Predictive Models in External Beam Radiotherapy for Clinically Localized Prostate Cancer

被引:49
作者
Roach, Mack, III [1 ,2 ]
Waldman, Fred [3 ]
Pollack, Alan [4 ]
机构
[1] Univ Calif San Francisco, Helen Diller Family Comprehens Canc Ctr, Dept Radiat Oncol, San Francisco, CA 94143 USA
[2] Univ Calif San Francisco, Dept Urol, San Francisco, CA 94143 USA
[3] Univ Calif San Francisco, Dept Lab Med, San Francisco, CA 94143 USA
[4] Univ Miami, Dept Radiat Oncol, Sylvester Comprehens Canc Ctr, Miami, FL USA
关键词
prostate cancer; radiotherapy; randomized trials; predictive models; LYMPH-NODE INVASION; LONG-TERM SURVIVAL; RADIATION-THERAPY; RADICAL PROSTATECTOMY; ANDROGEN DEPRIVATION; DISTANT METASTASIS; HORMONAL-THERAPY; PELVIC LYMPHADENECTOMY; PRETREATMENT NOMOGRAM; BIOCHEMICAL FAILURE;
D O I
10.1002/cncr.24348
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Predictive models are being used increasingly in effort to allow physician and patient expectations to be aligned with outcomes that are based on available data. Most predictive models for men who receive external beam radiotherapy for clinically localized prostate cancer are based on Gleason score, clinical tumor classification, and prostate-specific antigen (PSA) levels. More sophisticated models also have been developed that incorporate treatment-related variables, such as the dose of radiation and the use of androgen-deprivation therapy. Most of the predictive models applied to prostate cancer were derived using PSA recurrence rates as the major endpoint, but clinical endpoints have been incorporated increasingly into predictive models. Biomarkers also are increasingly being added to predictive models in an effort to strengthen them. The Radiation Therapy Oncology Group (RTOG) has completed studies on a wide range of markers using tissue from 2 phase 3 trials (RTOG 8610 and 9202). To date, preliminary assessments of p53; DNA ploidy; p16/retinoblastoma 1 protein; Ki-67; mouse double-minute p53 binding protein homolog; Bcl-2/Bcl-2-associated X protein; cytosine, adenine, and guanine repeats; cyclooxygenase-2; signal transducer and activator of transcription 3; cytochrome P450 3A4; and protein kinase A have been completed. Although they are not ready for widespread, routine use, there are reasons to believe that future models will combine these markers with traditional pretreatment and treatment-related variables and will improve our ability to predict outcome and select the optimal treatment. Cancer 2009;115(13 suppl):3112-20. (C) 2009 American Cancer Society.
引用
收藏
页码:3112 / 3120
页数:9
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