放射治疗睾丸恶性肿瘤

睾丸恶性肿瘤是种较为罕见的疾病,约占男性所有肿瘤的1%,发病率少于3/10万,大部分患者是年轻人。几乎90%的睾丸肿瘤属恶性。临床上分为精原细胞瘤和非精原细胞瘤。由狄克逊等建议的,莫斯托菲等修改的组织学分类法最近被世界卫生组织采用。该分类法的组织学标准如下。 A.以单一细胞形式出现的肿瘤 1.精原细胞瘤 2.胚胎瘤 3.绒毛膜瘤 4.畸胎瘤 B.以多种细胞形式出现的肿瘤 1.胚胎瘤和畸胎瘤 2.胚胎瘤和精原细胞瘤3.精原细胞瘤和畸胎瘤 4.其它复合瘤 [病例]1966～75年放射研究所治疗的88名恶性睾丸肿瘤患者,按组织学分类,49例为纯精原细胞瘤,34例为非精原细胞瘤。63例(76%)首发症状为睾     

18例睾丸恶性畸胎肿瘤综合治疗分析

睾丸恶性肿瘤占全部男性恶性肿瘤的1～2％,而生殖细胞肿瘤包括精原细胞瘤,胚胎癌,畸胎瘤及绒癌等占90％以上,其中畸胎瘤约占10.7％左右。胚胎癌和畸胎瘤多发生于20～30岁。临床上仍使用Boden和Gibbs分期法。近20年来由于放疗和化疗的迅速发展,对睾丸肿瘤的分期和综合治疗有了比较统一的认识,疗效亦明显提高。现将我们治疗并随访的18例睾丸恶性畸胎肿瘤报道如下: 临床资料 本组年龄20～48岁,平均34岁。右侧10例左侧8例;双侧隐睾、单侧隐睾及游动睾丸各1例;2例有外伤史。18例中单纯恶性畸胎瘤12例,恶性畸胎瘤合并精原细胞瘤2例,恶性畸胎瘤并发胚胎癌及畸胎瘤并     

睾丸生殖细胞肿瘤53例临床病理分析

本文分析了我院1962～1988年间经病理确诊的睾丸生殖细胞肿瘤53例,其中精原细胞瘤36例(占67.9%),胚胎癌3例(5.7%)、卵黄囊瘤5例(9.4%)、畸胎瘤4例(7.5%)、混合癌5例(9.4%)。53例睾丸肿瘤与隐睾有关者17例(32.0%)。     

睾丸肿瘤与肿瘤样病变的CT/MRI诊断

目的:探讨睾丸肿瘤与肿瘤样病变CT/MRI诊断与鉴别诊断特征,提高术前定性诊断的准确率.方法: 睾丸肿瘤与肿瘤样病变20例,所有患者均行CT或MRI检查;并最终经病理学证实.17例患者行CT检查,层厚3mm,层距3mm.MRI检查者为17例,采用T1WI、T2WI、T2WI脂肪抑制等序列扫描.结果: 20例均为单侧发病-左侧11例,右侧9例;其中精原细胞瘤14例,良性肿瘤或肿瘤样病变6例:包括成熟型囊性畸胎瘤3例、腺瘤样瘤2例、纤维性假瘤1例,这3种良性病变在密度或信号、是否合并钙化及病灶大小等方面均有不同于精原细胞瘤的影像学表现.结论: 睾丸肿瘤与肿瘤样病变的大小、密度、边缘、强化程度等情况,病灶内是否合并钙化及钙化的形态,对判断病变的良恶性有一定帮助.     

