前列腺基底细胞癌：29例临床病理分析

前列腺基底细胞增生性病变发生于移行区，表现为从基底细胞增生至基底细胞癌的增生性病变谱系。基底细胞增生有宽泛的形态学结构。由基底细胞组成的恶性肿瘤如果与涎腺的对应肿瘤有相同组织学特点，则被命名为“腺样囊性癌”或“腺样基底细胞肿瘤”；大多数缺乏这种相似性，多称为“基底细胞样癌”或“基底细胞癌”。作者研究了29例前列腺基底细胞癌，其中包括前列腺腺样囊性癌的病例。研究的目的是寻找基底细胞癌的形态学谱系的所有特点，以及免疫组化表型和长期生物学行为。     

涎腺基底细胞腺瘤和腺癌与腺样囊性癌的比较观察

目的 研究涎腺基底细胞腺瘤和基底细胞腺癌与腺样囊性癌的形态学特征、免疫表型和鉴别诊断。方法 对5例基底细胞腺瘤，5例基底细胞腺癌和7例腺样囊性癌进行了免疫组化和双重免疫电镜(2例)的观察。结果 基底细胞腺瘤和基底细胞腺癌在免疫表型方面非常相似；基底细胞腺瘤(癌)与腺样囊性癌之间在免疫表型和超微结构方面有一定的差别。结论 基底细胞腺瘤和基底细胞腺癌的鉴别诊断基于两者的生长方式和组织学特征。免疫组化和免疫电镜观察有助于基底细胞腺瘤(癌)与腺样囊性癌的鉴别诊断。     

前列腺基底细胞癌

前列腺基底细胞增生来自于移行区，形态学变化可从基底细胞增生到基底细胞癌。前列腺基底细胞癌比较少见，作者研究了29例基底细胞癌，病人年龄42～89岁（平均69岁）。组织学检查84％（24／29）病例为多种组织学构型，其中腺样囊样构型（AC—P）和小的实性巢伴巢周围细胞栅栏状排列是最主要的构型，各占64％。其他构型包括基底细胞增生样构型9例、小管状构型，部分管内侧偶见玻璃变的胶原纤维9例，其中4例混杂有条索状结构、大的实性巢8例，其中5例中央有坏死。[第一段]     

具有筛状结构的涎腺基底细胞腺瘤9例临床病理和分子遗传学分析

目的探讨具有筛状结构的涎腺基底细胞腺瘤(cribriform type of salivary basal cell adenoma, cSBCA)临床病理及分子遗传学特征。方法回顾性分析9例cSBCA的临床病理资料,采用免疫组化检测Ki-67、S-100、CD117、CK19、p63、SMA、β-catenin、LEF-1、E-cadherin及Cyclin D1的表达,应用FISH检测CTNNB1基因及MYB-NFIB融合基因。结果 9例cSBCA均有包膜,与周围组织分界清楚,筛状结构占10%～90%,主要分布于肿瘤边缘及包膜内,呈包膜内浸润性生长,大部分瘤巢的长轴与包膜呈平行关系,均未见神经、血管及周围组织侵犯。筛状结构由基底样/肌上皮样细胞构成,腔内见阿尔辛蓝阳性黏液物。免疫表型:Ki-67增殖指数1%～3%,β-catenin及LEF-1核阳性。分子遗传学显示均无CTNNB1扩增或缺失突变及MYB-NFIB融合基因。随访12～98个月,患者均无复发或转移。结论 cSBCA易被误诊为腺样囊性癌(adenoid cystic carcinoma, ACC),结合临床病理学特征可资鉴别。     

p63免疫组化染色在腺样囊性癌和基底样鳞状细胞癌鉴别诊断中的价值

腺样囊性癌与基底样鳞状细胞癌的鉴别有时非常困难，而诊断不明确则容易导致二者的治疗错误。p63作为一个新的上皮干细胞调控蛋白，可在人类多种正常组织如鳞状上皮、尿路上皮、乳腺和涎腺的肌上皮细胞等表达，也可表达于涎腺多形性腺瘤和癌中。为了探讨p63免疫组化染色在腺样囊性癌和基底样鳞状细胞癌鉴别诊断中的价值，     

前列腺基底细胞腺癌

目的：探讨前列腺基底细胞腺癌和腺瘤诊断和鉴别诊断标准。方法：对基底细胞腺瘤３例,基底细胞腺瘤１例,复习其临床和病理资料及进行随访。再次常规切片ＨＥ染色和采用ＬＳＡＢ法,对ＰＳＡ、ＰＡＰ、ＣＫ、ＣＥＡ、ＰＣＮＡ、ｂｃｌ－２、ｐ５３和ｃ－ｅｒｂＢ－２８种抗体标记结果进行观察。结果：前列腺基底细胞腺癌为分化差的帝体癌在底细胞癌样排列,核分裂象多,癌巢中央伴坏死,可见局灶性鳞状细胞,移行细胞或腺管分化,     

