molecular pathology of intraductal papillary mucinous neoplasms of the pancreas

Since the first description of intraductal papillary mucinous neoplasms(IPMNs)of the pancreas in the eighties,their identification has dramatically increased in the last decades,hand to hand with the improvements in diagnostic imaging and sampling techniques for the study of pancreatic diseases.However,the heterogeneity of IPMNs and their malignant potential make difficult the management of these lesions.The objective of this review is to identify the molecular characteristics of IPMNs in order to recognize potential markers for the discrimination of more aggressive IPMNs requiring surgical resection from benign IPMNs that could be observed.We briefly summarize recent research findings on the genetics and epigenetics of intraductal papillary mucinous neoplasms,identifying some genes,molecular mechanisms and cellular signaling pathways correlated to the pathogenesis of IPMNs and their progression to malignancy.The knowledge of molecular biology of IPMNs has impressively developed over the last few years.A great amount of genes functioning as oncogenes or tumor suppressor genes have been identified,in pancreatic juice or in blood or in the samples from the pancreatic resections,but further researches are required to use these informations for clinical intent,in order to better define the natural history of these diseases and to improve their management.

European vs 2015-World Health Organization clinical molecular and pathological classification of myeloproliferative neoplasms

The BCR/ABL fusion gene or the Ph^1-chromosome in the t(9;22)(q34;q11)exerts a high tyrokinase acticity,which is the cause of chronic myeloid leukemia(CML).The1990 Hannover Bone Marrow Classification separated CML from the myeloproliferative disorders essential thrombocythemia(ET),polycythemia vera(PV)and chronic megakaryocytic granulocytic myeloproliferation(CMGM).The 2006-2008 European Clinical Molecular and Pathological(ECMP)criteria discovered 3variants of thrombocythemia:ET with features of PV(prodromal PV),"true"ET and ET associated with CMGM.The 2008 World Health Organization(WHO)-ECMP and 2014 WHO-CMP classifications defined three phenotypes of JAK2^(V617F)mutated ET:normocellular ET(WHO-ET),hypercelluar ET due to increased erythropoiesis(prodromal PV)and ET with hypercellular megakaryocytic-granulocytic myeloproliferation.The JAK2^(V617F)mutation load in heterozygous WHO-ET is low and associated with normal life expectance.The hetero/homozygous JAK2^(V617F)mutation load in PV and myelofibrosis is related to myeloproliferative neoplasm(MPN)disease burden in terms of symptomaticsplenomegaly,constitutional symptoms,bone marrow hypercellularity and myelofibrosis.JAK2 exon 12mutated MPN presents as idiopathic eryhrocythemia and early stage PV.According to 2014 WHO-CMP criteria JAK2 wild type MPL^(515)mutated ET is the second distinct thrombocythemia featured by clustered giant megakaryocytes with hyperlobulated stag-horn-like nuclei,in a normocellular bone marrow consistent with the diagnosis of"true"ET.JAK2/MPL wild type,calreticulin mutated hypercellular ET appears to be the third distinct thrombocythemia characterized by clustered larged immature dysmorphic megakaryocytes and bulky(bulbous)hyperchromatic nuclei consistent with CMGM or primary megakaryocytic granulocytic myeloproliferation.

PVSG and WHO vs European Clinical,Molecular and Pathological Criteria for prefibrotic myeloproliferative neoplasms