睾丸精原细胞瘤的放射治疗——附119例临床分析

睾丸肿瘤是泌尿系统中常见的恶性肿瘤之一,其中生殖细胞瘤约占所有睾丸肿瘤的95％以上,非生殖细胞瘤占3～5％,生殖细胞瘤有四种基本组织类型:精原细胞瘤、胚胎瘤、畸胎瘤和绒毛膜癌。单纯一种细胞类型占睾丸肿瘤的60％,一种以上细胞类型占40％。     

成人睾丸畸胎瘤的临床分析

目的提高成人睾丸畸胎瘤的诊治水平.方法回顾了1 6例成人睾丸畸胎瘤患者的临床、病理及治疗资料.结果9例患者为成熟畸胎瘤,7例患者为未成熟畸胎瘤.11例就诊时为Ⅰ期肿瘤的患者中,有2例术后发生转移,5例患者就诊时已发生转移,转移率为43%.转移均发生在腹膜后淋巴结,转移灶病理:6例为畸胎瘤,1例为畸胎瘤合并卵黄囊瘤.结论成人睾丸畸胎瘤可发生转移,转移灶中可有其他非精原细胞瘤成分,Ⅰ期肿瘤转移率较低,但其治疗原则应与非精原细胞瘤一致.     

放射治疗恶性纵隔胚胎癌1例报告

1临床病例患者,男,5岁,2005年因右胸部隐痛不适1月余,行胸部CT检查提示:右侧前及中纵隔见类圆形边缘清楚之实行包块,其密度欠均匀,可见点状钙化灶,肿块压迫上腔静脉,考虑右侧纵隔肿瘤,穿刺活检并免疫组化证实为恶性纵隔胚胎癌(图1,2,3)。于2005年6月10日至2005年7月11日行直线加速器立体定向放疗;纵隔病灶6MV-X线照射,DT2.5Gy/次,治疗3次,患者反应不重,将放疗剂量改为DT3.5 Gy/次,照射3次后,行胸部透视检查,提示肿块明显缩小,重新定位修改计划DT3.5 Gy/次,照射7次,靶区总剂量DT42.5Gy/10f/32d。治疗过程顺利,患者无不适反应。治疗后1个月复查CT,肿块明显缩小(图4)。2007年3月,患者治疗后20个月复查CT提示:肿块几乎消失(图5)。2讨论纵隔生殖细胞肿瘤多位于前上纵隔,后纵隔少见。本例位于前纵隔,与文献报道相符。恶性纵隔生殖细胞肿瘤基本分为二大类,纵隔精原细胞瘤及非精原细胞瘤。非精原细胞瘤分为成熟型畸胎瘤、胚胎癌、畸胎癌、绒毛膜癌、卵黄囊瘤、混合瘤等[1]。纵隔生殖细胞肿瘤占所有纵隔肿瘤的1%-4%,占纵隔恶性肿瘤的5%-13%[2]。纵隔非精原细...     

27例睾丸混合性生殖细胞肿瘤临床病理分析

目的:探讨分析睾丸混合性生殖细胞肿瘤（MGCT）的临床病理特征、诊断及鉴别诊断、治疗及预后。方法:回顾性分析我院27例MGCT患者临床病理资料,并结合相关文献进行讨论。结果:MGCT占我院同一时期睾丸生殖细胞肿瘤的33.3%（27/81）,患者年龄1~44岁,平均年龄25.8岁,MGCT伴随精原细胞瘤成分的平均年龄31.63岁,MGCT不伴随精原细胞瘤成分的平均年龄17.36岁。MGCT伴精原细胞瘤患者年龄大于MGCT不伴精原细胞瘤患者,二者差异有统计学意义(P＜0.05)。全部MGCT病例均发生于单侧,左侧13例,右侧14例,左右侧之比0.93∶1。 睾丸的MGCT可由多种成分构成,其中成分包括精原细胞瘤16例（59.3%）,畸胎瘤20例（74.1%）,胚胎性癌20例（74.1%）,卵黄囊瘤10例（37.0%）,绒毛膜癌5例（18.5%）,其中,胚胎性癌伴有精原细胞瘤14例（51.9%）,是27例MGCT中最常见的成分组合,其次是胚胎性癌伴畸胎瘤13例（48.1%）。27例MGCT中,具有2种混合成分15例（55.6%）,3种混合成分9例（33.3%）,4种和5种混合成分均为1例（3.7%）。结论:睾丸 MGCT非常少见,好发于青壮年男性,不同的肿瘤成分导致其生物学行为、临床治疗和预后不同,因此准确的病理诊断非常必要,免疫组化标记对病理诊断与鉴别诊断具有重要作用。     