miR-98在涎腺腺样囊性癌组织中的表达及其对ACC-M细胞增殖、迁移的影响

目的探讨miR-98在涎腺腺样囊性癌组织中的表达及其对腺样囊性癌细胞系ACC-M增殖以及迁移能力的影响。方法通过实时PCR检测5例涎腺腺样囊性涎组织及癌旁正常组织miR-98的表达水平;将miR-98模拟物瞬时转入高转移腺样囊性癌细胞系(ACC-M)使miR-98过表达,并通过实时PCR方法验证;流式细胞仪分析转染后ACC-M细胞周期的改变,甲基噻唑基四唑比色法检测转染后ACC-M细胞的增殖,划痕实验检测转染后ACC-M细胞的迁移能力,免疫印迹法检测转染后ACC-M细胞细胞周期蛋白CyclinB与CDC2的表达变化。结果 miR-98在涎腺腺样囊性癌组织中的表达水平显著低于癌旁正常组织,P0.01。转染miR-98模拟物能够显著上调ACC-M细胞miR-98的表达水平,ACC-M细胞的S期比例明显下降,而G 0/G 1期的细胞明显增多,增殖受到明显抑制,迁移能力下降,显著降低ACC-M细胞CyclinB与CDC2的蛋白表达水平。结论过表达miR-98能够抑制涎腺腺样囊性癌细胞的增殖与迁移能力。     

miR-24-3p在涎腺腺样囊性癌组织中的表达及其对ACC-M细胞增殖、侵袭的影响

目的探讨miR-24-3p在涎腺腺样囊性癌组织中的表达及其对腺样囊性癌细胞系ACC-M增殖以及侵袭能力的影响。方法通过实时PCR检测5例涎腺腺样囊性涎组织及癌旁正常组织miR-24-3p的表达水平;将miR-24-3p模拟物瞬时转入高转移腺样囊性癌细胞系(ACC-M)使miR-24-3p过表达,并通过实时PCR方法验证;流式细胞仪分析转染后ACC-M细胞周期的改变,甲基噻唑基四唑比色法检测转染后ACC-M细胞的增殖,Transwell实验检测转染后ACC-M细胞的侵袭能力,蛋白质免疫印迹法检测转染后ACC-M细胞血小板源性生长因子受体B(PDGFRB)的表达变化。结果 miR-24-3p在涎腺腺样囊性癌组织中的表达水平显著低于癌旁正常组织。转染miR-24-3p mimics能够显著上调ACC-M细胞miR-24-3p的表达水平,ACC-M细胞的S期比例明显下降,而G_0/G_1期的细胞明显增多,增殖受到明显抑制,侵袭能力下降,显著降低ACC-M细胞PDGFRB的蛋白表达。结论 miR-24-3p在涎腺腺样囊性癌中低表达,过表达miR-24-3p能够抑制涎腺腺样囊性癌细胞的增殖与侵袭能力。     

涎腺腺样囊性癌预后因素与MYB基因融合及蛋白表达相关性的临床病理研究

正腺样囊性癌是涎腺常见的恶性肿瘤,复发率高和远期预后差。该文回顾性分析135例腺样囊性癌中MYB-NFIB基因融合和MYB蛋白的表达,并评估腺样囊性癌的预后因素,患者中位随访时间6.3年。5、10年局部无瘤生存率分别为94%和78%,5、10年远处转移生存率分别为77%和58%,     

子宫颈腺样基底细胞癌2例报道并文献复习

目的 探讨子宫颈腺样基底细胞癌的临床病理特点及其鉴别诊断.方法 应用组织学、免疫组织化学,对2例子宫颈腺样基底细胞癌进行分析,并复习相关文献.结果 2例子宫颈腺样基底细胞癌年龄均>50岁,无明显症状,为体检时发现.子宫颈无明显肿瘤外观,2例均行全子宫切除术.组织学:瘤细胞呈巢状、条索状向间质浸润性生长.瘤细胞体积小,形态一致,排列紧密,胞质稀少,胞核深染,瘤巢周边的细胞呈栅栏状排列,2例瘤巢中央见灶状腺腔样分化.其中例1伴灶状鳞状细胞分化及轻微的间质水肿,例2无明显间质反应.例1瘤细胞浸润深度2.8 mm,宽度6.5 mm;例2瘤细胞浸润深度3.5 mm,宽度2.5 mm,2例均伴CIN3.2例均随访1年,无异常发现.结论 子宫颈腺样基底细胞癌常伴有CIN,诊断需与腺样囊腺癌相鉴别.     

