绝经后子宫内膜癌癌周内膜病理学特征及其与预后的关系

目的：研究绝经后子宫内膜癌癌周内膜的病理学特点及其与预后的关系。方法：根据癌周内膜的组织学表现分为增生型和萎缩型两组，对２０４例子宫内膜癌患者的临床与病理特点和长期随访结果进行回顾性分析。结果：癌周内膜呈增生型的子宫内膜癌患者伴发高血压、肥胖、糖尿病、不孕及子宫内膜增生过长史的机率显著高于癌周内膜呈萎缩型的子宫内膜癌患者（Ｐ＜０．００１）；具有较高恶性程度的非内膜样腺癌（包括透明细胞型腺癌、鳞腺癌、浆液型腺癌）在癌周内膜呈萎缩型组占２７．０％，在增生型组占５．５％（Ｐ＜０．００１）。癌周内膜呈萎缩型者较增生型者呈低分化倾向及深肌层、脉管浸润（Ｐ＜０．００１）；５年生存率，癌周内膜呈增生型子宫内膜癌患者为９６．７％，萎缩型为８６．２％（Ｐ＜０．０１）。结论：子宫内膜癌癌周内膜的病理学特征与预后相关，癌周内膜呈增生型者的预后好于萎缩型。     

子宫乳头状浆液性癌与子宫内膜乳头状腺癌生物学行为的临床分析

目的：分析子宫乳头状浆液性癌及乳头状内膜腺癌的病理形态和生物学行为的特点。方法：对５６例含乳头状结构的子宫内膜癌患者行回顾性分析。其中子宫乳头状浆液性癌１５例，乳头状子宫内膜腺癌４１例。以普通子宫内膜腺癌１６０例作为对照。结果：各组诊断时，晚期病例的比例依次为２６．７％、１４．６％、５．６％（Ｐ＜０．０５）。宫外扩散率依次为５３．３％、２０．８％、１２．１％（Ｐ＜０．０１）。深肌层受侵犯的比例分别为７５．０％、４１．７％、３２．３％（Ｐ＜０．０１）。Ⅰ、Ⅱ期的５年生存率则各为４５．７％、６１．９％、９０．３％（Ｐ＜０．０１）。子宫乳头状浆液性癌以上腹部播散为主，未控率高达４６．２％。子宫内膜乳头状腺癌以盆内扩散为主，复发转移率达３１．０％。结论：乳头状结构的存在是子宫内膜癌的预后不良因素；子宫内膜乳头状腺癌的预后介于乳头状浆液性癌和普通子宫内膜腺癌之间。     

子宫乳头状浆液性癌临床生物学行为

回顾性分析近１０年收治的８０例子宫内膜癌。分Ａ组子宫乳头状浆液性癌８例；Ｂ组子宫内膜乳头状腺癌１０例；Ｃ组普通子宫内膜癌６２例。结果：Ａ组临床Ⅲ、Ⅳ期占５０．０％，远高于其他两组，Ｐ＜０．０１。宫外扩散，各组分别占６２．５％，３０．０％，８．１％，Ａ、Ｂ组显著高于Ｃ组，Ｐ＜０．０１。深肌层浸润依次为６２．５％，３０．０％，１６．１％，Ｐ＜０．０５。结论：ＵＰＳＣ与普通内膜癌的临床生物学行为截然不同。子宫内膜乳头状腺癌介于ＵＰＳＣ和普通子宫内膜癌之间。     

天狼猩红-偏振光法检测子宫内膜异位症中Ⅰ、Ⅲ型胶原

探讨子宫内膜异位症中Ⅰ、Ⅲ型胶原的含量和作用。方法：对子宫内膜异位症（内异症）２０例中的异位内膜组织红色病变期１２例（Ａ组）、黑色病变期８例（Ｂ组）和１１例非子宫内膜异位症患者的在位子宫内膜组织（Ｃ组）用天狼猩红染色,偏振光观察,ｐｈｏｔｏｓｈｏｐ分析,半定量研究Ⅰ、Ⅲ型胶原的含量。结果： Ｉ、Ⅲ型胶原在Ｃ组中含量最低（Ｐ＜０．０５）,Ⅲ型胶原在Ａ组中含量最高（Ｐ＜０．０５）,Ｉ型胶原在Ｂ组中含量最高（Ｐ＜０．０５）。Ｉ、Ⅲ型胶原在增生期和分泌期差异无显著性（Ｐ＞０．０５）。结论：Ⅰ、Ⅲ型胶原的异常沉积可引起内异症患者腹腔内发生异常的免疫反应。     

