The benign mimickers of prostatic acinar adenocarcinoma

As the most frequent malignant histological subtype in prostatic cancer, prostatic acinar adenocarcinoma （PAA） has a series of benign mimickers including prostatic or non-prostatic lesions and normal structures, which may lead to an erroneous diagnosis and inappropriate treatment. It is very important to be aware of the existence of these mimickers and to recognize their histological features. The differential diagnosis should be based on a comprehensive evaluation of clinical history, histological structure, cytological morphology and the results of immunohistochemistry （IHC） straining, rather than on single criteria （e.g., the presence of prominent nueleoli or basal cell layer）.

Comparison of pancreatic acinar cell carcinoma and adenocarcinoma using multidetector-row computed tomography

AIM:To distinguish acinar cell carcinoma(ACC)from pancreatic adenocarcinoma(AC)by comparing their computed tomography findings.METHODS:Patients with ACC and AC were identified on the basis of results obtained using surgically resected pancreatectomy specimens.The preoperative computer tomographic images of 6 acinar cell carcinoma patients and 67 pancreatic adenocarcinoma patients in 4 phases(non-contrast,arterial,portal venous,and delayed phase)were compared.The scan delay times were 40,70,and 120 s for each contrast-enhanced phase.The visual pattern,tomographic attenuation value,and time attenuation curve were assessed and compared between AC and ACC cases using the 2test,Wilcoxon signed-rank test,and Mann Whitney U test.RESULTS:The adenocarcinomas tended to be hypodense in all 4 phases.The acinar cell carcinomas also tended to be hypodense in the 3 contrast-enhancedphases,although their computed tomographic attenuation values were higher.Further,5 of the 6 acinar cell carcinomas(83%)were isodense in the non-contrast phase.The time attenuation curve of the adenocarcinomas showed a gradual increase through the 4 phases,and all adenocarcinomas showed peak enhancement during the delayed phase.The time attenuation curve of the acinar cell carcinomas showed peak enhancement during the portal venous phase in 4 cases and during the arterial phase in 2 cases.None of the 6 acinar cell carcinomas showed peak enhancement during the delayed phase.CONCLUSION:The tumor density in the non-contrast phase and time attenuation curve pattern clearly differ between acinar cell carcinomas and adenocarcinomas,and multidetector-row computed tomography can thus distinguish these tumors.

Therapeutic potential of targeting acinar cell reprogramming in pancreatic cancer

Pancreatic ductal adenocarcinoma(PDAC) is a common pancreatic cancer and the fourth leading cause of cancer death in the United States. Treating this life-threatening disease remains challenging due to the lack of effective prognosis, diagnosis and therapy. Apart from pancreatic duct cells, acinar cells may also be the origin of PDAC. During pancreatitis or combined with activating KRasG12 D mutation, acinar cells lose their cellular identity and undergo a transdifferentiation process called acinarto-ductal-metaplasia(ADM), forming duct cells which may then transform into pancreatic intraepithelial neoplasia(Pan IN) and eventually PDAC. During ADM, the activation of mitogen-activated protein kinases, Wnt, Notch and phosphatidylinositide 3-kinases/Akt signaling inhibits the transcription of acinar-specific genes, including Mist and amylase, but promotes the expression of ductal genes, such as cytokeratin-19. Inhibition of this transdifferentiation process hinders the development of Pan IN and PDAC. In addition, the transdifferentiated cells regain acinar identity, indicating ADM may be a reversible process. This provides a new therapeutic direction in treating PDAC through cancer reprogramming. Many studies have already demonstrated the success of switching Pan IN/PDAC back to normal cells through the use of PD325901, the expression of E47, and the knockdown of Dickkopf-3. In this review, we discuss the signaling pathways involved in ADM and the therapeutic potential of targeting reprogramming in order to treat PDAC.

SFRP1蛋白在前列腺腺癌中的表达及意义

目的:探讨分泌型卷曲相关蛋白1(Secreted Frizzled-related Proteins 1,SFRP1)在前列腺腺癌中的表达情况,并分析其与临床病理参数的关系。方法:采用免疫组化PV-9000二步法检测52例前列腺腺癌和68例良性前列腺增生组织中的SFRP1蛋白的表达。结果:在前列腺腺癌组织中SFRP1蛋白的阳性表达率为23.08%,显著低于良性前列腺增生组织的80.88%(X^2=39.928,P<0.001)。SFRP1蛋白的失表达与前列腺腺癌Gleason评分呈负相关(P<0.05),而与患者年龄、术前血PSA值、TNM分期、是否有骨转移均无关(X^2=0.177、1.915、0.751、1.631,P=0.739、0.200、0.513、0.300)。结论:SFRP1蛋白表达的降低及其对Wnt信号通路抑制作用的减弱,与前列腺腺癌的发生密切相关。

导管腺癌在前列腺癌中的研究进展

导管腺癌是前列腺癌的一种组织学亚型,因其独特的来源、形态学和病理特征而被公认为是一种不同于经典腺泡腺癌的独特病理类型。目前对导管腺癌的诊断主要是依据组织形态学,尚无确切的最佳治疗策略,其在前列腺癌中的预后价值亦不明确。本文通过回顾对导管腺癌的认识及其发展、病理特征和诊断标准、鉴别诊断、临床表现、治疗方法和预后,阐述导管腺癌在前列腺癌中的研究进展,探讨其在前列腺癌预后中的价值。

原发性前列腺平滑肌肉瘤合并腺泡腺癌1例报告

原发性前列腺平滑肌肉瘤罕见。本文报道1例前列腺平滑肌肉瘤合并腺泡腺癌。患者PSA异常升高,MRI检查提示前列腺恶性肿瘤,经会阴前列腺穿刺活检病理诊断平滑肌肉瘤。遂行腹腔镜根治性前列腺切除术,术后病理确诊为前列腺平滑肌肉瘤+腺泡腺癌。术后随访20个月未见复发和转移。

基于多排螺旋CT影像特征的胰腺腺泡细胞癌与胰腺导管腺癌的鉴别诊断

目的探讨基于多排螺旋CT(MDCT)影像特征的胰腺腺泡细胞癌(PACC)与胰腺导管腺癌(PDAC)的鉴别诊断。方法回顾性分析2013年11月至2021年4月间海军军医大学第一附属医院经手术病理证实的26例PACC(PACC组)和145例胰腺导管腺癌(PDAC组)患者的临床、病理学和影像学资料,比较两组患者的肿瘤位置、肿瘤大小、主胰管扩张、胆总管扩张、胰腺炎、淋巴结转移、囊肿、实质萎缩、侵犯十二指肠、侵犯胆总管及血管侵犯等影像特征,单因素及多因素logistic回归分析诊断PACC的独立预测因子。结果PACC组与PDAC组的肿瘤大小、胆总管扩张、淋巴结转移、实质萎缩、血管侵犯的差异均有统计学意义(P值均<0.05)。多因素回归分析结果显示,肿瘤大小(OR=1.07,95%CI1.028~1.105,P=0.001)、淋巴结转移(OR=0.23,95%CI0.065~0.800,P=0.02)、实质萎缩(OR=0.15,95%CI0.048~0.490,P=0.002)与PACC呈显著相关。结论依据MDCT影像特征评估的肿瘤大小、胆管扩张、淋巴结转移、实质萎缩、血管侵犯在PACC与PDAC的鉴别诊断中具有一定价值,其中肿瘤大小、淋巴结转移、实质萎缩是诊断PACC的独立预测因素。