235例卵巢畸胎瘤临床病理分析

目的：探讨卵巢畸胎瘤的临床病理特点。方法：对235例卵巢畸胎瘤患者的临床病理资料进行分析。结果：235例卵巢畸胎瘤病例中各个年龄均有发生,以20—40岁多发。其中卵巢成熟性囊性畸胎瘤228例,占97％;卵巢未成熟性畸胎瘤4例,占1．7％;卵巢成熟性囊性畸胎瘤恶变2例,占0．9％;卵巢畸胎瘤伴甲状腺类癌1例,占0．4％。结论：卵巢畸胎瘤绝大多数为良性,应及时手术,以减少并发症的发生,未成熟畸胎瘤及恶变者较少,应结合临床综合治疗。     

卵巢成熟性畸胎瘤恶变临床病理分析

目的:探讨卵巢成熟性囊性畸胎瘸恶变的临床病理特点.方法:收集8例卵巢成熟性囊性畸胎瘤恶变肿瘤,分析病变的临床表现、病理特征分期及随访结果.结果:卵巢成熟性囊性畸胎瘤恶变多发生于绝经后女性.8例中2例为类癌,2例为恶性甲状腺,1例黏液腺癌,1例上皮内癌,1例甲状腺肿类癌,1例鳞状细胞癌.8例均为临床Ⅰ期,除1例死亡外,其余7例均无瘤生存.结论:卵巢成熟性囊性畸胎瘤恶变率低,病理检查需细致全面,结合临床综合治疗1期患者预后良好.     

卵巢原发性类癌的临床病理观察

目的探讨卵巢类癌的临床病理、免疫组化特点及其与预后的关系。方法对10例卵巢类癌临床及病理资料进行复习,应用SP法免疫组织化学染色并随访。结果患者年龄26-72岁。肿块部位：右侧卵巢7例,左侧卵巢3例。光镜下癌细胞大小、形状、染色较一致,排列呈实性小巢状或岛状、梁状、腺泡状。10例CK、Syn均为（＋）,7例NSE、CgA为（＋）。TG、TTF-1、α-inhibin、ER和PR均（-）。7例获随访者均存活。结论卵巢类癌是少见的卵巢单胚层畸胎瘤,生物学行为低度恶性,需结合组织病理形态、免疫组织化学染色和临床资料对卵巢原发性类癌进行诊断和鉴别诊断。     

235例卵巢畸胎瘤临床病理分析

目的:探讨卵巢畸胎瘤的临床病理特点.方法: 对235例卵巢畸胎瘤患者的临床病理资料进行分析.结果: 235例卵巢畸胎瘤病例中各个年龄均有发生,以20-40岁多发.其中卵巢成熟性囊性畸胎瘤228例,占97%;卵巢未成熟性畸胎瘤4例,占1.7%;卵巢成熟性囊性畸胎瘤恶变2例,占0.9%;卵巢畸胎瘤伴甲状腺类癌1例,占0.4%.结论:卵巢畸胎瘤绝大多数为良性,应及时手术,以减少并发症的发生,未成熟畸胎瘤及恶变者较少,应结合临床综合治疗.     

卵巢原发甲状腺肿类癌的临床病理分析

目的:探讨卵巢原发甲状腺肿类癌的临床病理特征.方法:观察和分析2例卵巢原发甲状腺肿类癌病例的病理组织学及免疫表型的特点,并复习相关文献进行讨论.结果:例1卵巢类癌伴有成熟性囊性畸胎瘤成分,例2为单纯甲状腺肿类癌,类癌成分呈岛状与小梁状生长,甲状腺滤泡成分与类癌相互混杂.类癌的细胞比较一致,胞浆嗜酸性,染色质均匀,核分裂象少见.免疫组化2例类癌成分CK(+),CK19(+),CD56(+),NSE(+),Syn(+),TTF-1和TG散在阳性,甲状腺成分TTF-1(+)、TG(+).卵巢甲状腺肿类癌应与甲状腺癌鉴别,甲状腺癌的肿瘤细胞有高分裂活性,没有神经内分泌分化,细胞岛状或梁状分布不明显.结论:卵巢甲状腺肿类癌是罕见的低度恶性肿瘤,预后较好,病理形态学观察和免疫组化染色有助于明确诊断.     