放置IUD后宫腔微生物及子宫内膜病理学研究

研究ＩＵＤ与盆腔感染及子宫内膜恶变或其他病理改变的关系,探讨 ＩＵＤ长期使用的安全性。方法：将 ８８例分为 Ａ、Ｂ、Ｃ、Ｄ ４组,Ａ组 ２０例使用带尾丝活性 ＩＵＤ;Ｂ组２４例使用惰性 ＩＵＤ;Ｃ组 ２４例为正常对照组;Ｄ组 ２０例为盆腔感染组。所有病例取宫腔冲洗液进行需氧菌、厌养菌、解脲支原体、沙眼衣原体等培养,并取子宫内膜进行病理学检查,结果：Ａ、Ｂ组主要表现为正常增生期、分泌期或月经期子宫内膜,部分是单纯性或腺囊性增生,与Ｃ组、Ｄ组差异无显著性（Ｐ＞０．０５）,４组均未见不典型增生及恶变。Ａ、Ｂ、Ｃ３组子宫内膜均无慢性炎症改变,Ｄ组８例存在慢性子宫内膜炎改变,与Ａ、Ｂ、Ｃ组差异有显著性（Ｐ＜０．０５）。Ａ、Ｂ、Ｃ组淋巴细胞、浆细胞、中性白细胞、纤维细胞计数差异无显著性（Ｐ＞０．０５）,Ｄ组淋巴细胞、浆细胞、中性白细胞计数较以上３组明显增加（Ｐ＜０．０５）,间质细胞及纤维细胞计数与以上３组差异无显著性（Ｐ＞０．０５）。Ａ、Ｂ、Ｃ组宫腔微生物检出率分别为３０．０％,２９．２％,２０．８％,与Ｄ组（７０．０％）差异有显著性（Ｐ＜０．０５）。结论：使用ＩＵＤ５－１４年未增加子宫内膜癌、癌前病变及慢性子宫内膜炎发生率。Ｉ     

己酸孕酮、三苯氧胺及氨基导眠能对子宫内膜癌作用的研究

将子宫内膜癌７４例，分为７组单独或联合应用己酸孕酮，三苯氧胺和氨基导眠能治疗，光镜观察用药前后子宫内膜癌的形态学改变。结果：上述药物均能不同程度地抑制癌细胞生长，促其向成熟转化或发生退变，其中以三苯氧胺的作用尤为明显。癌细胞对上述药物的反应程度与癌分型、核分级有关，腺鳞癌、透明细胞癌和浆液乳头型腺癌反应不明显，而内膜型腺癌反应明显，两者的反应率有高度显著性差异（Ｘ２＝２０．８６Ｐ＜０．０１），粘液型腺癌反应介于两者之间。癌对药物反应程度随核分级增加而下降。     

