Endometriosis-associated endometrioid adenocarcinoma of the fallopian tube synchronized with endometrial adenocarcinoma:A case report

BACKGROUND Endometriosis is a common gynecological disorder that affects women of reproductive age.It is characterized by a cancer-like invasion of the extra-uterine endometrium and exhibits a strong association with ovarian clear cell cancer and endometrioid cancer.Endometriosis-associated fallopian tube endometrioid adenocarcinoma synchronized with endometrial adenocarcinoma was rarely reported.CASE SUMMARY A 49-year-old woman was referred to our hospital complaining about abnormal vaginal bleeding for three years following unsatisfactory medication.Intraop-erative frozen sections unexpectedly unveiled an endometrioid cancer of the left fallopian tube with superficial invasion surrounded by diffuse endometriosis synchronized with endometrioid endometrial cancer.CONCLUSION It was difficult to make a differential diagnosis when confronted with incidental findings of fallopian tube cancer lesions synchronized with endometrial cancer.The key differential diagnosis of primary endometriosis-associated endometrioid adenocarcinoma of the fallopian tube from endometrial adenocarcinoma invol-vement relies on the pathological identification of malignant transformation in fallopian tube endometriosis disease.

Pancreatic endometrial cyst mimics mucinous cystic neoplasm of the pancreas

Pancreatic cysts include a variety of benign, premalignant, and malignant lesions. Endometrial cysts in the pancreas are exceedingly rare lesions that are difficult to diagnose pre-operatively. This report describes the findings in a 43-year-old patient with a recent episode of acute pancreatitis who presented with a large cyst in the tail of the pancreas. Imaging demonstrated a loculated pancreatic cyst, and cyst fluid aspiration revealed an elevated amylase and carcinoembryonic antigen. The patient experienced an interval worsening of abdominal pain, fatigue, diarrhea, and a 15-pound weight loss 3 mo after the initial episode of pancreatitis. With concern for a possible pre-malignant lesion, the patient underwent a laparoscopic distal pancreatectomy with splenectomy, which revealed a 16cm×12cm×4cm lesion. Final histopathology was consistent with an intra-pancreatic endometrial cyst. Here we discuss the overlapping imaging and laboratory features of pancreatic endometrial cysts and mucinous cystic neoplasms of the pancreas.

Correlation between PTEN Expression and PI3K/Akt Signal Pathway in Endometrial Carcinoma

In order to investigate the role of the PTEN expression in carcinogenesis and development of endometrial carcinoma and clarify whether and how PTEN and PI3K/Akt pathway relate to endometrial carcinoma, the expression of PTEN and phospho-Akt was detected by semiquantitative reverse transcription-polymerase chain reaction （RT-PCR） methods and Western-blot from 24 cases of endometrial carcinoma, 10 cases of endometrial atypical hyperplasia, 10 cases of endometrial hyperplasia, and 10 cases of normal endometriurn. SP immunohistochemical methods were used to measure levels of PTEN protein expression in following 5 study groups： 31 cases of endometrium in proliferative phase, 30 cases of endometrium in secretory phase, 71 cases of endometrial hyperplasia, 25 cases of atypical hyperplasia and 73 cases of endometrial carcinoma. Immunostaining score of PTEN was 3.39±0.15 in proliferative phase, 1.90±0.21 in secretory phase, 3.34±0.29 in endometrial hyperplasia, 0.62±0.11 in atypical hyperplasia, and 0.74±0.19 in endometrial carcinoma, respectively. PTEN mRNA relative value in normal endometrium, endometrial hyperplasia, endometrial atypical hyperplasia, and endometrial carcinoma was 2.45±0.51, 2.32±0.32, 0.46±0.11, and 0.35±0.13 respectively. The expression levels of PTEN mRNA and protein in patients with endometrial carcinoma and atypical hyperplasia were significantly lower than in those of proliferative phase and with endometrial hyperplasia. The level of PTEN expression in patients with endometrial carcinoma was significantly related to tissue type （P〈0.005）, differentiation （P〈0.05） and clinical stage （P〈0.05）, but not to depth of myometrium invasion （P〉0.05）. Western blot analysis revealed that Phospho-Akt level in PTEN negative cases was significantly higher, and there was a negative correlation between PTEN and phospho-Akt （r=-0.8973, P〈0.0001）. It was suggested that loss of PTEN expression was an early event in endometrial tumorigenesis. The phosphorylation of Akt induced by the loss of PTEN took part in the tumorigenesis and development of endometrial carcinoma.

