联合检测子宫内膜样腺癌组织Ki-67、ER与CEA表达的临床诊断价值

目的探讨联合检测Ki-67、ER与CEA可否提高子宫内膜样腺癌的诊断和鉴别价值。方法采用免疫组织化学方法,对50例子宫内膜样腺癌和25例宫颈原发性腺癌组织检测Ki-67、ER与CEA,卡方检验分析两种类型腺癌组织的表达差异及各项指标之间的相关性,并统计比较Ki-67、ER与CEA三联检测和Ki-6与CEA两联检测的敏感性、特异性和准确度。结果在子宫内膜样腺癌组织中,ER和Ki-67的阳性表达率为82.0%和86.0%,明显高于宫颈腺癌组织,而CEA的表达低于宫颈腺癌组织,组间比较差异具有统计学意义(P0.05);在子宫内膜样腺癌组织中,在ER阳性组中Ki-67、CEA的阳性表达高于ER阴性组,两者呈正相关(P0.05)。三联检测诊断子宫内膜样腺癌的敏感性、特异性和准确度分别为65.3%、100%和80.2%,明显高于两联检测法(P0.05)。结论在子宫内膜样腺癌中存在明显的ER高表达,且与Ki-67、CEA的阳性表达呈负相关,在常规的Ki-67与CEA两项检测中加入ER可有效提高诊断的特异性和准确性,具有显著的临床价值。     

子宫内膜不典型息肉状腺肌瘤5例临床病理分析

目的探讨子宫内膜不典型息肉状腺肌瘤(atypical polypoid adenomyomas,APA)的临床与病理学特点。方法分析5例APA的临床资料、病理学形态、免疫组化标记及4例随访资料。结果5例APA中,1例合并子宫内膜样腺癌,1例局部分布分化良好的腺癌成分;免疫组化显示:间质SMA( ),desmin( )或局部( ),vimentin局部( )或(-);腺上皮ER、PR均( );p53、Ki-67(-)。随访的4例患者均健在(3~60个月)。结论APA需与高分化的子宫内膜样腺癌鉴别,后者可与APA并存,或起源于子宫内膜不典型息肉状腺肌瘤,具有低恶性潜能和潜在的复发性,长期随访十分必要。     

子宫内膜样腺癌中Stathmin和Ki-67的表达及意义

目的:研究Stathmin和Ki-67在子宫内膜样腺癌和正常子宫内膜中的表达差异,探讨Stathmin和Ki-67在子宫内膜样腺癌发生发展过程中的意义.方法:采用免疫组织化学法检测99例子宫内膜样腺癌及67例正常子宫内膜中Stathmin和Ki-67的表达情况.结果:子宫内膜样腺癌中Stathmin和Ki-67表达率分别为75.8%,70.7%,显著高于正常子宫内膜中的9.0%,4.5%,差异有统计学意义(P<0.05);Stathmin和Ki-67表达与子宫内膜样腺癌组织学分级相关(P<0.05),与患者年龄、临床分期、浸润深度、淋巴结转移及脉管侵犯无关(P>0.05);Stathmin表达和Ki-67表达呈正相关(r=0.672,P<0.05).结论:子宫内膜样腺癌中Stathmin和Ki-67高表达可能共同参与子宫内膜样腺癌发生和分化;Stathmin和Ki-67表达呈正相关,提示Stathmin高表达可能与子宫内膜样腺癌高增殖性相关.     

子宫颈鳞状细胞癌通过表面扩散累及子宫内膜1例并文献复习

目的探讨子宫颈鳞状细胞癌通过表面扩散累及子宫内膜的临床病理特征、诊断及鉴别诊断、治疗及预后。方法回顾性分析1例子宫颈鳞状细胞癌通过表面扩散累及子宫内膜的临床资料、病理学特征及免疫表型,并复习相关文献。结果眼观:子宫颈见隆起型肿物,子宫内膜局部见一菜花样肿物,余内膜均粗糙。镜检:子宫颈浸润性中分化鳞状细胞癌沿表面扩散至子宫内膜,子宫内膜中分化鳞状细胞癌伴肉瘤样化生及子宫腺肌症。免疫表型:子宫颈肿物:p16、CK8/18、CK19和PTEN均(+),CD138表面癌细胞及原位癌细胞着色强,深部癌细胞着色弱或阴性。子宫内膜肿物:p16、CK19和PTEN均(+),CK8/18(局灶+),CD138表面癌细胞及原位癌细胞着色强,深部癌细胞着色弱或阴性。子宫内膜鳞状细胞癌:CKpan、CK17和p63均(+),EMA(部分+),p53(散在+),CK7、ER和PR均(-),Ki-67增殖指数约70%;子宫内膜肉瘤样化生区:vimentin、CK17、p63均(+),CKpan(部分+),CD10、desmin、SMA、MyoD1和Myogenin均(-)。结论子宫颈鳞状细胞癌通过表面扩散累及子宫内膜较罕见,其扩散机制可能与基因改变和(或) CD138表达有关。     