The Polycythemia Vera Study Group(PVSG),World Health Organization(WHO) and European Clinical,Molecular and Pathological(ECMP) classifications agree upon the diagnostic criteria for polycythemia vera(PV) and advanced primary myelofibrosis(MF). Essential thrombocythemia(ET) according to PVSG and 2007/2008 WHO criteria comprises three variants of JAK2V617 F mutated ET when the ECMP criteria are applied. These include normocellular ET,hypercellular ET with features of early PV(prodromal PV),and hypercellular ET due to megakaryocytic,granulocytic myeloprolifera-tion(ET.MGM). Evolution of prodromal PV into overt PV is common. Development of MF is rare in normocellular ET(WHO-ET) but rather common in hypercellular ET.MGM. The JAK2V617 F mutation burden in heterozygous mutated normocellular ET and in heterozygous/homozygous or homozygous mutated PV and ET.MGM is of major prognostic significance. JAK2/MPL wild type ET associated with prefibrotic primary megakaryocytic and granulocytic myeloproliferation(PMGM) is characterized by densely clustered immature dysmorphic megakaryocytes with bulky(bulbous) hyperchromatic nuclei,which are never seen in JAK2V617 F mutated ET,and PV and also not in MPL515 mutated normocellular ET(WHO-ET). JAK2V617 mutation burden,spleen size,LDH,circulating CD34+ cells,and pre-treatment bone marrow histopathology are mandatory to stage the myeloproliferative neoplasms ET,PV,PMGM for proper prognosis assessment and therapeutic implications. MF itself is not a disease because reticulin fibrosis and reticulin/collagen fibrosis are secondary responses of activated polyclonal fibroblasts to cytokines released from the clonal myeloproliferative granulocytic and megakaryocytic progenitor cells in ET.MGM,PV and PMGM.

Pathological features and diagnosis of intraductal papillary mucinous neoplasm of the pancreas

Intraductal papillary mucinous neoplasm(IPMN) of the pancreas is a noninvasive epithelial neoplasm of mucinproducing cells arising in the main duct(MD) and/or branch ducts(BD) of the pancreas.Involved ducts are dilated and filled with neoplastic papillae and mucus in variable intensity.IPMN lacks ovarian-type stroma,unlike mucinous cystic neoplasm,and is defined as a grossly visible entity(≥ 5 mm),unlike pancreatic intraepithelial neoplasm.With the use of high-resolution imaging techniques,very small IPMNs are increasingly being identified.Most IPMNs are solitary and located in the pancreatic head,although 20%-40% are multifocal.Macroscopic classification in MD type,BD type and mixed or combined type reflects biological differences with important prognostic and preoperative clinical management implications.Based on cytoarchitectural atypia,IPMN is classified into low-grade,intermediategrade and high-grade dysplasia.Based on histological features and mucin(MUC) immunophenotype,IPMNs are classified into gastric,intestinal,pancreatobiliary and oncocytic types.These different phenotypes can be observed together,with the IPMN classified according to the predominant type.Two pathways have been suggested:gastric phenotype corresponds to less aggressive uncommitted cells(MUC1-,MUC2-,MUC5 AC +,MUC6 +) with the capacity to evolve to intestinal phenotype(intestinal pathway)(MUC1-,MUC2 +,MUC5 AC +,MUC6- or weak +) or pancreatobiliary /oncocytic phenotypes(pyloropancreatic pathway)(MUC1 +,MUC 2-,MUC5 AC +,MUC 6 +) becoming more aggressive.Prognosis of IPMN is excellent but critically worsens when invasive carcinoma arises(about 40% of IPMNs),except in some cases of minimal invasion.The clinical challenge is to establish which IPMNs should be removed because of their higher risk of developing invasive cancer.Once resected,they must be extensively sampled or,much better,submitted in its entirety for microscopic study to completely rule out associated invasive carcinoma.

Intraductal papillary-mucinous neoplasia of the pancreas:Histopathology and molecular biology

Intraductal papillary-mucinous neoplasm(IPMN) of the pancreas is a clinically and morphologically distinctive precursor lesion of pancreatic cancer,characterized by gradual progression through a sequence of neoplastic changes.Based on the nature of the constituting neoplastic epithelium,degree of dysplasia and location within the pancreatic duct system,IPMNs are divided in several types which differ in their biological properties and clinical outcome.Molecular analysis and recent animal studies suggest that IPMNs develop in the context of a field-defect and reveal their possible relationship with other neoplastic precursor lesions of pancreatic cancer.