抑癌基因P16与子宫内膜腺癌关系的研究

目的：研究抑癌基因Ｐ１６与子宫内膜腺癌的关系。方法：用免疫组化ＡＢＣ法检测１２３份石蜡包埋的子宫内膜腺癌标本（Ⅰ期８０份、Ⅱ期１２份、Ⅲ期２９份、Ⅳ期２份）和４０份增生期子宫内膜标本;用多聚酶链反应单股构象多态性分析（ＰＣＲ－ＳＳＣＰＡ）１０份子宫内膜腺癌Ｐ１６基因外显子１、２点突变。结果：Ｐ１６蛋白阳性表达率：增生期子宫内膜为７７５％,且均为高度阳性表达,子宫内膜腺癌为４３０８％,其中Ⅰ期为５１２５％、Ⅱ期为２５％、Ⅲ期为３１％、Ⅳ期为０;子宫内膜腺癌Ｐ１６阳性表达率明显低于正常增生期子宫内膜者（Ｐ＜００５）,且临床期别越晚,Ｐ１６蛋白阳性表达率越低（Ｐ＜００５）,阳性表达强度越弱（Ｐ＜００５）,Ⅰ期明显高于Ⅱ、Ⅲ、Ⅳ期（Ｐ＜００５）。１０份子宫内膜腺癌Ｐ１６基因外显子１、２均未检测出点突变。结论Ｐ１６基因蛋白的改变与子宫内膜腺癌的发生有关;临床期别越晚,其改变越明显,Ｐ１６基因的改变可能不以点突变为主。     

hMG对子宫内膜、卵泡发育及白细胞雌激素受体作用的探讨

目的：探讨ｈＭＧ对子宫内膜、卵泡发育及白血胞雌激素受体含量的变化及其临床意义。方法：应用阴道超声、放免法和放射配体结合法对１８例自然周期和１６例ｈＭＧ促排卵周期的不孕症患者子宫内膜厚度、分型、成熟卵泡数、血浆雌二醇及孕酮浓度和外周血白细胞雌激素受体含量进行测定比较。结果：①ｈＭＧ组围排卵期子宫内膜厚度大于自然周期组（Ｐ＜０．０５）;成熟卵泡数多于自然周期组（Ｐ＜０．０５）;子宫内膜Ａ、Ｂ型回声比例高于自然周期组（Ｐ＜０．０５）;②ｈＭＧ组围排卵期血浆雌二醇、孕酮浓度明显高于自然周期组（Ｐ＜０．０５）;③ｈＭＧ组围排卵期白细胞雌激素受体含量较自然周期组明显升高（Ｐ＜０．０１）。结论：①ｈＭＧ可使促排卵周期成熟卵泡数增加,子宫内膜分型改善,血浆Ｅ２浓度及白细胞雌激素受体含量升高,有改善子宫内膜容受性的作用;②ｈＭＧ可能有致卵泡过早黄素化的作用;③测定白细胞雌激素受体可间接反映子宫内膜雌激素受体的变化,具有无创、可靠、重复性好的优点     

绝经后应用利维爱妇女的子宫内膜组织学观察

目的：观察绝经后服用利维爱妇女子宫内膜组织学的变化。方法：通过统计分析４１例服药前和４３例服药后妇女的子宫内膜检查结果。结果：服药后增殖期内膜比例增加（Ｐ＜０．０５），萎缩性内膜比例减少（Ｐ＜０．０１）。出血组妇女服药前后内膜组织学变化无显著性差异（Ｐ＞０．０５）。出血组妇女服药前增殖期内膜比例显著高于无出血妇女（Ｐ＜０．０１），服药前、后萎缩性内膜比例显著低于无出血妇女（Ｐ＜０．０１，Ｐ＜０．０５）。出血组妇女服药前子宫内膜炎性细胞浸润比例显著高于无出血妇女（Ｐ＜０．０５）。提示：服用低剂量利维爱可明显地改善绝经后妇女的子宫内膜萎缩状况。ＨＲＴ期间的阴道出血与子宫内膜的组织学类型及炎性病变有关。     

妇癌患者腹腔冲洗液的相关因素

１０１例妇科肿瘤患者开腹探查前，先行腹腔冲洗，在道格拉斯氏陷凹取冲洗液做细胞学检查，其中妇科恶性肿瘤６５例，将细胞学检查与病理检查相对照。结果：冲洗液中８例检出癌细胞。子宫内膜癌Ⅰ～Ⅱ期阳性检出率８．３０％，卵巢癌Ⅰ～Ⅱ期阳性检出率９．０９％。单因素分析表明，腹腔冲洗液的细胞学阳性者，与淋巴转移（Ｐ＜０．０１）、盆腔转移（Ｐ＜０．０１）、组织学Ⅲ级（Ｐ＜０．０１）相关。腹腔冲洗液的细胞学检查可以指导术后治疗及评估预后     