子宫颈癌伴发印戒样细胞变化2例并文献复习

目的 探讨印戒样细胞变化与印戒细胞癌的组织学特点、免疫表型、诊断及鉴别诊断.方法 对2例子宫颈癌中印戒样细胞进行病理学分析,采用免疫组化EnVision法检测CK、CK7、E-cadherin、CEA、p53、Ki-67、vimentin、p16、p63、ER、PR表达并复习相关文献.结果 印戒样细胞变化与印戒细胞癌在形态上相似.印戒样细胞变化分非瘤性和肿瘤性印戒样细胞变化,子宫颈鳞癌和绒毛状管状腺癌可伴发非瘤性印戒样细胞变化.非瘤性印戒样细胞变化的细胞局限在基膜内,印戒细胞癌细胞在固有层内或更深组织内呈浸润性生长.非瘤性印戒样细胞变化免疫组化标记E-cadherin阳性,Ki-67低增殖指数和p53阴性,而印戒细胞癌E-cadherin阴性,Ki-67增殖指数高和p53阳性.肿瘤性印戒样细胞变化与肿瘤类型相关.结论 印戒样细胞变化的细胞在形态上与印戒细胞癌细胞相似,需仔细观察组织学结构,并结合病变器官,借助于免疫组化(CK、E-cadherin、CEA、p53等)和特殊染色(D-PAS)有助于做出正确的诊断.     

NEDD9在子宫内膜样腺癌中的表达及意义

目的 探讨NEDD9(neural precursor cell expressed developmentally down-regulated9)在子宫内膜样腺癌中的表达及意义。方法 应用免疫组化方法检测NEDD9在50例子宫内膜样腺癌和30例子宫内膜单纯性增生组织中的表达,并检测雌激素受体(ER)、孕激素受体(PR)在子宫内膜样腺癌的表达。结果 NEDD9在子宫内膜样腺癌中的表达高于在子宫内膜单纯性增生组织中的表达(p=0.226);在子宫内膜样腺癌中,NEDD9的高表达与肌层浸润≥1/2、FIGO分期III期和ER阴性表达相关(p=0.012,p=0.041及p=0.039)。结论 NEDD9促进子宫内膜样腺癌的侵袭,并与其ER表达状态负相关。     

子宫内膜样腺癌MUC1表达及其与ER、PR表达的相关性

目的 探讨跨膜型黏蛋白1(Mucin 1,MUC1)在子宫内膜样腺癌中的表达及其与ER、PR的相关性.方法 采用免疫组化EnVision法检测56例子宫内膜样腺癌、28例不典型增生性子宫内膜及18例增生性子宫内膜组织中MUC1蛋白的表达,同时检测子宫内膜样腺癌组织中ERα、PR的表达.结果 (1)在增生性子宫内膜、不典型增生性子宫内膜和子宫内膜样腺癌中,MUC1蛋白异质表达率分别为27.8%、71.4%和80.4%,差异有显著性(P=0.000).(2)子宫内膜样腺癌中,随着患者绝经的发生、组织学分级、分期的提高和肌层浸润加深,MUC1蛋白异质表达率有增加趋势(P>0.05);ERα、PR蛋白表达与组织学分级关系密切(P=0.003,P=0.008),与患者月经状态、肌层浸润、淋巴结转移及手术病理分期无关(P>0.05).(3)子宫内膜样腺癌中,MUC1蛋白表达与ERα蛋白有的负相关关系,与PR蛋白有部分呈正相关关系,但关系不密切(P>0.05).结论 子宫内膜样腺癌中MUC1蛋白异常表达率显著升高,并且与ER、PR有相互调节关系.     

