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本文引用的文献

1
Short-course adjuvant chemotherapy in high-risk stage I nonseminomatous germ cell tumors of the testis: a Medical Research Council report.
J Clin Oncol. 1996 Apr;14(4):1106-13. doi: 10.1200/JCO.1996.14.4.1106.
2
Expression of stem-cell factor and its receptor c-kit protein in normal testicular tissue and malignant germ-cell tumours.干细胞因子及其受体c-kit蛋白在正常睾丸组织和恶性生殖细胞肿瘤中的表达
J Cancer Res Clin Oncol. 1996;122(5):301-6. doi: 10.1007/BF01261407.
3
Tumor proliferative activity is predictive of pathological stage in clinical stage A nonseminomatous testicular germ cell tumors.
J Urol. 1996 Feb;155(2):579-86.
4
Flow cytometric and quantitative histological parameters to predict occult disease in clinical stage I nonseminomatous testicular germ cell tumors.用于预测临床I期非精原细胞瘤性睾丸生殖细胞肿瘤隐匿性疾病的流式细胞术和定量组织学参数。
J Urol. 1993 Sep;150(3):879-83. doi: 10.1016/s0022-5347(17)35638-0.
5
Primary retroperitoneal lymph node dissection in clinical stage A non-seminomatous germ cell testis cancer. Review of the Indiana University experience 1965-1989.
Br J Urol. 1993 Mar;71(3):326-35. doi: 10.1111/j.1464-410x.1993.tb15952.x.
6
Retroperitoneal lymphadenectomy for clinical stage A testis cancer (1965 to 1989): modifications of technique and impact on ejaculation.1965年至1989年临床分期为A期睾丸癌的腹膜后淋巴结清扫术:技术改进及其对射精功能的影响
J Urol. 1993 Feb;149(2):237-43. doi: 10.1016/s0022-5347(17)36046-9.
7
Mutations of the p53 gene do not occur in testis cancer.睾丸癌中不会发生p53基因的突变。
Cancer Res. 1993 Aug 1;53(15):3574-8.
8
Percentage of embryonal carcinoma and of vascular invasion predicts pathological stage in clinical stage I nonseminomatous testicular cancer.
Cancer Res. 1994 Jan 15;54(2):362-4.
9
Mutations of the p53 gene are not detectable in human testicular tumors.
Mod Pathol. 1994 May;7(4):435-9.
10
Immunohistochemical expression of P53 tumor suppressor gene protein in adult germ cell testis tumors: clinical correlation in stage I disease.P53肿瘤抑制基因蛋白在成人睾丸生殖细胞肿瘤中的免疫组化表达:I期疾病的临床相关性
J Urol. 1994 Aug;152(2 Pt 1):418-23. doi: 10.1016/s0022-5347(17)32753-2.

临床I期睾丸癌的治疗及新生物预后参数的可能作用。

Treatment of clinical stage I testicular cancer and a possible role for new biological prognostic parameters.

作者信息

Bokemeyer C, Kuczyk M A, Serth J, Hartmann J T, Schmoll H J, Jonas U, Kanz L

机构信息

Department of Internal Medicine II, Eberhard-Karls-University Tübingen, Germany.

出版信息

J Cancer Res Clin Oncol. 1996;122(10):575-84. doi: 10.1007/BF01221188.

DOI:10.1007/BF01221188
PMID:8879254
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12201354/
Abstract

Three different treatment strategies for patients with stage I non-seminomatous testicular cancer are available that will all result in long-term survival in more than 98% of the patients: a "wait and see" strategy with follow-up and chemotherapy in cases of tumour progression, retroperitoneal lymphadenectomy, with or without application of systemic chemotherapy, in cases of retroperitoneal metastases (pathological stage II disease) or primary adjuvant chemotherapy following inguinal orchiectomy. Each treatment strategy is associated with specific side-effects. In several studies histological characteristics of the primary tumour, particularly the presence of vascular invasion and of embryonal carcinoma cells, have been demonstrated to be significant prognostic factors for the risk of occult retroperitoneal metastases in patients with stage I disease. In addition, new biological prognostic factors determined by flow cytometry, cytogenetic analysis or molecular-biological DNA or RNA analysis have been investigated, among which alterations of the p53 tumour-suppressor gene may represent a promising new prognostic factor. Although alterations of p53 gene expression seem to be associated with advanced tumour stage and may predict retroperitoneal metastatic disease, the independent role of these molecular genetic alterations needs to be prospectively studied. Currently a risk-adapted treatment strategy based on the histological criteria of vascular invasion and the presence of embryonal carcinoma can be used to stratify patients into a "high-" and "low-risk" group with respect to tumour progression. While primary-nerve-sparing retroperitoneal lymphadenectomy or adjuvant chemotherapy with two cycles of platinum, etoposide and bleomycin may be appropriate for patients with a high risk (above 40%) for tumour progression, a "wait-and-see" strategy can be used for "low-risk" (less than 15% risk of progression) patients. Molecular investigations of prognostic factors may be able to improve further the stratification of patients into these different risk categories.

摘要

对于I期非精原细胞瘤性睾丸癌患者,有三种不同的治疗策略,所有这些策略都能使超过98%的患者长期存活:一种“观察等待”策略,即肿瘤进展时进行随访和化疗;对于腹膜后转移(病理II期疾病)的患者,进行腹膜后淋巴结清扫术,可应用或不应用全身化疗;或者在腹股沟睾丸切除术后进行原发性辅助化疗。每种治疗策略都伴有特定的副作用。在多项研究中,已证明原发性肿瘤的组织学特征,尤其是血管侵犯和胚胎癌细胞的存在,是I期疾病患者隐匿性腹膜后转移风险的重要预后因素。此外,还研究了通过流式细胞术、细胞遗传学分析或分子生物学DNA或RNA分析确定的新的生物学预后因素,其中p53肿瘤抑制基因的改变可能是一个有前景的新预后因素。虽然p53基因表达的改变似乎与肿瘤晚期相关,并且可能预测腹膜后转移疾病,但这些分子遗传改变的独立作用需要进行前瞻性研究。目前,基于血管侵犯的组织学标准和胚胎癌的存在的风险适应性治疗策略,可用于将患者按肿瘤进展情况分为“高风险”和“低风险”组。对于肿瘤进展风险高(超过40%)的患者,保留神经的原发性腹膜后淋巴结清扫术或两周期铂类、依托泊苷和博来霉素的辅助化疗可能是合适的,而对于“低风险”(进展风险低于15%)患者,可采用“观察等待”策略。对预后因素的分子研究可能能够进一步改善将患者分为这些不同风险类别的分层。