卵巢甲状腺肿类癌的临床病理分析

卵巢甲状腺肿类癌是由甲状腺组织和类癌组织密切混合构成的卵巢生殖细胞肿瘤[1]。自1970年Scully提出此命名以来,国内外报道鲜见[2]。本研究分析了7例卵巢甲状腺肿类癌患者的临床资料,并结合文献对其临床及病理学特点进行分析,以提高对这一疾病的认识。1临床资料1.1临床表现收集2001-01-01-2011-03-31中国医科大学附属盛京医院病理科卵巢甲状腺肿类癌7例,其中6例伴囊性成熟型畸胎瘤。患者均为女性。年龄34~65岁,平均年龄     

卵巢甲状腺肿性类癌并畸胎瘤一例报告（个案报告）

 病例报告 患者，女性，36 岁。因体检发现右附件包块于2005年8月1日入院，平素月经规律，无自觉症状。妇科检查：右侧附件区可扪及约6 cm×6 cm×5 cm大小包块，活动度好，边界清楚，质地中等，无压痛。超声示右侧卵巢肿瘤。8月4日行手术治疗，术中见右侧卵巢肿块为囊实性，包膜完整与周围组织无粘连，盆腔未见种植和转移。病理检查巨检：肿瘤大小为7 cm×6 cm×5 cm，包膜完整， 切面为多房性，分叶状、内见毛发、皮脂等畸胎瘤成分及灰黄色结节，无出血、坏死。镜检示：肿瘤由甲状腺和类癌组织混合组成，有畸胎瘤和软骨成分。类癌细胞以梁状结构为主，混有小管状结构，细胞呈短梭性，大小较一致，胞质丰富，嗜酸，核为卵圆胞，染色质均细，核仁不明显。混有大小不等甲状腺腺泡，腺泡内衬扁平和立方上皮，腺腔内胶质丰富。甲状腺滤泡的数量在肿瘤的不同区域差别很大。免疫组化染色：神经内分泌标记syn（突触素）、cgA（嗜铬蛋白A）阳性，甲状腺腺泡TG阳性。病理诊断：右侧卵巢甲状腺类癌合并囊性成熟性畸胎瘤。 讨论 卵巢甲状腺肿性类癌是非常罕见的卵巢生殖细胞肿瘤，由类癌和卵巢甲状腺肿两种成分构成。1970 年由Scully首先提出，迄今为止，国外报告约100余例，国内由范娜娣首报，至今约10例左右[1]。本病发病年龄21～77岁，40岁以上占2／3。临床上自觉症状不明显，可有下腹疼痛及月经不调，少数病例可伴有甲状腺功能亢进、男性化等症状，很少发生类癌综合征。其病理学特征独特，组织起源尚有争议。WHO（2003）肿瘤分类中将其归入单胚层畸胎瘤，认为肿瘤中的两种成分均为畸胎瘤内胚层起源。其中类癌成分含有淀粉样物及神经内分泌性颗粒，类似于甲状腺髓样癌，提示其来源于甲状腺滤泡旁细胞。也有人根据其类癌形态主要为梁状，认为是由内胚层的后肠或支气管上皮转化而来[2]。Robboy等[3]根据肿瘤的生长方式及所在部位将其分为三型：（1）瘤壁结节型，直径1～8 cm，位于皮样囊肿壁内，并突向囊腔。偶见瘤组织呈弥漫性分布，囊壁增厚。（2）纯型，肿瘤直径为012～20 cm，质地均匀，肿瘤内的类癌区呈灰白色或灰黄色，可有出血及坏死灶，甲状腺滤泡腔区充盈胶样物质。（3）混合型，类癌与畸胎瘤或其他肿瘤成分混合，本例即属于此型。通常畸胎瘤为囊性，囊内可见毛发及皮脂样物质，其他肿瘤则多为囊腺瘤。该瘤类癌成分中的腺泡样结构易与颗粒细胞瘤的Call-Exner 小体混淆，支持-间质细胞瘤具有小管或条索状瘤巢，也易与本瘤中小梁及岛状类癌成分混淆，免疫组化syn、CgA、TG染色有助于鉴别。本病预后良好，几乎全部为Ⅰ期，多为单侧，一般不转移[4]。手术无论行单纯患侧附件切除或双侧附件及子宫切除术，其预后相似。因此，若患者年轻，对侧卵巢无异常，行患侧附件切除术即可。若肿瘤内滤泡呈乳头状腺癌或滤泡癌变时，则术后应辅以化疗或放疗。     

