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排序方式: 共有1593条查询结果,搜索用时 15 毫秒
81.
82.
83.
Shen H Liu Z Strom SS Spitz MR Lee JE Gershenwald JE Ross MI Mansfield PF Duvic M Ananthaswamy HN Wei Q 《The Journal of investigative dermatology》2003,121(6):1510-1514
The p53 gene plays an important role in cell cycle control, facilitating DNA repair activities in response to DNA damage. Aberrant cell cycle control impairs DNA repair and increases the probability of mutations that can lead to carcinogenesis. The p53 gene is polymorphic at codon 72 (Arg/Pro) of its protein, which is functionally distinct, leading to inquiry into its role in carcinogenesis. In this hospital-based case-control study of 289 newly diagnosed patients with melanoma and 308 cancer-free control subjects, we evaluated whether the p53 codon 72 variant is associated with risk of cutaneous melanoma (CM). The controls were frequency-matched to the cases by age, sex, and ethnicity. The frequency of the p53 Arg allele was 78.2% in cases and 73.2% in controls (p=0.045), and the genotype frequencies of p53 Arg/Arg, Arg/Pro, and Pro/Pro were 62.6%, 31.1%, and 6.3%, respectively, in the cases, and 53.9%, 38.6%, and 7.5%, respectively, in the controls (p=0.096). Logistic regression analysis revealed that the p53 Arg/Arg genotype was associated with a significantly increased risk of melanoma (adjusted odds ratio (OR)=1.43; 95% confidence interval (CI)=1.02-2.02) compared with other genotypes, and this association was more evident in subgroups of older subjects (OR=2.32; 95% CI=1.39-388), and subjects with Fitzpatrick's skin type III or IV (OR=1.69; 95% CI=1.11-2.59). In conclusion, this study found some evidence that in subjects over 50, p53 Arg/Arg genotype is associated with increased risk of CM as compared to genotypes Arg/Pro or Pro/Pro. Further larger studies are needed to substantiate our findings. 相似文献
84.
The complement dependent cytotoxicity (CDC) immune effector mechanism contributes to anti-CD154 induced immunosuppression 总被引:4,自引:0,他引:4
BACKGROUND: In many situations, anti-CD154 (CD40 ligand) monoclonal antibody (mAb) treatment is very potent in producing allograft tolerance. In accordance to our previously reported results, combined donor specific transfusion (DST)3 plus anti-CD154 mAb (MR1) treatment enables the permanent engraftment of DBA/2 (H-2(d)) islets into B6AF1 (H-2(b/kd)) recipients in all cases. It has been widely assumed that the MR1 anti-154 is a noncytolytic neutralizing mAb, and it exerts immune suppressive effects by blockade of CD40/CD154 signal pathway. In this study, we sought to test the role of complement dependent cytotoxicity (CDC) immune effector mechanism in MR1 anti-CD154 induced immunosuppression. METHODS: We have evaluated the contributions of CDC in the context of the potent tolerizing effects of DST plus anti-CD154 mAb treatment regiment in recipients of islet allografts. We have used CD40 knockout (KO) mice and complement C5 deficient mice DBA/2 as islet allograft recipients as well as cobra venom factor (CVF), a complement blocker, treatment. RESULTS: The absence of direct and indirect CD40/CD154 pathway signals does not prevent islet allograft acute rejection. Interestingly, MR1 anti-CD154 induces islet allograft tolerance in the absence of CD40/CD154 pathway. In a wild-type major histocompatibility complex (MHC) mismatched strain combination, DST results in accelerated islet allograft rejection. Combination of DST and MR1 anti-CD154 treatment prevents presensitization and permits permanent engraftment. However, administration of CVF abolishes the tolerance induction. Moreover, DST plus MR1 anti-CD154 regiment, a potent tolerizing therapy, does not prevent acute islet allograft rejection when complement C5 deficient DBA/2 mice are used as recipients. Thus, the mechanisms of the tolerizing effects by MR1 anti-CD154 are not limited to blockade of CD40/CD154 signals. The CDC immune effector mechanism contributes to MR1 anti-CD154 induced immunosuppression. 相似文献
85.