Papillary Serous Carcinoma of the Uterus: Increased Risk of Subsequent or Concurrent Development of Breast Carcinoma

OBJECTIVE: Some women with endometrial cancer may be at increased risk for developing breast cancer. The histologic type of endometrial cancer associated with synchronous or subsequent breast cancer has not been clearly established. Our purpose was to determine if a certain histologic type of endometrial cancer was associated with an increased risk of synchronous or subsequent breast cancer. METHODS: The University of Iowa Hospitals and Clinics tumor registry was queried to ascertain all patients with the diagnosis of uterine cancer from January 1, 1983, to December 31, 1994. Statistics were performed utilizing SPSS for Windows version 9.0 (SPSS Inc., Chicago, IL), including Student's t tests and chi(2) tests. RESULTS: Five hundred ninety-two patients had endometrial adenocarcinoma during the study period. Five hundred thirty-six women had endometrioid adenocarcinoma, 23 women had papillary serous carcinoma (UPSC), 21 women had adenosquamous carcinoma, 10 women had clear-cell carcinoma, and 1 woman each had mucinous or squamous carcinoma. Twelve patients had previously been diagnosed with breast carcinomas. Twenty-five patients were diagnosed with breast cancer either concurrently or subsequent to their diagnosis of endometrial cancer. Synchronous or subsequent breast cancers developed in 3.2% of patients with endometrioid carcinoma and in 25% of patients with UPSC (P < 0.001). CONCLUSION: Patients with UPSC have an increased risk of development of breast cancer as compared to patients with endometrioid adenocarcinoma of the uterus.     

基于TCGA数据库分析KIF20 A在子宫内膜癌中的表达和意义

目的:检测驱动蛋白家族成员20A(KIF20A)在子宫内膜癌中的表达及其预后价值.方法:下载癌症基因组图谱(TCGA)中子宫内膜癌组织和癌旁组织样本的基因表达谱数据和临床数据,比较KIF20 A在子宫内膜癌组织和癌旁组织中的表达,并检测KIF20 A表达水平与患者生存预后的关系.结果:子宫内膜癌组织中KIF20 A表达...     

Endometrial carcinosarcomas have a different prognosis and pattern of spread compared to high-risk epithelial endometrial cancer

OBJECTIVE: The endometrial origin of uterine carcinosarcoma has recently been well established. The current study investigates whether uterine carcinosarcomas can be included in protocols on high-risk endometrial cancer, given the similarities in biologic behavior of both entities. METHODS: Pathological and surgical notes of patients diagnosed with grade 3 endometrioid, carcinosarcoma, serous and clear cell endometrial cancer subtypes were retrospectively analyzed with special attention to the spread pattern of the different subtypes. Information on site of relapse and time to recurrence was obtained. RESULTS: We traced 146 patients of which 9 patients were ineligible. Histological subtypes of the remaining 137 patients were as follows: 50 (37%) grade 3 endometrioid carcinoma, 54 (39%) serous or clear cell carcinoma (non-endometrioid carcinoma), and 33 (24%) carcinosarcomas. Distribution of early stage disease (I and II) was 67, 46, and 78% for grade 3 endometrioid, non-endometrioid, and carcinosarcoma, respectively. Although we could not trace differences in hematogenic and transperitoneal spread among the three subtypes, non-endometrioid and carcinosarcomas were more likely to spread to pelvic and paraaortic lymph nodes (P < 0.01). Using univariate analysis, both stage (P < 0.006, Wald statistic) and histological type appear to determine the outcome, whereas lymphovascular space infiltration (P < 0.25) and age (P < 0.07) were not significantly different between the three histological subtypes. Cox Regression multivariate analysis on 127 women suffering from the three histological subtypes suggested that both stage III-IV disease (P < 0.00001) and histological type (carcinosarcoma) (P < 0.003) were of prognostic significance [hazard ratio (CI 95%) were, respectively, 3.8 (2.1-7.0) and 3.2 (1.7-5.9)]. Analyzing cases limited to stage I-II endometrial cancer, 24/28 (86%) grade 3 endometrioid, 18/24 (75%) non-endometrioid, and 11/25 (44%) carcinosarcomas survived, suggesting a worse outcome for endometrial carcinosarcoma when compared to the other subtypes (P < 0.008, Log Rank). A higher incidence of pulmonary metastases explained the worse outcome for early stage carcinosarcoma (P < 0.006), whereas the incidence of liver metastasis, transperitoneal spread, or recurrences in lymph nodes or vagina were comparable between the three pathologic subtypes. CONCLUSIONS: Although endometrial carcinosarcoma originates from epithelial cancer, the intrinsic more aggressive tumor biology suggests that this subtype should not be incorporated in studies on high-risk epithelial endometrial cancer.     