卵巢囊性畸胎瘤伴恶性黑色素瘤及良性黑色素痣各1 例报告及文献复习

 引言 卵巢囊性畸胎瘤在临床上比较多见,但囊性畸胎瘤伴有黑色素成分的病例极为罕见,至今国内外报道的卵巢囊性畸胎瘤伴恶性黑色素瘤的病例不到20 例[1] ,卵巢畸胎瘤伴良性色素痣的更少。因其组织发生不甚明确,临床表现与其他卵巢肿瘤相比无明显特殊,故术前确诊比较困难。本文报告卵巢囊性畸胎瘤伴恶性黑色素瘤1例及卵巢囊性畸胎瘤伴良性黑色素痣1例,并结合文献对其组织发生、临床及病理特征等进行探讨。     

囊性肾透明细胞癌1例及文献复习

目的：探讨囊性肾透明细胞癌的临床病理特征、诊断及鉴别诊断。方法：对1例囊性肾透明细胞癌进行光镜观察,行组织化学及免疫组化染色,并复习文献。结果：肿瘤细胞主要由透明细胞组成。癌细胞免疫表型Ckpan、EMA、CEA呈阳性表达,CD68阴性。结论：囊性肾透明细胞癌是一种罕见的肾癌病理类型。其诊断依赖组织病理学和免疫组化标记。     

卵巢甲状腺肿类癌5例临床病理分析

原发性卵巢类癌因组织形态不同,可分为岛状型、梁索型、甲状腺肿型、黏液型及混合型等。甲状腺肿类癌(strumal carci-noid)属于生殖细胞肿瘤中单胚层高度特殊性的畸胎瘤,由不同比例的甲状腺组织和类癌混合而成,绝大部分为原发且预后良好[1]。我们就本院近年收治的5例甲状腺肿类癌病例进行分析回顾。     

胸腺类癌1例及文献复习

目的：探讨胸腺类癌的病理学特点及临床表现。方法：对1例胸腺类癌进行组织学表现、电镜和免疫组化染色观察及文献复习。结果：组织学特点：瘤细胞多排列为不规则巢状,条索状,伴有大量坏死,瘤细胞大小较一致,胞质弱嗜酸,颗粒状,边界不清,胞核呈圆形或椭圆。免疫组化特点：肿瘤细胞表达Syn（＋）、CgA（＋）、NSE（＋）。电镜：部分瘤细胞及突起内见有神经内分泌颗粒。结论：胸腺类癌是前纵隔一种少见的恶性肿瘤,主要与胸腺瘤相鉴别,治疗以手术切除的疗效为最好。     

Renal carcinoid tumor: An immunohistochemical and molecular genetic study of four cases

Few genetic studies of renal carcinoid tumor have been conducted thus far. We performed immunohistochemical and genetic examinations on four renal carcinoid tumors. Histologically, the tumors consisted of neoplastic cells with round to oval nuclei. Various growth patterns such as tightly packed cords and trabeculae, ribbon-like, trabecular, sheet-like or solid growth were observed. Nuclear chromatin showed a coarse and granular pattern. Immunohistochemically, tumors were positive for chromogranin A and synaptophysin. In the fluorescence in situ hybridization study, three of four tumors revealed monosomy of chromosome 3 (D3Z1), but one tumor showed monosomy of chromosome 13 (D13S319/13q34). Using PCR amplification and fragment analysis of three microsatellite markers (D3S1300, D3S666 and D3S1768) of chromosome arm 3p, one tumor showed loss of heterozygosity at D3S1300 and D3S1768, one tumor was not informative and the analysis of two tumors failed due to low DNA quality. In three cases, the VHL gene status was tested. Two tumors showed wild-type, but the analysis of one tumor failed to provide adequate results. In conclusion, we suggest that the abnormality of chromosome 3 is involved in the pathogenesis of renal carcinoid tumor.     