小儿睾丸肿瘤

小儿睾丸原发恶性肿瘤是比较罕见的肿瘤,约占日本小儿全部恶性肿瘤的2～7%。一般都发生在二岁以下的幼儿。近年来,由于肿瘤标记物研究的进步,使肿瘤的病理及治疗有所发展。睾丸肿瘤分胚胎细胞性肿瘤及非胚胎细胞性肿瘤两大类,前者占大多数。按Dexon 分类,有精原细胞瘤、胚胎癌、畸胎瘤、绒癌及混合型五种,目前广泛使用的是这个分类。近年来,因为已知卵黄囊产生AFP;能产生AFP的睾丸肿瘤叫作卵黄囊肿瘤,如胚胎癌、恶性畸胎瘤     

睾丸肿瘤,特别是精原细胞瘤的放射治疗

日本群马大学从1961年至1976年底进行放射治疗的睾丸肿瘤60例中,单纯精原细胞瘤42例,非单纯精原细胞瘤18例,其中混合型精原细胞瘤5例,胚胎癌10例、畸胎癌2例,畸胎瘤1例。治疗装置:1969年以前使用钴~(60),以后使用10MeV X线。治疗方法:单纯精原细胞瘤采用睾丸高位切除,并尽可能行开腹探查,以明确有无腹腔淋巴结转移。术后对患侧骨盆、髂动脉、腹主动脉旁淋巴结放疗、剂量为4000拉得/4-5周。可能有腹膜后淋巴结转移者尚需照射纵隔及左锁骨上区,剂量为3000拉得/3-4     

Risk of bilateral testicular germ cell cancer in Denmark: 1960-1984.

The incidence of a second primary testicular germ cell cancer among 2850 (96.6% of eligible) men with a histologically verified first primary germ cell cancer diagnosed in the period 1960-1979 in Denmark was established. Of these 2850 men, 73 (2.6%) developed a contralateral testicular cancer. In five of these patients (0.18%), the tumors were synchronous. The cumulative risk of developing a contralateral cancer 25 years after diagnosis of the first testicular germ cell cancer was 5.2% according to a Kaplan-Meier estimate. It was higher among men with a nonseminoma as the first tumor (8.4%) than among men with a seminoma as the first tumor (3.6%). Of the second tumors, 12% were stage II and 17% were stage III at the time of diagnosis. Based on 24,588 person-years at risk and 68 nonsimultaneously occurring bilateral testicular germ cell cancers, the overall relative risk (RR) of developing a second primary cancer in the contralateral testicle following a first germ cell cancer was found to be 24.8 (95% confidence interval = 19-38). Among men with a nonseminoma, the risk was higher (RR = 27.1) than among men with a seminoma (RR = 22.5). The excess risk was not affected by age at diagnosis, calendar period, or time since diagnosis. Close surveillance by screening for and treatment of carcinoma in situ of the remaining testicle in testicular cancer patients are advised.     