The accuracy of magnetic resonance imaging and ultrasound in evaluating the size of early-stage breast neoplasms

Objective Breast cancer is the most frequently diagnosed cancer in women. Accurate evaluation of the size and extent of the tumor is crucial in selecting a suitable surgical method for patients with breast cancer. Both overestimation and underestimation have important adverse effects on patient care. This study aimed to evaluate the accuracy of breast magnetic resonance imaging(MRI) and ultrasound(US) examination for measuring the size and extent of early-stage breast neoplasms.Methods The longest diameter of breast tumors in patients with T_(1–2)N_(0–1)M_0 invasive breast cancer preparing for breast-conserving surgery(BCS) was measured preoperatively by using both MRI and US and their accuracy was compared with that of postoperative pathologic examination. If the diameter difference was within 2 mm, it was considered to be consistent with pathologic examination.Results A total of 36 patients were imaged using both MRI and US. The mean longest diameter of the tumors on MRI, US, and postoperative pathologic examination was 20.86 mm ± 4.09 mm(range: 11–27 mm), 16.14 mm ± 4.91 mm(range: 6–26 mm), and 18.36 mm ± 3.88 mm(range: 9–24 mm). US examination underestimated the size of the tumor compared to that determined using pathologic examination(t = 3.49, P < 0.01), while MRI overestimated it(t =-6.35, P < 0.01). The linear correlation coefficients between the image measurements and pathologic tumor size were r = 0.826(P < 0.01) for MRI and r = 0.645(P < 0.01) for US. The rate of consistency of MRI and US compared to that with pathologic examination was 88.89% and 80.65%, respectively, and there was no statistically significant difference between them(χ~2 = 0.80, P > 0.05).Conclusion MRI and US are both effective methods to assess the size of breast tumors, and they maintain good consistency with pathologic examination. MRI has a better correlation with pathology. However, we should be careful about the risk of inaccurate size estimation.

Intraductal papillary mucinous neoplasm originating from a jejunal heterotopic pancreas:A case report

BACKGROUND Intraductal papillary mucinous neoplasm(IPMN)is a rare pancreatic tumor and has the potential to become malignant.Surgery is the most effective treatment at present,but there is no consensus on the site of resection.Heterotopic pancreas occurs in the gastrointestinal tract,especially the stomach and duodenum but is asymptomatic and rare.We report a case of ectopic pancreas with IPMN located in the jejunum.CASE SUMMARY A 56-year-old male patient suffered from severe pain,nausea and vomiting due to a traffic accident and sought emergency treatment at our hospital.Contrast-enhanced computed tomography of the whole abdomen suggested splenic congestion,which was considered to be splenic rupture.Emergency laparotomy was performed,and the ruptured spleen was removed during the operation.Unexpectedly,a cauliflower-like mass of about 2.5 cm×2.5 cm in size was incidentally found about 80 cm from the ligament of Treitz during the operation.A partial small bowel resection was performed,and postoperative pathology confirmed the small bowel mass as heterotopic pancreas with low-grade IPMN.CONCLUSION Ectopic pancreas occurs in the jejunum and is pathologically confirmed as IPMN after surgical resection.

中老年肠道炎性肌纤维母细胞瘤临床病理及预后特点

目的探讨中老年肠道炎性肌纤维母细胞瘤(inflammatory myofibroblastic tumours,IMT)的临床病理及预后特点。方法回顾性分析5例中老年肠道IMT的临床、病理形态、免疫表型及随访结果。结果4例IMT发生在右半结肠,1例在回肠。3/5患者有肠道损伤史,首发消化道症状且白细胞增高。瘤组织由梭形肌纤维母细胞和纤维母细胞构成,席纹状排列,浸润性生长,伴较多淋巴细胞、浆细胞浸润,可见胶原化及黏液水肿。其中一例异型性明显,核大且畸形。免疫表型:瘤细胞vimentin(5例)、SMA(5例)、desmin(3例)、ALK(3例)、CK(2例)阳性,Caldesmon、CD34、β-catenin、MC、CD117、DOG1、S-100、BCL-2、CD99、CD68均阴性,Ki-67增殖指数1.28%~10.01%。5例均完整切除肿瘤,随访53~137.5个月,其中1例83岁患者,于术后27个月影像学考虑肿瘤复发;另一例术后无瘤生存122个月,因其他原因去世;其余均无瘤生存,基本状况良好。结论(1)本组中老年肠道IMT多见于右半结肠,多有肠道损伤史,多首发消化道症状,白细胞多升高;(2)Vimentin和SMA同时阳性,多伴ALK阳性;(3)4/5的患者手术切除治疗效果好,1/5的患者术后2~3年可复发;高龄且ALK阳性、Ki67达10%、异型性明显很有可能是中老年肠道IMT复发的重要危险因素,其中ALK阳性者复发的风险或许为1/3。