OVARIAN METASTASIS IN PATIENT WITH ENDOMETRIAL CARCINOMA

Objective： To study the clinical pathological characteristics of ovarian metastasis of endometrial carcinoma and the factors affecting prognosis. Methods： Retrospective analysis was made to the clinical pathological outcome of endometrial carcinoma patients receiving surgical treatment in our hospital from January 1990 to December 2002. Results： Among the 191 cases of endometrial carcinoma patients, 17 cases （8.9%） had ovarian metastasis and young patients were more likely to have ovarian metastasis. The multiple factor analysis showed that the independent risk factors of ovarian metastasis in endometrial carcinoma included the depth of myometrial invasion, lymph node metastasis and pathological types. Conclusion： Ovarian metastasis in patients with endometrial carcinoma is associated with poor prognosis, the depth of myometrial invasion, lymph node metastasis and histologic types are independent risk factors affecting the prognosis. For young patients at early stage of the disease, it should be prudent as to whether to retain the ovary.

Correlation between single nucleotide polymorphisms of 17β-HSD-1 and endometrial adenocarcinoma

Objective: To investigate the correlation between 17-beta-hydroxysteroid dehydrogenase type1(17β-HSD-1) gene polymorphisms and risk of endometrial adenocarcino-ma.Methods: Forty-one patients with endometrial adenocarcinoma were selected as experimen-tal group and twenty-seven healthy women were selected as control group.The three common single nucleotide polymorphism of 17β-HSD-1 gene at sites + 1004,+ 1322 and + 1954 were detected by allele-specific PCR(ASA-PCR).The allele frequencies were analyzed by SPSS13.0 software between endometrial cancer cases and controls.Results: We observed no significant difference in various frequency distribution between experimental group and control group.P1004= 0.994,P1322 = 0.974,and P1954 = 0.981.Conclusion: We found that three common SNPs with the 17β-HSD-1 gene were not associated with endometrial adenocarcinoma.We suggest that more research for 17β-HSD needs to explore.

The relationship between single nucleotide polymorphisms in estrogenmetabolizing genes CYP1A1,CYP17,COMT and estrogen receptor alpha and the risk of endometrial adenocarcinoma among the Chinese women

Objective:To explore whether polymorphisms of the genes responsible for catechol estrogen(CE)formation via estrogen biosynthesis(CYP17)and hydroxylation (CYP1A1)and CE inactivation(COMT)and ERa are associated with an elevated risk for en- dometrial adenocarcinoma in Chinese women.Methods:A multigenic case-control study was conducted,eighty-seven endometrial adenocarcinoma patients and ninety controls were recrui- ted.PCR-RFLP assays were used to determine the genotypes of estrogen-metabolizing genes and ERa gene.Results:The endometrial adenocarcinoma risk associated with individual susceptibili- ty genotypes varied among the six polymorphic sites and was the highest for CYP17,followed by CYP1 A1 Ile-Val,CYP1A1 MspI,COMT,ERa XhaI and ERa PvuII.Multivariate logistic regres- sion showed the CYP1A1 MspI genotype was the most significant determinant for endometrial adenocarcinoma development and was associated with a 3.61 fold increase in risk(95% confi- dence interval,1.73～7.55).Furthermore,a trend of increasing risk for developing endometrial adenocarcinoma was found in women harboring higher numbers of high-risk genotypes.Conclu- sion:The CYP1A1,CYP17 and ERa XbaI genotypes are related to the susceptibility of endome- trial adenocarcinoma,they may be useful markers for predicting endometrial adenocarcinoma susceptibility.The allele encoding for low acticity COMT,ERa PvuII may not be a genetic risk factor for endometrial adenocarcinoma.