Bcl-2蛋白、Ki-67抗原、雌激素受体及孕激素受体在子宫腺肌病子宫内膜中的表达

目的检测与分析细胞凋亡抑制因子(Bcl-2蛋白)、细胞核相关抗原(Ki-67抗原)、雌激素受体(ER)、孕激素受体(PR)在子宫腺肌病(AM)在位内膜、异位内膜和正常子宫内膜中的表达情况及相关性,探讨其在AM发病机制中的作用。方法采用免疫组织化学PicTureTM二步法检测40例AM在位内膜、异位内膜及38例正常子宫内膜中Bcl-2蛋白、Ki-67抗原、ER、PR的表达情况。采用Spearman等级相关分析这些因素间表达的相关性。结果(1)Bcl-2蛋白、Ki-67抗原在AM在位内膜和正常子宫内膜中表达有周期性变化,增生期高于分泌期(P<0.05);而在AM异位内膜中表达无明显周期性变化。(2)Bcl-2蛋白、Ki-67抗原在3种内膜的表达情况:AM异位内膜>AM在位内膜>正常子宫内膜,差异有统计学意义(P<0.05)。(3)AM在位内膜、正常子宫内膜中Bcl-2蛋白、Ki-67抗原的表达与ER、PR的表达呈正相关(P<0.05);AM异位内膜中Bcl-2蛋白、Ki-67抗原的表达与ER、PR的表达无相关。结论AM在位、异位内膜中Bcl-2蛋白、Ki-67抗原的异常表达可能与AM的发生、发展有关。     

Bcl-2蛋白、Ki-67抗原、雌激素受体及孕激素受体在子宫腺肌病子宫内膜中的表达

目的 检测与分析细胞凋亡抑制因子(Bcl-2蛋白)、细胞核相关抗原(Ki-67抗原)、雌激素受体(ER)、孕激素受体(PR)在子宫腺肌病(AM)在位内膜、异位内膜和正常子宫内膜中的表达情况及相关性,探讨其在AM发病机制中的作用.方法 采用免疫组织化学PicTureTM二步法检测40例AM在位内膜、异位内膜及38例正常子宫内膜中Bcl-2蛋白、Ki-67抗原、ER、PR的表达情况.采用Spearman等级相关分析这些因素间表达的相关性.结果 (1)Bcl-2蛋白、Ki-67抗原在AM在位内膜和正常子宫内膜中表达有周期性变化,增生期高于分泌期(P＜0.05);而在AM异位内膜中表达无明显周期性变化.(2)Bcl-2蛋白、Ki-67抗原在3种内膜的表达情况:AM异位内膜＞AM在位内膜＞正常子宫内膜,差异有统计学意义(P＜0.05).(3)AM在位内膜、正常子宫内膜中Bcl-2蛋白、Ki-67抗原的表达与ER、PR的表达呈正相关(P＜0.05);AM异位内膜中Bcl-2蛋白、Ki-67抗原的表达与ER、PR的表达无相关.结论 AM在位、异位内膜中Bcl-2蛋白、Ki-67抗原的异常表达可能与AM的发生、发展有关.     

腹壁异位子宫内膜恶变为透明细胞腺癌临床病理特征及鉴别诊断

目的 探讨腹壁异位子宫内膜恶变为透明细胞腺癌临床病理特点、诊断及鉴别诊断.方法 对1例腹壁异位子宫内膜恶变为透明细胞腺癌的临床及病理资料进行分析,并复习相关文献.结果 腹壁异位子宫内膜恶变为透明细胞腺癌的形态,与发生在子宫内膜和卵巢等部位的形态学改变相似.肿瘤细胞呈巢状实性或腺样排列,实性区域胞质透亮,伴广泛凝固性坏死.腺样区域腺体拉长及相互连接形成隧道样结构,肿瘤细胞呈鞋钉状,胞质嗜酸性,核大突向腺腔.免疫表型:CK7、CK、CEA(多克隆)、EMA和vimentin均阳性;ER灶性阳性.CEA(单克隆)、PR、CK20、MC、CR、S-100、CK5/6和Moc31均阴性.结论 腹壁异位子宫内膜恶变为透明细胞腺癌非常少见,免疫表型无特异性,确诊主要依靠病史及HE形态特点.需与汗腺来源的腺癌、转移性腺癌和恶性上皮型间皮瘤进行鉴别.     

