigen (PSA) era has not been investigated previously. METHODS A multivariate Cox regression analysis was used to evaluate the ability of pretreatment risk group and age at diagnosis to predict time to all causes of death and time to death from prostate carcinoma for 381 patients who underwent RT for clinically localized prostate carcinoma. RESULTS Age at diagnosis, as a continuous variable (Pcontinuous = 0.04), and risk group (Pcategorical = 0.02) were independent predictors of time to death from prostate carcinoma, whereas only age at diagnosis (Pcontinuous = 0.01) was a predictor of time to all causes of death. When analyzed as a categorical variable, beginning at age 73 years, age at diagnosis was an independent predictor (Pcategorical < 0.04) of time to death from prostate carcinoma. Upon further analysis, this finding was limited to high-risk patients. For example, age , 75 years at diagnosis predicted for a shorter median time to death from prostate carcinoma (6.3 years vs. 9.7 years; P = 0.002) in high-risk patients. CONCLUSIONS Patients with clinically localized, high-risk prostate carcinoma who were diagnosed at age , 73 years and were treated with RT had a worse prognosis compared with patients who were diagnosed age < 73 years, raising the possibility that a more aggressive prostate carcinoma biology may develop during andropause. Cancer 2003;97:56,62. © 2003 American Cancer Society. DOI 10.1002/cncr.11053 [source] Long-term outcome of patients with insular carcinoma of the thyroidCANCER, Issue 10 2002The insular histotype is an independent predictor of poor prognosis Abstract BACKGROUND Insular thyroid carcinoma was described originally as a tumor with aggressive behavior. However, whether a predominant insular component is an independent factor for poor prognosis is unclear. METHODS The authors compared the clinical behavior of tumors in three groups of patients with thyroid carcinoma,13 patients with insular thyroid carcinoma, 18 patients with follicular thyroid carcinoma, and 26 patients with papillary thyroid carcinoma,who were selected based on similar tumor size and similar age. Disease free survival and disease specific deaths were assessed in the three groups with a Kaplan,Meier analysis and were compared using the log-rank test. Cox regression analysis was used to evaluate the influence of histotype and other prognostic factors on the occurrence of distant metastases and disease specific death. RESULTS Patient follow-up ranged from 5.2 months to 190.0 months. At last follow-up, only 1 of 13 patients (7.7%) with insular carcinoma, compared with 8 of 18 patients (44.4%) with follicular carcinoma and 12 of 26 patients (46.1%) with papillary carcinoma, were disease free. The disease specific death rate was 61.5% among patients in the insular carcinoma group compared with 16.7% and 15.4% among patients in the follicular carcinoma group (P = 0.006) and the papillary carcinoma group (P = 0.025), respectively. At multivariate analysis, the insular histotype was the only variable that was related independently to disease specific death (hazard ratio = 4.27; P = 0.005). Distant metastases occurred in 84.6% of patients in the insular carcinoma group compared with 50% and 19.2% of patients in the follicular carcinoma group (P = 0.039) and the papillary carcinoma group (P = 0.0003), respectively. All metastases from patients with insular carcinomas (n = 11 patients) showed radioiodine uptake, but a clinical benefit from this treatment was observed only in 1 patient. CONCLUSIONS Patients with insular thyroid carcinoma have a poorer outcome compared with patients of similar age who have differentiated types of thyroid carcinoma with tumors of a similar size. Because radioiodine rarely is effective in the treatment of patients with metastatic insular thyroid carcinoma, novel and possible multimodal therapies should be explored for the treatment of patients with these aggressive tumors. Cancer 2002;95:2076,85. © 2002 American Cancer Society. DOI 10.1002/cncr.10947 [source] | ||||||||||