Trends in the incidence of testicular germ cell tumors in the United States

BACKGROUND: Recent reports have suggested that the increasing rates of testicular germ cell tumors in some populations have begun to plateau. This study was conducted to examine whether rates among white men in the United States have begun to stabilize and whether rates among black men in the United States have remained low. METHODS: Testicular germ cell tumor incidence data from in the Surveillance, Epidemiology, and End Results Program were analyzed for the years 1973-1998. Trends were examined separately for seminoma and nonseminoma. Using age-period-cohort analyses with 5-year age intervals and 5-year calendar-period intervals, changes in the slope of the trends in birth-cohort and calendar-period effects were examined. RESULTS: Among white men, rates of seminoma continued to increase, but the rate of increase steadily declined throughout the 26-year time span. Nonseminoma rates among whites increased more slowly during the first three time intervals, then plateaued in the final interval. Rates of both seminoma and nonseminoma in black men fluctuated throughout the first three time intervals. In the final interval, the rates of seminoma increased almost 100%, whereas the rates of nonseminoma increased more modestly. Age-period-cohort modeling of the incidence data in white men found that, whereas the dominant effect was that of birth cohort, there also was a period effect. CONCLUSIONS: Among white men in the United States, the incidence of testicular germ cell tumors varied by histology, with a continuing increase in risk only for seminoma. Among black men in the United States, the surprising increases seen between 1988 and 1998 were likely to be a calendar-period effect.     

C-myc蛋白在睾丸肿瘤中的表达及意义

目的　探讨C myc基因蛋白与睾丸肿瘤生物学行为及预后的关系。方法　采用免疫组化S P法对 38例睾丸肿瘤和 10例正常睾丸组织中C myc蛋白表达进行了定量分析。结果　 31例 (81.6 % )睾丸肿瘤显示阳性反应 ,正常睾丸组织为阴性反应。肿瘤组和正常组组织阳性细胞率分别为 2 4 .99%和 3.2 6 % ,两者相比有非常显著性差异 (P <0 .0 1)。在睾丸肿瘤中C myc蛋白的表达程度与肿瘤病理分级、临床分期无关 (P >0 .0 5 )。C myc表达在精原细胞瘤组及非精原细胞瘤组间无显著性差异 (P >0 .0 5 )。结论　C myc蛋白的异常表达可能在睾丸肿瘤的发生、发展过程中起着促进作用。     

上皮源性腮腺恶性肿瘤的CT征象与病理对照研究

背景与目的:上皮源性腮腺恶性肿瘤种类繁多,CT为腮腺占位的常用影像学检查方法,本研究旨在通过回顾性分析上皮源性恶性肿瘤的CT征象,探讨CT在上皮源性腮腺恶性肿瘤的诊断价值.方法:对经病理确诊的29例上皮源性腮腺恶性肿瘤的CT征象,包括病灶的部位、形态、边界、强化程度、均匀性、邻近组织的浸润、淋巴结转移等进行回顾性分析,并与病理进行对照研究.结果:(1)腮腺低度恶性肿瘤组:共8例,4例为高分化粘液表皮样癌、3例为腺泡细胞癌、1例为上皮-肌上皮癌;3例病灶边缘清楚,3例病灶边缘部分欠清,2例病灶边缘不清;5例病灶形态规则,3例病灶形态不规则;8例病灶均呈明显强化,2例病灶内密度均匀,6例病灶内可见低密度区;所有的病灶均未见侵犯邻近肌群的CT征象,有3例出现淋巴结转移征象.(2)腮腺中高度恶性肿瘤组:共21例,5例为低分化鳞癌、8例为恶性混合瘤、2例为腺癌、1例为淋巴上皮癌、4例为粘液表皮样癌、1例为腺样囊性癌;5例病灶边缘清楚,7例病灶边缘部分欠清,9例病灶边缘不清;10例病灶形态规则,1l例病灶形态不规则;17例病灶呈明显强化,4例恶性混合瘤病灶呈轻度强化;9例病灶内密度均匀,12例病灶内可见低密度区;8例病灶侵犯邻近肌群,8例病灶与腮腺床的脂肪间隙消失,6例出现淋巴结转移征象.结论:上皮源性腮腺恶性肿瘤的CT征象在一定程度上和肿瘤的恶性程度存在相关性,但是,还须结合肿瘤的大小、肿瘤的病理组织学类型才能做出更精确的影像学诊断.     