术前Sonazoid超声造影评估肝细胞癌病理分化程度的价值

目的分析肝细胞癌(HCC)Sonazoid超声造影(CEUS)的特点与病理分化程度的相关性。方法纳入行CEUS检查并经病理确诊为HCC的患者64例,共64个病灶,根据病理分化程度将其分为高、中、低分化组,分别为6、48和10例。比较不同病理分化程度HCC的CEUS动脉期增强形态、增强水平和增强模式。结果动脉期增强形态分为均匀增强和不均匀增强2种,低分化组所有病灶及58.3%中分化组病灶呈不均匀高增强;高分化组病灶可呈均匀高增强、均匀等增强和不均匀高增强3种表现。动脉期,所有中、低分组病灶和66.7%高分化组病灶呈高增强,不同分化程度HCC的增强水平差异有统计学意义(P<0.01);门脉期,高、中、低分化组分别有16.7%、25.0%和70.0%的病灶消退成低增强,不同分化程度HCC的增强水平差异有统计学意义(P<0.05);延迟期,75%中分化组病灶和所有低分化组病灶呈低增强,66.7%高分化组病灶呈等增强,不同分化程度HCC的增强水平差异有统计学意义(P<0.01);Kupffer期,所有低分化组和95.8%中分化组病灶呈低增强,高分化组中仍有50%的病灶呈等增强,不同分化程度HCC的增强水平差异有统计学意义(P<0.01)。高分化组病灶表现为多种CEUS模式,中分化组病灶以“快进快退”、“快进慢退”为主,90.0%低分化组病灶呈“快进快退”模式,不同分化程度HCC的CEUS模式差异有统计学意义(P<0.01)。结论Sonazoid-CEUS在评估HCC病理分化程度方面具有一定价值。

外阴良性肿瘤的病理特征及临床分析

目的 探讨外阴良性肿瘤的临床特点、病理特征及治疗预后,总结相关的临床诊治经验。方法 收集2018年1月至2022年12月因外阴肿物收入首都医科大学附属北京妇产医院妇科微创中心住院治疗的24例经病理检查证实为外阴良性肿瘤患者的临床及病理资料进行回顾性分析。探讨发病年龄、临床症状体征、肿物性状特点、病理类型、治疗及转归情况。结果 24例患者中仅2例(8.3%)为多发病灶,其余患者均为单发。发病年龄为14~78岁,中位发病年龄为38岁,围绝经期患者2例(8.3%)。所有患者表现为自触和/或在妇科检查时发现外阴肿物,有2例伴异味及破溃;病程为2周~70年;3例表现为外阴囊性肿物,21例表现为外阴实性肿物(包括8例外阴皮赘),包块大小为0.5~8 cm。术后病理诊断为外阴软纤维瘤者8例,平滑肌瘤4例,外阴皮内痣、纤维瘤、乳头状汗腺腺瘤、血管肌纤维母细胞瘤各2例,多发鳞状细胞乳头状瘤、脂肪瘤、细胞性血管纤维瘤、孤立性纤维性肿瘤各1例。除1例外阴多发鳞状细胞乳头状瘤患者行单纯外阴切除术,其余患者均采用局部病灶切除术。术后随访3个月~5年,均未见复发。结论 外阴良性肿瘤多为单发,实性肿物多见,常无明显自觉症状,病理类型呈多样性,预后较好,建议尽早手术切除,术后加强随访。