Prognostic significance of the infiltrative pattern invasion in endometrioid adenocarcinoma of the endometrium

The prognostic significance of the invasive type of carcinoma cells in endometrial carcinoma is not defined. We evaluated the prognostic significance of the invasive type, as well as the immunostains of p53, c-erbB-2, Ki-67 antigen and MDM2 in endometrial endometrioid adenocarcinoma. This prospective analysis comprised 112 patients with endometrioid adenocarcinoma of the uterine corpus who had undergone surgery and were traced for more than 5 years after the operation. They were divided into recurrence (16 patients) and non-recurrence (96 patients) groups. The invasive type of carcinoma cells was divided into expansile, mixed (expansile and infiltrative) and infiltrative pattern. The difference in the invasive type (P < 0.001) and p53 expression (P = 0.004) between the recurrence and non-recurrence groups was significant in the univariate analysis. Moreover, the invasive type was significant in the multivariate analysis (P = 0.004). In contrast, the difference in MDM2 expression, c-erbB-2 expression and the Ki-67 labeling index in both groups was not significant in the univariate analysis. The infiltrative pattern of the invasive type (P < 0.001) and p53 expression (P = 0.043) were significantly related to a poor prognosis in the Kaplan-Meier method using the log-rank test. In conclusion, the current study indicated that the infiltrative pattern of the carcinoma cells is a predictor for poor prognosis in endometrioid adenocarcinoma in the uterine corpus. It was also indicated that p53 immunostains are useful as a predictor, but Ki-67 antigen, c-erbB-2 and MDM2 stains are not.     

Endometrioid adenocarcinoma of the uterus with a minimal deviation invasive pattern

AIMS: Minimal deviation adenocarcinoma of endometrioid type is a rare pathological entity. We describe a variant of typical endometrioid adenocarcinoma associated with minimal deviation adenocarcinoma of endometrioid type. METHODS AND RESULTS: One 'pilot' case of minimal deviation adenocarcinoma of endometrioid type associated with typical endometrioid adenocarcinoma was encountered at our institution in 2001. A second case of same type was received in consultation. We reviewed 168 consecutive hysterectomy specimens diagnosed with 'endometrioid adenocarcinoma' specifically to identify areas of minimal deviation adenocarcinoma of endometrioid type. Immunohistochemistry was done with the following antibodies: MIB1, p53, oestrogen receptor (ER), progesterone receptor (PR), cytokeratin 7 (CK7), cytokeratin 20 (CK20), carcinoembryonic antigen (CEA), and vimentin (VIM). Four additional cases of minimal deviation adenocarcinoma of endometrioid type were identified. All six cases of minimal deviation adenocarcinoma of endometrioid type were associated with superficial endometrioid adenocarcinoma. In two cases with a large amount of minimal deviation adenocarcinoma of endometrioid type, the cervix was involved. The immunoprofile of two representative cases was ER+, PR+, CK7+, CK20-, CEA-, VIM+. MIB1 immunostaining of four cases revealed little proliferative activity of the minimal deviation adenocarcinoma of endometrioid type glandular cells (0-1%) compared with the associated 'typical' endometrioid adenocarcinoma (20-30%). The same four cases showed no p53 immunostaining in minimal deviation adenocarcinoma of endometrioid type compared with a range of positive staining in the associated endometrioid adenocarcinoma. CONCLUSIONS: Minimal deviation adenocarcinoma of endometrioid type more often develops as a result of differentiation from typical endometrioid adenocarcinoma than de novo. Due to its deceptively benign microscopic appearance, minimal deviation adenocarcinoma of endometrioid type may be overlooked and may lead to incorrect assessment of tumour depth and pathological stage. There was a tendency for tumour with a large amount of minimal deviation adenocarcinoma of endometrioid type to invade the cervix.     

Immunoprofile of cervical and endometrial adenocarcinomas using a tissue microarray