Risk of germ cell tumors among men with HIV/acquired immunodeficiency syndrome.

BACKGROUND: Men with HIV/acquired immunodeficiency syndrome (AIDS) are reported to be at increased risk for germ cell tumors (GCT), particularly testicular seminoma. We investigated correlates of this association to improve understanding of GCTs. METHODS: Testicular and extratesticular seminoma and nonseminoma cases were found by linking population-based cancer and HIV/AIDS registry data for 268,950 men who developed AIDS in 1980 to 2003. Standardized incidence ratios (SIR) with 95% confidence intervals (95% CI) were used to compare these cases with the number of cases expected in the demographically matched population. RESULTS: Overall, seminoma risk (161 cases: SIR, 1.9; 95% CI, 1.6-2.2) was increased significantly with HIV/AIDS, whereas nonseminoma risk was not (56 cases: SIR, 1.3; 95% CI, 0.96-1.7). Extratesticular GCT risk also was increased (11 cases: SIR, 2.1; 95% CI, 1.1-3.7). Seminoma risk was elevated regardless of age, race, or HIV/AIDS transmission group. It was highest for disseminated disease (SIR, 4.7; 95% CI, 2.9-7.2) and within 9 months of AIDS onset (SIR, 7.6; 95% CI, 5.8-9.6), but it was unrelated to CD4 count and duration of HIV/AIDS. The excess risk of seminoma declined in more recent calendar periods, and it was no longer elevated (SIR, 1.4; 95% CI, 0.9-1.9) in the highly active antiretroviral treatment era. CONCLUSIONS: Men with HIV/AIDS had an increased risk of seminoma, but this risk may have attenuated with improving anti-HIV/AIDS treatments. Although detection bias could partly explain the excess of this cancer, various lines of evidence support a causal relationship. Possible mechanisms underlying this association include impaired tumor immunosurveillance or AIDS-related testicular atrophy.     

Second cancers after testicular cancer diagnosed after 1980 in Sweden

BackgroundTesticular cancer treatment has become standardized in the 1980s involving radiotherapy preferentially for seminoma and chemotherapy for nonseminoma. The late effects of these therapeutic practices have not been properly evaluated because of the relatively short time since their application.Patients and methodsWe conducted a study among 5533 survivors of testicular cancer on the basis of Swedish Family-Cancer Database for which the cancer data were retrieved from the nationwide Cancer Registry. Standardized incidence ratios (SIRs) of second cancer were calculated by comparing with the rates of the first cancers. The follow-up was started in 1980 and carried on through 2006.ResultsA total of 370 second cancers (6.7% of all patients) were recorded, more in seminoma than in nonseminoma patients. Second testicular cancer showed an SIR of 29 after seminoma and an SIR of 13 after nonseminoma. A total of 10 discordant sites were increased after seminoma compared with seven sites after nonseminoma. Gastrointestinal tract cancers occurred mainly after seminoma and bladder cancers (SIR 8.6 when diagnosis before age 30) occurred after nonseminoma.ConclusionsOf the selective affected second tumors, it will be important to confirm the association of bladder cancer with nonseminoma treatment.     

Gene expression profiling in seminoma and nonseminoma.