PTEN coding product:a new marker for tumorigenesis and progession of endometrial carcinoma

Objective:To investigate the expression of PTEN in carcinogenesis and development of endometrial carcinoma.Methods:The expression of PTEN was detected by reverse transcription-polymerase chain reaction(RT-PCR)methods from 24 cases with endometrial carcinoma,10 cases with endometrial atypical hyperplasia,10 cases with endometrial hyperplasia and 10 cases with normal endometrium and by SP immunohistochemical methods from 73 cases with endometrial carcinoma,25 cases with endometrial atypical hyperplasia,71 cases with endometrial hyperplasia and 31 cases with normal endometrium.Results:PTEN expression of both RNA and protein in patients with endometrial carcinoma and endometrial atypical hyperplasia was significantly lower than that of patients with endometrial hyperplasia and normal endometrium.mRNA relative value was 0.35±0.13,0.46±0.11,2.32±0.32,2.45±0.51,respectively.Loss of PTEN expression rates were 66.67%(38/57),76.00%(19/25),5.63%(4/71),0(0/31),repectively.The results were also compared with clinical parameters.Loss of PTEN expression in patients with endometrial carcinoma was significantly related to histological classification(P<0.0001)and differentiation(P<0.05).It was not related to depth of myometrium invasion and clinical stage(P>0.05).Conclusion:Loss of PTEN expression is an early event in endometrial tumorigenesis.Detection of PTEN protein may be a diagnostic biomarker for endometrial precancers and adenocarcinoma.

MRI基于2023版国际妇产科联盟分期评估子宫内膜癌进展

子宫内膜癌(EC)是常见妇科恶性肿瘤;MRI对EC评估具有重要价值。2023年国际妇产科联盟(FIGO)分期做出重大修订,以更细致地对EC进行风险分层,也使MRI面临新的挑战。本文就MRI基于2023版FIGO分期评估EC进展进行综述。

组织中MMP-9、E-cadherin与子宫内膜样癌伴MELF浸润方式及肿瘤侵袭程度的关系

目的分析子宫内膜样癌组织中基质金属蛋白酶(matrix metalloproteinase,MMP)-9、E-钙黏蛋白(E-cadherin)与微囊性、伸长及碎片状(microcystic,elongation,and fragmentation,MELF)浸润方式及肿瘤侵袭程度之间的关系,探讨能够识别子宫内膜样癌伴MELF浸润的指标,抑制肿瘤侵袭能力。方法回顾性分析在河北北方学院附属第一医院接受手术治疗的112例子宫内膜样癌患者临床资料,全部患者均顺利完成改良根治性子宫切除术,并获得肿瘤标准,根据病理检查结果对112例患者进行分组,分为MELF组和N-MELF组。统计112例患者一般临床资料,血液检查项目包括肿瘤标志物,免疫组织化学检查项目包括组织中MMP-9、E-cadherin,根据检查结果,构建Logistic回归模型,分析组织中MMP-9、E-cadherin及相关指标与子宫内膜样癌MELF浸润方式及肿瘤侵袭程度的关系。结果研究中112例子宫内膜样癌患者,评估为MELF浸润患者21例(18.75%);MELF浸润患者病理等级低级别,国际妇产科联盟(International Federation of Gynecology and Obstetrics,FIGO)ⅣA期,淋巴脉管间隙浸润(lymphatic vascular space,LVSI)、组织中MMP-9阳性患者占比多于N-MELF浸润患者,E-cadherin阳性患者占比少于N-MELF浸润患者,人附睾蛋白(humanepididymisprotein 4,HE4),甲壳质酶蛋白(human cartilageglycopmtein,YKL-40)水平高于N-MELF患者,差异有统计学意义(P<0.05)。多元Logistic回归分析提示,组织中E-cadherin表达率低、MMP-9表达率高,MELF浸润与子宫内膜样癌FIGO分期进展有关(P<0.05)。结论子宫内膜样癌发生MELF浸润与组织中MMP-9、E-cadherin有关,MMP-9表达率高和E-cadherin表达率低能够通过导致MELF浸润发生,从而增强肿瘤侵袭能力。

PARP抑制剂与免疫检查点抑制剂联合治疗在妇科恶性肿瘤中的应用

近年来肿瘤靶向和免疫治疗的研究进展迅速,如多腺苷二磷酸核糖聚合酶抑制剂[poly(ADP-ribose)polymerase inhibitor,PARPi]、免疫检查点抑制剂(immune checkpoint inhibitors,ICI)等已改变了妇科肿瘤的传统治疗模式,但部分患者疗效有限或出现耐药。临床前研究发现,PARPi损伤DNA修复过程,可造成肿瘤突变负荷与肿瘤特异性抗原增加,调节肿瘤微环境,刺激肿瘤浸润淋巴细胞(tumor infiltrating lymphocytes,TIL)产生并促进抗肿瘤免疫反应,为PARPi与ICI联合治疗提供了理论基础。近年多项临床研究发现PARPi与ICI联合使用可显著改善妇科恶性肿瘤患者的预后。