Zhu Y Spitz MR Strom S Tomlinson GE Amos CI Minna JD Wu X 《International journal of cancer. Journal international du cancer》2002,102(5):536-540
Cytogenetic aberrations on chromosome 9 have been reported to be one of the most frequent genetic changes in lung tumorigenesis. Although many of these changes have been detected in lung carcinoma specimens, there is growing evidence showing the concordance between chromosomal alterations in primary lung tumors and peripheral blood lymphocytes (PBLs). We investigated whether spontaneous aberrations on chromosome 9 in PBLs are associated with the presence of lung cancer and with a family history of cancer. A personal interview, to construct a detailed epidemiologic profile including family history of cancer, was conducted on 174 lung cancer cases and 162 matched controls. One hundred metaphases from PBLs of each subject were analyzed for chromosome 9 aberrations using the whole chromosome painting technique. Overall, the mean proportion of individuals with chromosome 9 abnormalities in their PBLs was significantly higher in cases (96.0%) than in controls (60.5%) (p < 0.05). After adjustment by age, gender, ethnicity, family size, and pack-years, there was a 16.63-fold significantly elevated odds ratio (OR) for lung cancer associated with chromosome 9 aberrations. When subjects were categorized by frequencies of the chromosome 9 lesions, we observed significantly increased odds ratios of 11.13 (4.66, 26.58) and 27.45 (11.15, 67.54) for individuals with 1 chromosome 9 aberration and >/=2 chromosome 9 aberrations, respectively. By performing family history analyses, we further observed that control individuals with chromosome 9 aberrations were more likely to report a family history of any cancer (OR = 1.67 [0.84, 3.32]) and lung cancer (OR = 2.49 [0.81, 7.67]). Our findings suggest that chromosome 9 aberrations in PBLs might be considered a marker of lung cancer predisposition and may be associated with familial aggregation of cancer. 相似文献
86.
Breast IMRT: new tools leading to new vision 总被引:2,自引:0,他引:2
Strom EA 《International journal of radiation oncology, biology, physics》2002,54(5):116-1298
87.
Predictors of locoregional recurrence among patients with early-stage breast cancer treated with breast-conserving therapy 总被引:15,自引:2,他引:13
Mirza NQ Vlastos G Meric F Buchholz TA Esnaola N Singletary SE Kuerer HM Newman LA Ames FC Ross MI Feig BW Pollock RE McNeese M Strom E Hunt KK 《Annals of surgical oncology》2002,9(3):256-265
Background Our aim was to identify predictors of locoregional recurrence (LRR) in patients with early-stage breast cancer treated with
breast-conserving therapy (BCT) and long-term follow-up.
Methods From 1970 to 1994, 1153 patients with stage I to II breast cancer underwent BCT and radiotherapy at our institution. Patients
with prior breast cancer or other primary malignancies were excluded. Clinical and pathologic characteristics evaluated were
age, race, tumor size, stage, pathologic tumor margins, axillary nodal involvement, estrogen and progesterone receptor status,
Black's nuclear grade, type of surgery, and use of adjuvant therapy.
Results Of 1083 patients, 54% presented with stage I disease and 46% with stage II disease. Median age was 50 years, and median follow-up
was 9 years. Axillary nodes were positive in 31% of the patients who underwent axillary dissection. LRR developed in 6%, LRR
followed by systemic recurrence in 5%, and systemic recurrence alone in 13%, 76% had no evidence of recurrence at last follow-up.
Age, tumor size, positive lymph nodes, and not receiving chemotherapy or hormonal therapy were independent predictors of LRR.
Disease-specific survival among patients with LRR was similar to that among patients with no recurrence.
Conclusions Multidisciplinary treatment strategies should be used to accomplish durable locoregional control after BCT.
Presented at the 54th Annual Cancer Symposium of the Society of Surgical Oncology, Washington, DC, March 15–18, 2001. 相似文献
88.