PURPOSE: Gene expression profiles of seminoma were compared with nonseminoma to get insights into tumorigenesis. MATERIALS AND METHODS: Eleven testicular tumor biopsies (five pure seminoma, six nonseminoma; pT1N0M0 to pT2N2M1) and biopsies from unaffected sites were analyzed once per patient using a macroarray (1,176 genes). On the same patients, six genes were validated using real-time quantitative (RTQ) polymerase chain reaction (PCR). Additionally, in a separate cohort of 19 patients, 24 genes selected from the macroarray were measured using RTQ-PCR. RESULTS: (1) The agreement in gene expression was 94% between the two methods and two different patient cohorts. (2) Two features in gene expression were independent of the tumor entity: Most changes of gene expression occurred in five functional groups like "cell cycle" and "apoptosis." Genes within these groups were almost similarly (> 80%) up- or downregulated. (3) Nonseminoma were characterized by downregulated genes (75%), but in seminoma, upregulated genes (64%) prevailed. Furthermore, 64.4% of those genes that were differentially expressed in both tumor entities were usually upregulated in seminoma but downregulated in nonseminoma. A reverse pattern was found in 24.4% of such genes. Eleven percent of these genes showed a similar up- or downregulation in gene expression in both tumor entities. CONCLUSION: Seminoma in this preliminary study can be differentiated from nonseminoma due to almost opposing gene expression profiles (89% of the significantly differentially expressed genes) and are in line with the histological discrimination of both tumor entities. Underlying mechanisms and implications regarding the origin and tumor progression of both entities are discussed.     

A case-control investigation of immune function gene polymorphisms and risk of testicular germ cell tumors.

There is reason to suspect that testicular germ cell tumor (TGCT) development may be influenced by cytokines, secreted proteins that modulate tumor immune surveillance activity as well as a variety of processes in the testis. To address this hypothesis, we conducted a case-control analysis (508 cases, 608 controls) of 32 putatively functional single-nucleotide polymorphisms (SNP) in 16 immune function genes among non-Hispanic Caucasian participants in the U.S. Servicemen's Testicular Tumor Environmental and Endocrine Determinants Study. The TGFB1 Ex5-73C>T variant was positively associated with TGCT (CT/TT versus CC: odds ratio, 1.73; 95% confidence interval, 1.01-2.95; P(trend) = 0.05); additionally, haplotypes of the assessed TGFB1 SNPs (-509C>T, 327C>T, Ex1-282C>G, and Ex5-73C>T) differed in frequency between cases and controls (all TGCT, P 0.07; seminoma, P 0.04; nonseminoma, P 0.11). We also observed excess frequencies among TGCT cases versus controls of LTA 252G (P(trend) = 0.08) and of the TNF variants -1042C (P(trend) = 0.06), -1036T (P(trend) = 0.07), and -238G (P(trend) = 0.09). Analyses of haplotypes for LTA-TNF SNPs (LTA -91C>A, LTA 252A>G, TNF -863C>A, TNF -857C>T, TNF -308G>A, and -238G>A) were similarly suggestive of an association with TGCT (P = 0.06) and nonseminoma (P = 0.04), but not seminoma (P = 0.21). Polymorphisms in other genes were found to be associated only with seminoma (IL2) or nonseminoma (IFNGR2 and IL10). However, none of the associations remained noteworthy after applying the false discovery rate method to control for multiple testing. In conclusion, our findings suggest that polymorphisms in TGFB1 and LTA/TNF, and possibly other immune function genes, may influence susceptibility to TGCT.     

Testicular cancer.

In testicular cancer epidemiology, the increasing recognition that germinal epithelial atrophy is the final common pathway in the development of this tumor has developed along with reports that elevated follicule-stimulating hormone levels at the time of diagnosis of first tumor correlate with risk of developing a second tumor. There is also evidence from experimental studies that atrophy is a complication of vasectomy, a recently reported risk factor. In the area of new diagnostic approaches, correlation of the rate of rise of tumor markers after orchiectomy in patients with metastases has defined a new risk factor for predicting drug-resistant disease. In the treatment of nonseminoma, it has been reported that use of adjuvant chemotherapy for stage I tumors with two courses of combination chemotherapy produces a relapse rate lower than that seen after surgical staging. For seminoma, chemotherapy results have improved, with nearly 100% of patients cured by combination regimens and 80% cured by single-agent carboplatin. This success is finally leading to questioning of the role of radiotherapy as adjuvant therapy for stage I tumors. A study using two courses of adjuvant carboplatin produced equivalent results and possibly less toxicity.