Matrix metalloproteinases 2 and 9, E-cadherin, and beta-catenin expression in endometriosis, low-grade endometrial carcinoma and non-neoplastic eutopic endometrium

OBJECTIVES: Endometriosis and endometrial endometrioid carcinoma are both capable of invasion and metastasis, but their biological behavior is strikingly different. Matrix metalloproteinases (MMPs) and changes in adhesion molecules have a role in the pathogenesis of various physiological and pathological processes, as well as in the development of endometriosis and endometrioid endometrial carcinoma. We hypothesized that endometriosis, being a benign process, will show different MMPs and adhesion molecules expressions, compared to endometrioid endometrial carcinoma, a disease with potential of malignant behavior. STUDY DESIGN: We performed an immunohistochemical study to investigate expression of matrix metalloproteinase-2 (MMP-2), matrix metalloproteinase-9 (MMP-9), E-cadherin and beta-catenin in endometriosis, low-grade endometrial endometrioid carcinoma, and eutopic proliferative endometrium. Endometriotic tissues (n=15), low-grade endometrial endometrioid carcinomas (n=15), and unremarkable proliferative endometrium from women without endometriosis or carcinoma (n=10) were examined. RESULTS: Endometriotic tissues showed statistically significantly stronger staining for MMP-9 and reduced beta-catenin expression when compared with proliferative endometrium. Endometrial endometrioid carcinoma showed decreased E-cadherin expression in comparison with proliferative endometrium. MMP-2 and MMP-9, and E-cadherin expressions were significantly higher and beta-catenin expression was significantly lower in endometriosis as compared to endometrioid carcinoma. CONCLUSIONS: We suggest that increased MMPs and altered beta-catenin may play a role in the pathogenesis of endometriosis. Decreased E-cadherin may be important in the development of endometrial endometrioid carcinoma. The changes in MMPs, E-cadherin and beta-catenin differ in endometriosis from those in endometrioid carcinoma, an interesting finding in view of the fact that both these diseases are capable of invasion and metastasis, but have different biological behavior.     

Ⅰ期子宫内膜癌盆腔淋巴清扫术的意义

目的:探讨Ⅰ期子宫内膜癌患者预后的相关因素及盆腔淋巴清扫术对其预后可能的影响。方法:收集1997年8月至2005年3月浙江大学医学院附属妇产科医院临床Ⅰ期子宫内膜癌患者202例,分析影响预后的各项临床病理指标,寿命表法计算生存率,比较盆腔淋巴清扫组与平行淋巴结清扫组的复发率,并发症。结果:Ⅰ期子宫内膜癌盆腔淋巴转移率1·53%。病理类型、腹腔细胞学、盆腔淋巴转移、手术-病理分期、肌层浸润及CA125值是影响预后的独立因素。Ⅰ期低危患者,盆腔淋巴清扫术无助于提高生存率(P>0.05),其复发率也无明显差异(P>0.05),手术并发症率明显增高(P<0.05);Ⅰ期高危患者,盆腔淋巴清扫术未能延长其生存期(P>0·05),但可减少复发的例数,并发症率无明显增多(P>0.05)。结论:特殊病理类型,腹腔细胞学阳性,手术-病理分期高,盆腔淋巴转移,深肌层浸润及CA125>100U/ml的患者预后较差(P<0.05)。Ⅰ期高危子宫内膜癌患者盆腔淋巴清扫术具有一定的临床意义。     