前列腺癌多参数MRI诊断及误诊原因分析

目的 探讨前列腺癌临床特点、多参数MRI表现,总结其误诊原因及防范措施。方法 对2020年4月—2022年2月收治的多参数MRI检查后误诊为膀胱癌、前列腺增生的前列腺癌10例的临床资料进行回顾性分析。结果 10例年龄54~73岁。6例因尿急、尿频、尿潴留、排尿困难就诊,直肠指诊示前列腺肥大,查血清前列腺特异性抗原升高,多参数MRI及前列腺穿刺活组织病理检查未发现前列腺肿瘤证据,误诊为前列腺增生,后经术后病理检查确诊T1期前列腺癌。4例以尿痛、血尿、排尿困难就诊,经多参数MRI检查误诊为膀胱癌,查血清前列腺特异性抗原升高,直肠指诊发现前列腺肥大,再次行多参数MRI和前列腺组织穿刺活组织病理检查证实为前列腺癌累及膀胱。误诊时间4~10 d。误诊为前列腺增生6例接受根治性手术,误诊为膀胱癌4例予内分泌和放射治疗,随访至今病情控制尚可。结论 临床接诊以尿急、尿频、尿潴留、排尿困难等症状就诊的中老年男性患者时应考虑到前列腺癌可能。加强对前列腺癌影像学特征认识,行多参数MRI检查时重点观察前列腺结构、包膜完整与否、膀胱壁连续性等重要特征,必要时可行前列腺穿刺活组织病理检查,以提高该病术前诊断正确率。

结直肠癌组织中错配修复蛋白的表达及其与临床病理特征的关系

目的分析结直肠癌组织中错配修复蛋白(MMR)的表达情况及与临床病理特征的关系,并探讨MMR检测在临床工作中的价值。方法收集2021年12月至2023年7月山东省济宁市第一人民医院胃肠外科经外科手术治疗的212例结肠癌及直肠癌患者的相关临床病历资料,分析MMR蛋白Mut L蛋白同系物1(MLH1)、Mut S蛋白同系物2(MSH2)、Mut S蛋白同系物6(MSH6)、减数分裂后分离蛋白2(PMS2)的表达情况并将错配蛋白缺失(dMMR)与其他临床病理数据进行分析。结果212例患者中存在MLH1缺失5例(2.4%),PMS2缺失10例(4.7%),MSH2与MSH6分别缺失2例(0.9%),MLH1、PMS2共同缺失5例(2.4%),MSH2、MSH6共同缺失2例(0.9%)。212例结直肠癌组织中dMMR 12例占5.7%;dMMR与结直肠癌患者的性别、年龄、分化程度、TNM分期、T分期、N分期、有无脉管癌栓及有无神经侵犯均无关;与肿瘤部位、组织学类型相关(P<0.05)。结论MMR表达缺失与肿瘤部位及组织学类型相关,通过对MMR的检测可对术后治疗方案提供指导并对判断癌症患者的预后有重要意义。

骨髓增殖性肿瘤临床病理学特征分析

目的探讨骨髓增殖性肿瘤的骨髓病理组织形态学特点,探讨其临床诊断价值。方法选取2020年1月至2023年3月本院收治的MPN患者138例,对骨髓活检组织作组织学观察及免疫组化行表型分析,同时进行基因学检测。结果138例确诊MPN患者中,BCR ABL阳性CML 39例,BCR ABL阴性MPNs中PV 13例、ET 72例和PMF 11例。经典型MPN骨髓活检组织各具有诊断性形态学特点。CML粒红系比例明显增大伴粒系核右移,巨核细胞均为胞体小、分叶少的巨核细胞,PV粒红系比例明显减小,巨核细胞形态多样,混杂分布;ET粒红系比例大致正常,巨核细胞则为胞体大、分叶多的巨核细胞;PMF巨核细胞形态怪异,核染色质深染浓集,多伴网状纤维显著性增生。结论骨髓活检组织形态在MPN精准诊断和分型中具有重要临床意义。