Adenocarcinomas of the uterine cervix show a wide range of morphological features, and can be confused with endometrial adenocarcinoma in biopsy or curetting specimens. The objective of this study was to use tissue microarray technology to evaluate the immunoprofile of a large set of uterine adenocarcinomas with an extended panel of antibodies, comparing the profile of primary cervical and endometrial adenocarcinomas. A tissue microarray was constructed using paraffin-embedded, formalin-fixed tissues from 141 hysterectomy specimens. Duplicate 0.6-mm cores were obtained from 57 cervical adenocarcinomas (16 in situ and 41 invasive) and 84 endometrial adenocarcinomas. Tissue array sections were immunostained with 21 commercially available antibodies [B72.3, CD 99, carcinoembryonic antigen (CEA), c-kit, pancytokeratin, CK 5/6, CK 7, CK8/18, CK19, CK 20, CK 22, EMA, estrogen receptor (ER), KP-1, melan-A, p53, PLAP, S-100, synaptophysin, TTF-1, and vimentin] utilizing the avidin-biotin (ABC) technique. Hierarchical clustering analysis of the tumors was done based on the immunostaining results. Only ER ( P<0.001), CEA ( P=0.04), vimentin ( P<0.001), and CK 8/18 ( P=0.002) showed a significantly different frequency of positivity in endometrial relative to cervical adenocarcinomas. ER, vimentin, and CK 8/18 were more likely to be expressed in endometrial adenocarcinomas, while cervical adenocarcinomas more frequently expressed CEA. We were able to identify immunoprofiles that were highly specific for endocervical adenocarcinoma (ER(-), vimentin(-), CK 8/18(-), CEA(+)) or endometrial adenocarcinoma (ER(+), vimentin(+), CK 8/18(+), CEA(-)), but most tumors showed an intermediate, non-specific immunophenotype. Hierarchical clustering analysis was useful in the interpretation of these intermediate immunophenotypes. Papillary serous adenocarcinoma of the endometrium was less likely to express vimentin ( P=0.002) than endometrioid carcinoma of the endometrium.     

Carcinomas of Bartholin's gland. Histogenesis and the etiological role of human papillomavirus.

In this study, we examine 10 primary carcinomas of Bartholin's gland, including seven squamous carcinomas, two adenoid cystic carcinomas, and one adenocarcinoma, as well as four non-neoplastic Bartholin's gland. Six of seven squamous cell carcinomas contained human papillomavirus (HPV) type 16 DNA detectable by the polymerase chain reaction; one of these demonstrated HPV type 16 by in situ hybridization. The two adenoid cystic carcinomas, the adenocarcinoma, and the non-neoplastic Bartholin's gland epithelium showed no evidence of HPV DNA by polymerase chain reaction or in situ hybridization. A panel of eight antibodies (Cam 5.2, B72.3, CEA, EMA, MCA, Lewis X, ER, and PR) demonstrate that the squamous, transition zone, duct, acinar, and myoepithelial cells or Bartholin's gland are antigenically distinct, and are similar to those reported in analogous areas of the uterine cervix. Squamous carcinoma and adenocarcinomas of Bartholin's gland are antigenically similar, and seem to arise from the transition zone of the Bartholin's gland duct. The origin of adenoid cystic carcinomas is more difficult to determine; it is distinct from squamous and adenocarcinomas and seems more likely to arise from myoepithelial cells. We conclude that adenocarcinoma and squamous cell carcinoma of Bartholin's gland arise in the transition zone of Bartholin's gland, which is similar to the transition zone of the uterine cervix. We also show that HPV is associated with Bartholin's gland carcinoma and may play a role in the genesis of malignancy.     

p16INK4A overexpression and HPV infection in uterine cervix adenocarcinoma

Human papillomaviruses (HPVs) are causally involved in the genesis of cervical carcinomas and their precursors, and there is a strong relationship between the cyclin-dependant kinase inhibitor p16^INK4A and HPV infection. This study was carried out to assess the correlations between p16^INK4A expression as an early biomarker of the endocervical adenocarcinoma and HPV infection. p16^INK4A expression and HPV typing were performed on 46 samples including 5 normal endocervix, 9 benign lesions of the endocervix, 25 endocervical adenocarcinomas, and 7 endometrioid adenocarcinomas of the uterine corpus. A semiquantification of the p16^INK4A immunostaining was realized (using both the staining intensity and the percentage of positive cells) and was graded from 0 to 15. All of the 25 endocervical adenocarcinomas overexpressed p16^INK4A; the adjacent epithelium and the connective tissue were strictly negative. No p16^INK4A was detected in nine benign endocervical lesions and in five normal endocervix. Few endometrioid adenocarcinomas of the uterine corpus that infiltrate the endocervix exhibited a low immunoreactivity (score 0/15 or 1/15). This pattern of expression is significantly associated with HPV infection (p<10 ⁻³), mainly high-risk HPV types (p=0.02). Our results suggest that p16^INK4A is a putative molecular biomarker that consistently discriminates uterine cervix adenocarcinomas from benign lesions and from endometrioid adenocarcinomas of the uterine corpus .     