Association between uterine serous carcinoma and breast cancer

OBJECTIVE: Endometrial cancer and breast cancer are two common malignancies found in women. As a result of estrogen dependency, an association is thought to exist between these entities. This study was undertaken to determine if the endometrial carcinomas, which develop in women with a history of breast cancer, were more likely to be of the endometrioid or the serous histology, which is generally considered non-estrogen-dependent. METHODS: A retrospective chart review was conducted for the years 1984-2001. All women who were diagnosed at our institution with endometrial carcinoma were identified. The women who also had a prior history of breast cancer were identified and comprise the cohort for this study. Information regarding age at diagnosis, tumor stage, histologic subtype, and tamoxifen exposure were recorded and analyzed. RESULTS: About 1166 women were diagnosed with endometrial cancer during the study period, of whom 54 (4.6%) had a pre-existing diagnosis of breast cancer. Of the 54 women in this study, 41 had tumors of the endometrioid histology and 13 had a tumor of the serous subtype. There was no difference with regards to median age at the time of diagnosis or years of tamoxifen exposure. Women with breast cancer were more likely to develop uterine serous carcinoma (USC) as compared to one of endometrioid histology (OR 2.6; 95% CI 1.29-5.23). CONCLUSIONS: Women with breast cancer who subsequently developed endometrial cancer exhibited a 2.6-fold increased risk of developing a USC as compared to an endometrioid carcinoma. These findings suggest that there may be an underlying genetic predisposition linking breast cancer and USC.     

Pathological findings in early-stage endometrial cancer

OBJECTIVE: The aim of this study was to assess the pathological characteristics of early-stage endometrial cancer, with regard to endometrioid versus serous papillary adenocarcinoma. METHODS: Sixty-six cases of early-stage endometrial carcinoma were classified into two groups: group I--36 cases of endometrioid endometrial cancer, staged IA-IB and graded G1-G2; group II--30 cases of Stage I serous papillary endometrial cancer. The pathological characteristics compared between the two groups included features such as tumor location in the uterine cavity, tumor focality, lymphovascular invasion, as well as the status of the uninvolved endometrium, adjacent to the tumor. Patient clinical characteristics were obtained from the medical records. RESULTS: Significantly more patients with endometrioid endometrial cancer were premenopausal (p < 0.0001), obese (p < 0.02), had hypertension (p < 0.00001) and familial cancer (p < 0.0001). On the other hand, significantly more patients with serous papillary cancer had another primary malignancy (p < 0.001). Considering the pathological characteristics, 75% of endometrioid as compared with 6.7% of serous papillary cancer cases were found in the upper uterine segment only (p < 0.0001). Multifocality was observed in 16.7% of endometrioid as compared with 100% of serous papillary cancer cases (p < 0.0001). Lymphovascular space invasion was absent in all cases of endometrioid cancer, while present in 90% of serous papillary cancer cases (p < 0.0001). Seventy-five percent of endometrioid and 100% of serous papillary cancer cases were associated with an atrophic endometrium. CONCLUSION: The clinical and pathological features of early-stage endometrial cancer differ according to the histological type of the cancer. The majority of endometrioid cancers are probably associated with an atrophic or normally cycling endometrium, and not with endometrial hyperplasia.     

Expression of COX-2, Ki-67, cyclin D1, and P21 in endometrial endometrioid carcinomas.