应用深度学习进行基于前列腺癌转移报告和数据系统指南的晚期前列腺癌盆腔外脏器及转移灶分割

目的探讨应用深度学习进行基于前列腺癌转移报告和数据系统指南的晚期前列腺癌患者盆腔外脏器及转移灶分割的可行性。资料与方法回顾性收集北京大学第一医院2017年1月—2022年1月不同扫描部位(头部、颈部、胸部、腹部)的经临床综合诊断存在转移灶的数据集(头部、颈部、胸部及腹部转移患者分别为68、91、57、263例),用于进行扫描范围的分类模型及不同区域脏器和转移灶的分割模型训练。另收集90例经病理证实为前列腺癌且行全身MRI患者用于模型的外部验证。以手工标注的区域(脑实质、颈椎、肺实质、纵隔、胸椎、肝、腰椎)及转移灶标签为“金标准”,评估模型的分割性能。评价指标包括Dice相似系数(DSC)、体积相似度(VS)。结果在外部验证数据集中,分类模型在头部、颈部、胸部和腹部的符合率分别为100%(90/90)、98.89%(89/90)、96.67%(87/90)和94.44%(85/90);分割模型对不同区域脏器分割的DSC、VS范围分别为(0.86±0.10)~(0.99±0.01)、(0.89±0.10)~(0.99±0.01);分割模型对不同转移灶分割的DSC、VS范围分别为(0.65±0.07)~(0.72±0.13)、(0.74±0.04)~(0.82±0.13)。结论基于深度学习的3D U-Net模型可实现晚期前列腺癌患者的盆腔外区域及转移灶分割。

同时性双侧乳腺癌分子分型与乳腺影像表现的相关性

目的分析同时性双侧乳腺癌不同分子分型与乳腺影像特征的相关性。资料与方法回顾性分析2016年1月—2022年5月青岛大学附属医院经手术病理证实的同时性双侧乳腺癌81例,其中80例接受X线检查,38例接受MRI检查。影像学特征参照第5版乳腺影像报告和数据系统。分子分型参照2013年St.Gallen国际专家共识。比较同时性双侧乳腺癌中首发癌与对侧癌的临床病理及影像表现差异以及首发癌、对侧癌不同分子分型的影像表现差异。结果首发癌与对侧癌组织学类型及分子分型差异均有统计学意义(χ^(2)=39.72、12.23,P<0.05)。X线示首发癌多为单纯肿块(51.9%,40/77),对侧癌多为单纯钙化(38.4%,28/73);首发癌多为多形性钙化(68.8%,22/32),对侧癌多为无定形钙化(45.2%,19/42)(χ^(2)=33.15、10.47,P<0.05)。MRI示首发癌与对侧癌强化方式差异有统计学意义(χ^(2)=6.79,P<0.05)。对侧癌X线示4种分子分型表现形式、肿块密度以及MRI示强化方式、早期强化程度、时间-信号强度曲线差异有统计学意义(P<0.05),对侧癌X线luminalA型多为肿块(51.3%,20/39),luminalB型(36.4%,8/22)、HER-2过表达型(50%,5/10)多为钙化,TNBC型为肿块伴钙化(χ^(2)=26.72、7.49、8.95、13.44、12.85,P<0.05)。首发癌X线示4种分子分型钙化分布差异有统计学意义(χ^(2)=20.15,P<0.05)。结论同时性双侧乳腺癌分子分型及部分影像学特征存在差异,部分影像学特征可为预测分子分型提供参考。