铜死亡在妇科恶性肿瘤中的研究进展

铜离子作为重要的辅酶,参与了广泛的代谢过程,包括有氧呼吸、肽酰胺化、铁转运、超氧化物歧化和细胞外基质的生物合成。铜稳态是维持细胞活性的重要机制。铜死亡是由铜离子积累引发的细胞死亡形式,其特点是铜稳态失衡,细胞内铜积累,选择性地扰乱三羧酸循环,使脂酰化线粒体酶聚集和铁硫蛋白丢失,引起线粒体蛋白质毒性应激,细胞膜裂解,最终导致细胞死亡。妇科恶性肿瘤是引起女性癌症死亡的重要原因。研究发现,铜死亡与妇科恶性肿瘤的发生、发展、预后及耐药密切相关。一些铜死亡调节剂可通过抑制血管生成、调节癌细胞的耐药性,抑制肿瘤转移和复发,因此铜死亡是治疗妇科恶性肿瘤有价值的研究方向。

子宫内膜腺纤维瘤1例报告并文献复习

子宫内膜腺纤维瘤是一种苗勒管起源的良性混合肿瘤,具有组织学良性、诊断困难、高复发率的特点。本文对该病的发病特点、临床表现、影像学表现、诊断及治疗进行分析,并复习相关文献,为了解该病特点、指导临床诊治提供帮助。

m6A修饰与妇科恶性肿瘤相关性的研究进展

N6-甲基腺苷(m6A)修饰是一种常见的表观遗传学修饰,动态调控RNA代谢的整个过程。m6A包括甲基转移酶、去甲基酶及m6A结合蛋白。m6A的甲基化修饰通过调节RNA的衰变、运输、剪切、翻译来调节细胞的增殖和分化,m6A与妇科恶性肿瘤的发生发展有关。笔者就近年来m6A甲基化修饰在宫颈癌、子宫内膜癌和卵巢癌中的相关研究进展进行回顾,分析m6A通过作用于RNA的修饰调节妇科恶性肿瘤发生发展的机制,为妇科恶性肿瘤的治疗、改善预后提供新的方向。

免疫细胞和免疫因子在子宫内膜癌中的作用

子宫内膜癌是常见的妇科恶性肿瘤,严重威胁女性的生活质量和生命健康。近年研究显示,在子宫内膜癌免疫微环境中,树突状细胞等免疫细胞与免疫增强因子相互作用可增强抗肿瘤的免疫效应,而肿瘤相关巨噬细胞等免疫细胞与免疫抑制因子通过抑制免疫应答可发挥促肿瘤的免疫效应。综述子宫内膜癌免疫微环境中部分免疫细胞、免疫抑制因子及免疫增强因子的研究进展,为深入研究子宫内膜癌的发病机制及免疫治疗方法提供新思路。

米非司酮对子宫内膜癌细胞系E-钙粘素和核因子kappa B表达的影响

目的:探讨米非司酮(Mifepristone,MIF)对子宫内膜癌细胞中核因子kappaB(nuclear factor kappa B,NF-κB)与E-钙粘素表达的影响,及NF-κB与E-钙粘素之间的关系。方法:体外培养子宫内膜癌细胞系HHUA,以不同浓度MIF(0、0.1×10-6、0.1×10-5、1×10-5、5×10-5、1×10-4mol/L)分别作用细胞24h、48h和72h,用免疫组化法检测NF-κB p65与E-钙粘素的蛋白表达水平。结果:MIF显著抑制HHUA细胞生长。MIF显著降调NF-κB p65的蛋白表达水平(P<0.05),增加E-钙粘素的蛋白表达水平(P<0.05)。NF-κB p65表达与E-钙粘素表达呈显著负相关(r=-0.94)。结论:MIF可抑制子宫内膜癌细胞系HHUA的生长,其机制可能通过抑制NF-κB的表达,进而增加其靶基因E-钙粘素的表达,来达到抑制子宫内膜癌细胞生长的作用。

miR-20a在妇科常见恶性肿瘤中的作用机制

宫颈癌、子宫内膜癌及卵巢癌作为妇科最常见的三大恶性肿瘤,其发病率近年来在各年龄段中呈上升趋势,已严重威胁我国女性健康。尽管多种靶向药物的应用已使该类患者的生存期明显延长,但其仍是一类无法被精准诊断和治疗的疾病。miR-17-92基因簇作为最早被确定为癌基因的微小RNA(micro RNA,miRNA)家族,其作用机制一直被广泛关注。miR-20a是miR-17-92基因簇中的一员,可通过降低或上调表达的方式发挥转录后调控功能,进而影响下游基因通路,调控恶性肿瘤细胞的增殖、侵袭及转移,并最终实现恶性肿瘤的发生及进展。根据目前研究进展,miR-20a在宫颈癌、子宫内膜癌及卵巢癌中表达特异性升高通常与疾病的恶性进展有关,综述miR-20a在妇科常见三大恶性肿瘤发病机制中作用的最新研究。