COX-2, the isoform of cyclooxygenase inducible by cytokines, mitogens, and growth factors, appears to play an important role in inflammation and carcinogenesis. In the colon, COX-2 overexpression results in cell cycle alterations, and NSAIDs have proven effective in cancer chemoprevention. HNPCC (hereditary nonpolyposis colon cancer) is a clinically defined cancer susceptibility syndrome in which women are also at significantly increased risk for the development of endometrial carcinoma. The purpose of this study was to evaluate expression of COX-2 in benign and malignant endometrium in the context of other cell cycle and proliferation markers, including Ki-67, cyclin D1, and the cyclin-dependent kinase inhibitor, p21. Immunostains with COX-2, Ki-67, cyclin D1, and p21 antibodies were performed on formalin-fixed and paraffin-embedded tissue sections from 40 cases: 10 benign (5 atrophic and 5 proliferative) endometria, 6 hyperplasias (complex without atypia), and 24 endometrioid carcinomas (9 well, 4 moderately, and 11 poorly differentiated). Ki-67 was positive in all proliferative and neoplastic endometria. Cyclin D1 and p21 were both overexpressed in endometrial hyperplasia and endometrioid carcinomas. COX-2 was negative in the nonneoplastic endometrium, stained minimally in the well-differentiated endometrioid carcinomas, and stained most strongly in the moderately and poorly differentiated endometrioid carcinomas. Because cyclin D1 may function as an oncogene, its effects may dominate the usual inhibitory effect of a rising p21. Alternatively, it has been shown that p21 can promote cell cycle function by stabilizing cell cycle complexes. The overexpression of COX-2 in poorly differentiated endometrioid carcinoma and lack of expression in hyperplasia and well-differentiated carcinoma suggests that in this form of cancer, COX-2 may play a role in tumor progression rather than tumor initiation.     

Development of endometrial cancer following radiation therapy for cervical carcinoma

The clinical and histologic findings in five cases of endometrial cancer, which developed following radiation therapy for squamous cell carcinoma of the cervix, are described. The mean age at endometrial cancer diagnosis was 69 years and average latency period from initial therapy to development of endometrial carcinoma was 13.4 years. For endometrial cancer, one patient had Stage Ib, one patient had Stage IIIa, two patients had Stage IIIc, and one patient did not undergo laparotomy. The histological types were carcinosarcoma in two patients, endometrioid adenocarcinoma, grade 3 in one patient, and clear cell carcinoma in one patient. All patients died of disease within 33 months of diagnosis. Endometrial cancers that develop after radiation treatment have a preponderance of high-risk histological subtypes, and consequently have a poor prognosis. Long-term follow-up should be mandatory for patients surviving radiation therapy for cervical cancer in order to detect and effectively treat second malignancies.     

p53 Expression as a Prognostic Indicator of 5-Year Survival in Endometrial Cancer

BACKGROUND: One of the most common genetic alterations to occur in human cancers is an alteration of the p53 tumor suppressor gene. The purpose of this article was to build upon the authors' previous work with p53 and determine whether p53 was a prognostic indicator of 5-year survival. METHODS: One hundred thirty-seven consecutively surgically treated patients with endometrial cancer had their p53 expression studied by immunoperoxidase staining and quantified by image analysis. All patients were evaluable for 5-year survival. RESULTS: One hundred three patients had endometrioid adenocarcinoma; 6, adenosquamous carcinoma; 14, papillary serous carcinoma; 10, clear cell carcinoma; and 4, undifferentiated carcinoma. p53 expression ranged from 0.0 to 58.2% positive nuclear area with a mean of 11.5% (median 2.6%) for the cohort. For the patients with endometrioid carcinoma, the mean p53 expression was 7.1% while for the nonendometrioid tumors it was 24.6% (P<0.001). Fifty-nine of the 103 endometrioid tumors (57.3%) stained positive for p53 while 32 of the 34 nonendometrioid (94.1%) tumors stained positive (P<0.001). Increasing histologic grade correlated with an increasing p53 expression (P = 0.003). The percentage of tumors expressing p53 was found to be higher in FIGO stage II, III, and IV than in FIGO stage I cancer (P = 0.003). However, mean p53 expression did not differ between early (stage I) and advanced (stage II, III, and IV) cancers (P = 0.088). Utilizing 5-year survival as the endpoint for multivariate analysis, FIGO stage (P = 0.0028) and p53 expression (P<0.001) were the only independent prognostic indicators found. CONCLUSION: p53 expression is more commonly found in nonendometrioid than in endometrioid adenocarcinoma of the endometrium. It, along with FIGO stage, is an independent prognostic indicator of 5-year survival.