Features of basal cell carcinomas in basal cell nevus syndrome

Basal cell nevus syndrome (BCNS) is an autosomal dominant genodermatosis that is characterized by early onset basal cell carcinomas (BCCs) that define the disease and often lead to diagnosis of the underlying syndrome. The objective of this study was to investigate the anatomic location, subtypes, and impact of BCCs on a group of 61 individuals affected with BCNS attending a research colloquium. Fifty individuals had at least one prior BCC with 22 participants having over 100 lesions. The median age of syndrome diagnosis was 11 years and median age of first BCC was 16 years. Males had more lesions on the upper back, upper extremities, and M-zone of the face, while females had more lesions on the scalp, back, and lower extremities. Pigmented BCCs were concentrated on the neck, upper trunk, and extremities. Subjects with >100 lesions showed wider anatomic distribution. The number of BCCs did not correlate with any of the other major features of the syndrome. Eighty percent of affected individuals reported great concern related to BCCs, citing the limitations and morbidity of available treatments. Vigilant surveillance, which was found to be inconsistent for participants in this study, is warranted. Future work should include development of a consensus guideline on skin examinations and strategies to optimize therapy of BCCs in this syndrome.     

Clear cell basal cell carcinoma

We describe a case of clear cell basal cell carcinoma of the superficial type, presenting as a crusted eruption on the abdomen. Histological examination showed a solid proliferation of clear cells attached to the under-surface of an atrophied epidermis. In addition, distinct pagetoid infiltration was seen within the overlying epidermis. A focal connection between the clear cell portion and a deeper lying nodular basal cell carcinoma was demonstrated, elucidating the true nature of the lesion. Immunohistochemical studies and electronmicroscopy confirmed the epithelial derivation of the tumour. The clear cell appearance was due to multiple cytoplasmic electronlucent vacuoles which were not surrounded by membranes.     

The hedgehog pathway and basal cell carcinomas

Developmental pathways first elucidated by genetic studies in the fruit fly, Drosophila melanogaster, are conserved in vertebrates, and disruption of these pathways has been associated with various human congenital anomalies. Many developmental genes continue to play an important role in regulation of cell growth and differentiation after embryogenesis, and mutations in some of these genes can result in cancer. Basal cell carcinoma (BCC) of the skin is the most common type of cancer in humans. Although most BCCs are sporadic, in rare cases, individuals have a hereditary disease, Gorlin syndrome, that predisposes to multiple skin tumors as well as a variety of birth defects. Mutations in the human homolog of a Drosophila gene, patched, underlie Gorlin syndrome. Genetic studies in Drosophila show that patched is part of the hedgehog signaling pathway, important in determining embryonic patterning and cell fate in multiple structures of the developing embryo. Human patched is mutated in sporadic as well as hereditary BCCs, and inactivation of this gene is probably a necessary if not sufficient step for tumor formation. Delineation of the biochemical pathway in which patched functions may lead to rational medical therapy for skin cancer and possibly other tumors.     

Clear cell basal cell carcinoma with sialomucin deposition

Clear cell basal cell carcinoma (BCC) is a variant of BCC with a characteristic clear cell component that may occupy all or part of the tumor islands. Periodic acid-Schiff (PAS) staining for glycogen is variably positive, and mild deposition of sulfated mucin has been noted. However, to our knowledge, clear cell BCC with sialomucin deposition has not been reported. Here we report a case of clear cell BCC showing sialomucin deposition. The clear tumor cells stained with PAS and showed incomplete diastase-resistance. In addition, mucin staining with alcian blue was positive at pH 2.5 but not at pH 0.5.     

Role of apoptosis in basal cell and squamous cell carcinoma formation

Long-term ultraviolet-light (UV) exposure of human skin epidermis is associated with an increased risk for the development of skin cancers, such as melanoma, basal cell carcinoma (BCC) and squamous cell carcinoma (SCC). UV radiation not only induces DNA damage in epidermal cells, it also interferes with skin homeostasis, which is maintained by a unique distribution pattern of apoptosis-inducing and -preventing molecules. If the DNA damage is not repaired or the damaged cells are not eliminated by apoptosis, the consequence can be cell transformation, uncontrolled proliferation and eventually skin tumor formation. An important "repair" gene is the p53 suppressor gene. Excessive UV exposure can mutate the p53 gene leading to the loss of its repair function and thus apoptosis resistance of the DNA-damaged cell. For BCC formation an additional pathway has been identified. Mutation of genes of the Hedgehog signaling pathway evokes the downregulation of apoptotic genes and upregulation of anti-apoptotic genes preventing the elimination of damaged cells. In addition, BCC and SCC strongly express the apoptosis-inducing Fas-ligand (FasL) which may help the tumor to escape the attack of immune effector cells. Silencing the genes involved in tumor formation by RNA interference might become a promising new approach to treat skin tumors.     

Why classify basal cell carcinomas?

Basal cell carcinoma of the skin is the commonest form of cancer in the white population. A simple pathological classification is presented and recommended for general use to aid clinicians in their management of cases. Basal cell carcinoma can be classified as nodular, infiltrative, superficial apparently multifocal and mixed in terms of the histological growth pattern. These patterns can be related to the likelihood of complete excision and, if excision is incomplete, to the frequency of recurrence.