^(18)F-FDG PET/CT代谢参数预测胸腺上皮肿瘤恶性程度

目的观察^(18)F-FDG PET/CT代谢参数对预测胸腺上皮肿瘤(TET)恶性程度的价值。方法回顾性分析95例经病理诊断的TET患者,根据病理结果进行组织学分型(低危型胸腺瘤、高危型胸腺瘤、胸腺癌)及临床分期(Ⅰ~Ⅳ期)。基于^(18)F-FDG PET/CT获取原发灶最大标准摄取值(SUV_(max))、峰值标准摄取值(SUV_(peak))、原发灶SUV_(max)与纵隔血池平均标准摄取值的比值,即靶区本底比值(TBR),分别以SUV=2.5及40%SUV_(max)为阈值,获得病灶糖酵解总量(TLG_(2.5)、TLG_(40%))及肿瘤代谢体积(MTV_(2.5)、MTV_(40%))。比较不同类型及临床分期TET各代谢参数的差异。针对两两比较差异均有统计学意义的代谢参数绘制受试者工作特征(ROC)曲线,计算曲线下面积(AUC),评估其预测不同组织学分型TET的效能。结果95例中,27例低危型胸腺瘤、15例高危型胸腺瘤、53例胸腺癌;临床分期Ⅰ期28例、Ⅱ期8例、Ⅲ期12例、Ⅳ期47例。不同类型TET间SUV_(max)、SUV_(peak)及TBR差异均有统计学意义(P均<0.05),高危型胸腺瘤及胸腺癌TLG_(2.5)和MTV_(2.5)均高于低危型胸腺瘤(P均<0.05),胸腺癌TLG_(40%)高于低危型胸腺瘤(P<0.05);其他代谢参数差异均无统计学意义(P均>0.05)。临床Ⅳ期TET的SUV_(max)、SUV_(peak)、TBR、TLG_(2.5)、TLG_(40%)、MTV_(2.5)均高于Ⅰ期(P均<0.05),Ⅲ期TET的TLG_(2.5)高于Ⅰ期(P<0.05),不同临床分期TET其余代谢参数差异均无统计学意义(P均>0.05)。以SUV_(max)、SUV_(peak)及TBR预测低危型与高危型胸腺瘤的AUC分别为0.857、0.840及0.857,预测高危型胸腺瘤与胸腺癌的AUC分别为0.769、0.758及0.755。结论^(18)F-FDG PET/CT代谢参数可有效预测TET恶性程度。

基于乳腺癌超声特征及临床病理指标的列线图预测腋窝淋巴结转移风险

目的探讨基于超声特征联合临床病理指标的列线图预测乳腺癌腋窝淋巴结转移风险的价值。资料与方法回顾性分析2014年1月—2021年10月于石河子大学第一附属医院经病理证实的1038例乳腺癌患者(共1099个肿块)的超声图像及病理资料,按检查时间分为训练组和验证组。基于多因素Logistic回归筛选与腋窝淋巴结转移相关的独立预测因素,建立回归模型并制作列线图,利用验证组数据及校准曲线验证列线图。绘制受试者工作特征曲线、决策曲线评估列线图的预测效能。结果多因素Logistic分析结果显示,乳腺癌肿块最大径(OR=1.906,95%CI 1.397~2.609,P<0.001)、纵横比(OR=0.425,95%CI 0.284~0.634,P<0.001)、边界(OR=0.373,95%CI 0.267~0.520,P<0.001)、Adler血流分级(OR=3.188,95%CI 2.049~5.107,P<0.001)、病理类型(OR=2.975,95%CI 1.759~5.267,P<0.001)及人表皮生长因子受体2表达状态(OR=1.439,95%CI 1.048~1.982,P=0.025)是预测腋窝淋巴结转移的危险因素。基于以上6个指标构建列线图预测模型,其训练组和验证组一致性指数分别为0.712和0.749,校准曲线(绝对平均误差分别为0.019、0.014)及决策曲线均提示该模型预测能力较好。结论基于乳腺癌原发病灶超声特征及临床病理指标联合构建的预测腋窝淋巴结转移风险列线图模型,可为临床诊断、后期治疗及预后评估提供参考信息。