Trichoadenoma in a mature Cystic Teratoma: A Rare Finding

Skin adnexal tumors arising in dermoid cysts of the ovary are exceedingly rare. We report a trichoadenoma arising in a dermoid cyst in a 42-year-old female. The histopathology of trichoadenoma has also been described briefly. Mature teratomas, which are almost all cystic (dermoid cysts), account for approximately 25% of all ovarian tumors, and 30% of benign ovarian tumors. They usually develop in children or women of the reproductive age group. Histologically, they are composed of variable proportions of tissue originating from the ectoderm, mesoderm, and endoderm. Cystic cavities are lined by mature epidermis. Although skin appendages and neural tissue are extremely common, there are only few case reports of skin adnexal tumors arising in a mature teratoma. We report a case of ovarian teratoma with a trichoadenoma. To the best of the authors' knowledge, this is the first report describing this rare benign skin adnexal tumor, in a mature cystic teratoma of the ovary. Keywords: trichoadenoma, mature cystic teratoma.     

肾上腺成熟畸胎瘤的临床特征及治疗

目的探讨肾上腺成熟畸胎瘤的临床特征及治疗方法。方法回顾性分析6例经手术切除肿瘤、术后结合病理证实为肾上腺成熟畸胎瘤患者的临床、影像、病理学特点,评价手术治疗效果。结果6例患者中,肿块位于左侧肾上腺2例,右侧4例;患侧腰痛3例,体检发现肾上腺肿物3例。6例患者均无高血压史。CT平扫检查示肿物位于肾上腺区域,为椭圆形或哑铃状的囊、实性混合包块,其直径3～6cm,内有钙化灶,多表现为斑块状或弧形,包块内可见脂肪样密度灶。B型超声示肾上腺区囊实性肿物,边界清晰。CT增强后肿物边缘和内部软组织成分可见强化。病理示镜下可见钙化、软骨、脂肪、鳞状上皮及黏液柱状上皮等。6例患者均行肾上腺肿瘤切除,术中见肿瘤边界清楚,血供不丰富。术后随访1—8年未见肿瘤复发。结论成熟畸胎瘤发生于肾上腺罕见,以女性多见,多发于年轻人,临床症状不典型,对其术前诊断主要依靠影像学检查。肾上腺成熟畸胎瘤宜行手术切除,预后良好。     

Germ cell origin of testicular carcinoid tumors.

PURPOSE: Carcinoids are neuroendocrine tumors and most frequently occur within tissues derived from the embryonic gut. These tumors can occur in any organ site but are rare in the testis. The cell type giving rise to testicular carcinoid is unknown. We hypothesized that testicular carcinoid may have a germ cell origin. EXPERIMENTAL DESIGN: We describe our analysis of protein and genetic markers of germ cell neoplasia, using immunohistochemistry and fluorescence in situ hybridization, in four testicular carcinoid tumors. RESULTS: All four cases of testicular carcinoid tumor arose in a background of mature teratoma. Isochromosome 12p was identified in carcinoid tumor cells in all four samples. 12p overrepresentation was also observed in three cases. Isochromosome 12p and 12p overrepresentation were present in cells of coexisting mature teratoma in three cases. Carcinoid tumors showed strong immunoreactivity for synaptophysin and chromogranin, but no immunoreactivity for OCT4, CD30, c-kit, TTF-1, and CDX2. Membranous and cytoplasmic staining for beta-catenin was detected in three cases. CONCLUSION: Our findings suggest that testicular carcinoid represents a phenotypic expression of testicular teratoma and is of germ cell origin.     

Familial pulmonary carcinoid tumors

BACKGROUND: Pulmonary carcinoid tumors are rare and usually occur sporadically. Infrequently, they arise in association with multiple endocrine neoplasia type 1 (MEN1). Familial pulmonary carcinoid tumors not associated with MEN1 have not been described. METHODS: Two sets of first-degree relatives diagnosed with primary pulmonary carcinoid tumors with no clinical features of MEN1 were identified in a pair of siblings and in a mother and daughter. Mutations in the MEN1 gene were sought using polymerase chain reaction analysis on paraffin embedded tissue from two members of one of the families. RESULTS: Histopathologic and immunohistochemical studies confirmed the diagnoses of carcinoid tumors. None of these patients and no family members had features of MEN1. DNA analysis did not detect germline mutations in the MEN1 gene. CONCLUSIONS: The occurrence of familial pulmonary carcinoid tumors in the absence of MEN1 suggests a novel, rare germline mutation specific to the development of pulmonary carcinoids.