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.

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。

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.

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.

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.

HSPA5 CD44v6在子宫内膜癌的表达及临床价值

目的探讨热休克蛋白5(HSPA5)和CD44v6在子宫内膜癌中的表达及临床价值。方法选取2018年1月至2020年12月上海市长宁区妇幼保健院手术切除的93例子宫内膜癌标本,用免疫组织化学方法作HSPA5和CD44v6的表达检测,结合其临床病理指标,进行统计学分析。结果在93例子宫内膜癌中,HSPA5、CD44v6表达的阳性率分别为71.0%(66/93)和65.6%(61/93)。HSPA5在子宫内膜癌的不同病理分期、是否绝经及肿瘤浸润子宫壁深度不同(浸润子宫壁深度<1/2组;浸润子宫壁深度≥1/2组)的表达结果差异无统计学意义(均为P>0.05);而HSPA5在子宫内膜癌的不同组织学类型、淋巴结有无转移组的表达结果差异均有统计学意义(P<0.01,P<0.005)。CD44v6在子宫内膜癌的不同临床分期、是否绝经及不同组织学类型的表达结果差异无统计学意义(均为P>0.05);而CD44v6在肿瘤浸润子宫壁不同深度(浸润子宫壁深度<1/2组;浸润子宫壁深度≥1/2组)、淋巴结有无转移组的表达结果差异均有统计学意义(P<0.001,P<0.005)。结论HSPA5、CD44v6在子宫内膜癌中存在高表达,二者与子宫内膜癌的生物学行为有关,在子宫内膜癌的发生、发展中有着重要的调控作用。同步进行HSPA5、CD44v6在子宫内膜癌的表达检测,在判断其预后和指导其临床治疗上有重要价值。

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。

子宫内膜样腺癌中TBX2、PAX9的表达及其相关性

目的探讨TBX2、PAX9在正常子宫内膜、子宫内膜增殖症和子宫内膜样腺癌(endometrioid adenocarcinoma,EA)组织中的表达及临床病理学意义。方法采用组织芯片技术和免疫组化检测30例正常子宫内膜组织、30例单纯性增生内膜、30例复杂伴不典型性增生内膜、82例EA组织中TBX2、PAX9蛋白的表达。结果 TBX2蛋白在子宫内膜样腺癌中的阳性表达率明显高于正常子宫内膜和子宫内膜增殖症(P均<0.01),TBX2过表达与组织学分级、临床分期、浸润程度均有相关性(P<0.01,P<0.05,P<0.01),与淋巴结转移无相关性(P>0.05);PAX9蛋白在子宫内膜样腺癌中的阳性表达率明显高于正常子宫内膜、子宫内膜单纯性增生(P均<0.01),而和复杂伴不典型性增生之间没有统计学意义(P>0.05),在复杂伴不典型增生中表达明显高于正常子宫内膜和单纯性增生内膜(P均<0.01),PAX9阳性表达与组织学分级、临床分期、浸润程度均有相关性(P<0.01,P<0.01,P<0.05),但与淋巴结转移无相关性(P>0.05)。TBX2与PAX9蛋白呈正相关(rs=0.427,P<0.01)。结论 TBX2和PAX9均在子宫内膜样腺癌中发生、发展中发挥重要作用,联合检测其表达可为子宫内膜样腺癌的早期诊断、预后判断提供有价值的指标。

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。

COX-2、u-PA和TSP-1在胃癌及周围淋巴结中的表达及意义

目的:研究COX-2、u-PA和TSP-1在胃癌及周围淋巴结中的表达状况,探讨它们在胃癌浸润和淋巴结转移中的作用和意义。方法:用组织芯片技术和免疫组化法检测COX-2、u-PA和TSP-1的表达。结果:COX-2、u-PA和TSP-1在胃癌组阳性表达率分别为67.7%、78.1%和78.6%,均显著高于对照组(40.0%、6.7%和40.0%,P<0.05)。COX-2表达与浸润深度有关(P<0.05)。u-PA表达与浸润深度和淋巴结转移均有关(P<0.05)。TSP-1表达与浸润深度和淋巴结转移均无关(P>0.05)。COX-2、u-PA和TSP-1在转移淋巴结和对应癌组织间的表达差异无显著性(P>0.05)。COX-2和u-PA、TSP-1的表达呈正相关,u-PA和TSP-1的表达无相关关系。结论:胃癌中COX-2、u-PA和TSP-1高表达;COX-2表达与胃癌的浸润深度有关,u-PA表达与浸润深度和淋巴结转移有关。

子宫内膜样腺癌中MDM2、Livin和Caspase-3蛋白及mRNA的表达

目的探讨鼠双微体基因(MDM2)、凋亡蛋白抑制因子(Livin)、半胱氨酸天冬氨酸特异性蛋白酶3(Caspase-3)蛋白及mRNA在正常子宫内膜、子宫内膜增殖症和子宫内膜样腺癌(EA)中的表达及临床病理学意义。方法采用组织芯片技术结合免疫组化SP法及原位分子杂交方法,检测30例正常子宫内膜、30例单纯性增生、30例复杂伴不典型性增生、72例EA组织中MDM2、Livin、Caspase-3蛋白及mRNA的表达。结果 MDM2、Livin、Caspase-3蛋白及mRNA在EA中的表达率分别为80.6%(58/72)、80.6%(58/72)、33.3%(24/72)及73.6%(53/72)、75.0%(54/72)、27.8%(20/72),MDM2和L ivin表达率明显高于正常增生内膜(P<0.01),而Caspase-3阳性率明显低于正常增生内膜(P<0.01)。MDM2蛋白及mRNA过表达与组织分化、临床分期、浸润深度和淋巴结转移均无相关性;Livin和Caspase-3蛋白及mRNA阳性表达与组织分化有关(P<0.01或P<0.05),与临床分期、浸润深度及淋巴结转移均无相关性。MDM2、Livin、Caspase-3蛋白与相应的mRNA呈正相关;Livin与Caspase-3表达在蛋白及mRNA水平均呈负相关。结论 MDM2、Livin和Caspase-3蛋白及mRNA异常表达与EA的发生发展相关,有望成为EA早期诊断和预后判断的有价值标记物。

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。

EPAS1、VEGF在胰腺癌中表达及其相关性

目的研究胰腺癌组织中缺氧诱导因子2(EPAS1/HIF-2α)、血管内皮生长因子(VEGF)和微血管密度(MVD)的表达及与临床病理特征之间的关系。方法应用逆转录聚合酶链反应(RT-PCR)、免疫印迹Western blot、免疫组化SP法检测60例胰腺癌及相应正常胰腺组织中EPAS1、VEGF mRNA和蛋白的表达和分布,同时检测MVD作为判断血管生成的指标,分析其间的相关性以及与肿瘤临床病理特征之间的关系。结果EPAS1、VEGF和MVD在胰腺癌组织中的表达明显高于正常胰腺组织,VEGF在mRNA和蛋白水平均增高(P<0.01),但EPAS1只在蛋白水平增高(P<0.01)。此外,三者之间的表达具有显著相关性(P<0.01)。EPAS1和VEGF的阳性表达与胰腺癌的TNM分期、肿瘤大小有关。结论胰腺癌组织中EPAS1和VEGF呈过量表达,且EPAS1的表达与VEGF及MVD呈显著正相关。EPAS1可通过上调VEGF表达来促进胰腺癌血管生成从而在胰腺癌的发生、发展中起重要作用。