Endometrioid adenocarcinoma of the vagina with a microglandular pattern arising from endometriosis after hysterectomy

Primary endometrioid adenocarcinoma rarely occurs in the vagina. Occasionally, endometrioid adenocarcinoma has a microglandular pattern. Herein, a case of primary endometrioid adenocarcinoma of the vagina with a microglandular pattern arising from pre‐existing endometriosis long after a hysterectomy, is described. A 57‐year‐old postmenopausal woman developed a vaginal discharge over one decade after undergoing a hysterectomy. Microscopic examination of the vaginal smear and a biopsy specimen demonstrated an atypical glandular proliferation composed of columnar cells with occasional intracytoplasmic mucin and bland nuclear morphology, showing microcysts and numerous neutrophils within and around cysts. Immunohistochemically, the neoplastic cells were diffusely positive for CK7, MUC1, ER, and PR, and focally positive for vimentin, CEA, CK5/6, p63, p16^INK4a, and p53. A portion of residual endometrioid adenocarcinoma was identified adjacent to foci of endometriosis in the vaginectomy specimen. The patient has done well without evidence of recurrent disease for 1 year after surgery. Pathologists are encouraged to be aware of the occurrence of endometrioid adenocarcinoma associated with endometriosis in the vaginal stump after hysterectomy, and microglandular morphology which might be a source of misinterpretation.     

Clinicopathologic study of endometrial dedifferentiated endometrioid adenocarcinoma: a case report

In 2006, dedifferentiated endometrioid adenocarcinoma (undifferentiated carcinoma associated with low-grade endometrioid carcinoma) of the uterus was first proposed. Dedifferentiated endometrioid carcinoma is part of the spectrum of undifferentiated carcinoma of the endometrium which is a highly aggressive tumor even when the undifferentiated component represents only 20% of the entire neoplasm. Therefore, accurate diagnosis and appropriate classification of this neoplasm are important in patient management. Lack of the recognition may lead to misclassification of dedifferentiated endometrioid adenocarcinoma as a pure endometrioid adenocarcinoma which is less aggressive. Only 4 papers have appeared in the literature so far on the topic of dedifferentiated endometrioid carcinoma. We report herein a first case of endometrial dedifferentiated endometrioid carcinoma in a 51-year old woman in Chinese population. We performed immunoperoxidase studies for 12 markers. Among them, cytokeratins, keratin 7, keratin 18, EMA, estrogen receptor (ER), progesterone receptor (PR), and vimentin show significantly differential expression between differentiated and undifferentiated area.     

Immunohistochemical profile of endometrioid adenocarcinoma of the uterus: ER, PR, HER-2, Ki-67 and their prognostic value

76 endometrioid adenocarcinomas of the uterine body were studied. Expression of the above markers is of essential value together with metastatic involvement of regional lymph nodes, stage of the disease and pathogenetic variant for determining prognosis of carcinoma aggressiveness and disease outcome. Positive hormonal-receptor status of the tumor is characterized by well-differentiated tumor cells, small depth of invasion, rare metastases to regional lymph nodes and higher survival (5 year--81%) of patients comparing with cases where ER and PR were not determined (53%). On the contrary, overexpression of oncoprotein HER-2 and Ki-67 higher than median (42%) was associated with high tumor aggression resulting finally in a significant fall in the survival (from 75% to 58% and from 79% to 60%, respectively). Combination of HER-2 overexpression with a high level of Ki-67 is particularly unfavourable (5-year survival--43%).     

P16-positive continuous minimal deviation adenocarcinoma and gastric type adenocarcinoma in a patient with Peutz-Jeghers syndrome

We report a case of Peutz-Jeghers syndrome (PJS) in a 33-year-old female patient with synchronous uterine cervical minimal deviation adenocarcinoma (MDA) and gastric type adenocarcinoma (GTA). The patient was diagnosed with PJS at the age of 10. At the time of consultation, she complained of watery discharge. Magnetic resonance imaging of the pelvis showed a poorly circumscribed mass in the uterine cervix. Histologically, both MDA and GTA components, as well as their transitional area, were observed. Both components were diffusely positive for MUC6, CK7 and, robustly, for p16. Moreover, the components were negative for ER, PgR and CEA, while HIK1083 and CK20 positive cells were found focally. Ki-67 labeling index in the MDA component was 5% while that in the GTA component was 50%. This case of GTA accompanied by MDA in a patient with PJS is distinct from the single previously-reported comparable case of which we are aware, with respect to the overexpression of p16 protein, an event considered rare in these tumors, and the continuity between the MDA and GTA components. This continuity favors the hypothesis that GTA arises from the dedifferentiation of MDA.