脂肪酸合酶及其抑制剂在子宫内膜癌中的研究进展

脂肪酸合酶(fatty acid synthase,FASN)是脂肪酸合成的关键酶,可催化脂质从头合成。正常组织中的脂肪酸大多来源于食物,而在子宫内膜癌细胞中脂肪酸依赖于脂质的从头合成。既往研究表明,FASN的表达与子宫内膜癌的发生、发展及预后不良相关,FASN的过表达与丝裂原细胞外激酶(mitogen extracellular kinase,MEK)/细胞外信号调节激酶(extracellular signal-regulated kinase,ERK)/丝裂原激活的蛋白激酶(mitogen-activated protein kinase,MAPK)和磷脂酰肌醇3激酶(phosphoinositide 3-kinase,PI3K)/蛋白激酶B(protein kinase B,Akt)/哺乳动物雷帕霉素靶蛋白(mammalian target of rapamycin,mTOR)信号转导通路相关。因此,特异性阻断FASN的活性可显著抑制肿瘤细胞的生长和增殖。综述子宫内膜癌中FASN的作用机制、FASN抑制剂(如C75、C93、奥利司他等)在子宫内膜癌或其他肿瘤中的研究进展,旨在为子宫内膜肿瘤的治疗提供新思路。

2023版子宫内膜癌FIGO分期更新对病理诊断内容的影响

子宫内膜癌是女性生殖系统最常见的恶性肿瘤,近年来子宫内膜癌诊疗中备受关注的热点问题,如淋巴脉管间隙浸润的定量评价、前哨淋巴结超分期和子宫内膜癌分子分型等,已经逐渐用于临床实践。目前,子宫内膜癌相关的新进展已被写入2023版国际妇产科联盟(International Federation of Gynecology and Obstetrics,FIGO)子宫内膜癌分期修订版本,并在临床推广应用。规范的病理诊断是评估子宫内膜癌患者预后和指导辅助治疗的重要依据,介绍2023版FIGO子宫内膜癌分期更新对病理诊断内容的影响,旨在帮助提高病理医生子宫内膜癌病理诊断的规范化及标准化水平,辅助临床医生更准确地理解和应用新分期。

合成MRI联合基于复合灵敏度编码弥散加权成像(MUSE-DWI)鉴别子宫内膜良、恶性病变

目的观察合成MRI联合基于复合灵敏度编码的弥散加权成像(MUSE-DWI)鉴别子宫内膜良、恶性病变的价值。方法回顾性分析112例经病理证实子宫内膜病变患者资料,根据病理诊断结果将其分为恶性组(n=72)及良性组(n=40)。测量病变合成MRI及MUSE-DWI定量参数,包括T1、T2、质子密度(PD)及表观弥散系数(ADC);比较2组临床资料及病变ADC、T1、T2及PD值。对组间差异有统计学意义的参数行单因素及多因素logistic回归分析,建立单变量及联合模型用于鉴别子宫内膜良、恶性病变,绘制受试者工作特征曲线,计算曲线下面积(AUC)评估其诊断效能并以DeLong检验加以比较。结果恶性组患者年龄大于良性组(P<0.05);子宫内膜恶性病变长径大于,而ADC、T2及PD值均低于良性病变(P均<0.05);组间T1值差异无统计学意义(P=0.074)。ADC单变量模型的AUC为0.966,与ADC+T2+PD联合模型的AUC(0.970)差异无统计学意义(校正P>0.05),而均高于T2单变量模型(0.618)、PD单变量模型(0.664)及T2+PD联合模型(0.668)(校正P均<0.05)。结论以合成MRI联合MUSE-DWI参数构建的ADC单变量模型及与其他参数构建的联合模型均能较有效鉴别子宫内膜良、恶性病变。