Long-term complications associated with breast-conservation surgery and radiotherapy 总被引:5,自引:0,他引:5
Meric F Buchholz TA Mirza NQ Vlastos G Ames FC Ross MI Pollock RE Singletary SE Feig BW Kuerer HM Newman LA Perkins GH Strom EA McNeese MD Hortobagyi GN Hunt KK 《Annals of surgical oncology》2002,9(6):543-549
Background Breast-conservation surgery plus radiotherapy has become the standard of care for early-stage breast cancer; we evaluated
its long-term complications.
Methods We selected patients treated with surgery and radiotherapy between January 1990 and December 1992 (an era in which standard
radiation dosages were used) with follow-up for at least 1 year. Patients were prospectively monitored for treatment-related
complications. Median follow-up time was 89 months.
Results A total of 294 patients met the selection criteria. Grade 2 or higher late complications were identified in 29 patients and
included arm edema in 13 patients, breast skin fibrosis in 12, decreased range of motion in 4, pneumonitis in 2, neuropathy
in 2, fat necrosis in 1, and rib fracture in 1. Arm edema was more common after lumpectomy plus axillary node dissection than
after lumpectomy alone. Arm edema occurred in 18% of patients who underwent surgery plus irradiation of the lymph nodes and
10% who underwent surgery without nodal irradiation.
Conclusions Breast-conservation surgery plus radiotherapy was associated with grade 2 or higher complications in only 9.9% of patients.
Half of these complications were attributable to axillary dissection, it is hoped that lower complication rates can be achieved
with sentinel lymph node biopsy. 相似文献
89.
90.
Polymorphisms in the DNA repair genes XPC, XPD, and XPG and risk of cutaneous melanoma: a case-control analysis. 总被引:2,自引:0,他引:2
Chunying Li Zhibin Hu Zhensheng Liu Li-E Wang Sara S Strom Jeffrey E Gershenwald Jeffrey E Lee Merrick I Ross Paul F Mansfield Janice N Cormier Victor G Prieto Madeleine Duvic Elizabeth A Grimm Qingyi Wei 《Cancer epidemiology, biomarkers & prevention》2006,15(12):2526-2532
Sunlight causes DNA damage, including bulky lesions that are removed effectively by the nucleotide-excision repair (NER) pathway. There are at least eight core NER proteins participating in the pathway, and genetic variations in their genes may alter NER functions. We hypothesized that some NER variants are associated with risk of cutaneous melanoma. In a hospital-based case-control study of 602 non-Hispanic White patients with cutaneous melanoma and 603 age- and sex-matched cancer-free controls, we genotyped five common non-synonymous single-nucleotide polymorphisms identified to date and assessed their associations with risk of cutaneous melanoma. We found that a significantly increased risk of cutaneous melanoma was associated with XPD 751Lys/Gln [adjusted odds ratio (OR), 1.55 and 95% confidence interval (95% CI), 1.12-2.16] and XPD 751Gln/Gln (OR, 1.66; 95% CI, 1.03-2.68) genotypes compared with the XPD 751Lys/Lys genotype as well as XPD312Asp/Asn (OR, 1.54; 95% CI, 1.11-2.12) and XPD312Asn/Asn (OR, 1.75; 95% CI, 1.05-2.90) genotypes compared with the XPD 312Asp/Asp genotype. This increased risk was not observed in the other three XPC and XPG single-nucleotide polymorphisms. Moreover, the number of the observed XPD at-risk genotypes (i.e., 312Asn/Asn+Asn/Asp and 751Gln/Gln+Lys/Gln) was associated with cutaneous melanoma risk in a dose-response manner (OR, 1.47; 95% CI, 0.97-2.23 for one at-risk genotype; OR, 1.83; 95% CI, 1.29-2.61 for two at-risk genotypes; P(trend) < 0.001). However, we found no evidence of any interaction between XPD genotypes with XPC and XPG genotypes or the known risk factors. We concluded that genetic variants of the XPD gene might serve as biomarkers for susceptibility to cutaneous melanoma. 相似文献