PI3K/AKT信号通路与乳腺病变弹性特征的相关性

目的探讨磷脂酰肌醇-3-激酶/丝苏氨酸蛋白激酶(PI3K/AKT)信号通路与乳腺病变弹性特征的相关性。资料与方法前瞻性分析2021年5月—2022年5月于解放军总医院接受手术的114例患者共115个乳腺病变,术前行超声和剪切波弹性成像检查。采用免疫组化染色检测组织标本中PI3K/AKT蛋白水平的表达,分析染色结果与剪切波弹性成像最大弹性模量值、平均弹性模量值、最小弹性模量值、病变与周围组织弹性比值的相关性。结果115个乳腺病变中,手术病理显示乳腺良性病变50个,恶性病变65个(25个伴腋窝淋巴结转移)。良性病变与恶性病变不伴腋窝淋巴结转移、恶性病变伴腋窝淋巴结转移的最大弹性模量值(F=40.47)、平均弹性模量值(F=45.11)、病变与周围组织弹性比值(F=48.98)、“硬环征”检出率(χ^(2)=62.25)、PI3K/p-PI3K表达水平(F=15.19、58.95)及AKT/p-AKT表达水平(F=46.94、74.21)比较,差异均有统计学意义(P<0.05)。PI3K/pPI3K及AKT/p-AKT表达水平与最大弹性模量值、平均弹性模量值、病变与周围组织弹性比值均呈正相关(r=0.475、0.475、0.451;r=0.533、0.540、0.542;r=0.371、0.402、0.445;r=0.482、0.455、0.545,P均<0.05)。结论乳腺病变的PI3K/AKT表达水平与弹性特征具有相关性,提示其在乳腺病变弹性特征调控中发挥重要作用。

TRIM44蛋白在前列腺癌中的表达及其临床意义

目的探讨三结构域蛋白44(TRIM44)在前列腺增生与前列腺癌中的表达差异,分析其表达与前列腺癌的临床病理及预后的关系。方法采用免疫组织化学染色的方法检测96例前列腺癌和60例前列腺增生组织中TRIM44蛋白的表达,并分析TRIM44表达与前列腺癌临床病理参数以及预后的关系。结果前列腺癌组中TRIM44的阳性表达率(64.16%)明显高于前列腺增生组织(20.00%),差异有显著性(χ^(2)=25.591,P<0.05);T3~T4分期、N1分期前列腺癌组织TRIM44高表达率明显高于T1~T2分期、N0分期(χ^(2)=5.629~5.721,P<0.05);前列腺特异性抗原(PSA)>20μg/L前列腺癌中的TRIM44高表达率明显高于PSA≤20μg/L组(χ^(2)=10.532,P<0.05);Gleason高评分组的前列腺癌组织中TRIM44的高表达率高于Gleason低评分组(χ^(2)=6.097,P<0.05)。Kaplan-Meier生存分析显示,TRIM44高表达病人的总生存率明显低于TRIM44低表达病人(χ^(2)=5.494,P<0.05);单因素生存分析显示,T分期、N分期、M分期、Gleason评分以及TRIM44表达与前列腺癌病人的不良预后相关(HR=1.968~7.416,95%CI=1.099~13.342,P<0.05);Cox多因素回归分析显示,TRIM44高表达是前列腺癌病人的独立预后因素(HR=1.873,95%CI=1.051~3.337,P=0.033)。结论TRIM44在前列腺癌组织中高表达,其表达与前列腺癌病人的临床分期、Gleason评分以及不良预后密切相关。

母细胞性浆细胞样树突细胞肿瘤2例并文献复习

目的探讨母细胞性浆细胞样树突细胞肿瘤的临床病理特征、治疗及预后。方法结合相关文献,回顾性分析2例母细胞性浆细胞样树突细胞肿瘤患者的临床表现、组织学形态、免疫表型、治疗方案及预后。结果2例组织形态均符合母细胞性浆细胞样树突细胞肿瘤的病理改变,免疫组织标记CD4、CD56、CD123、TCL1阳性,排除淋巴系、髓系及NK细胞来源,2例EBER原位杂交检测结果均为阴性;例l累及骨髓及淋巴结,对症支持治疗,2月后死亡;例2经CHOP方案化疗8周期,半年后病情进展,全身多发红疹,后予吉西他滨、奥沙利铂及培门冬酶化疗9周期,目前病情稳定。结论母细胞性浆细胞样树突细胞肿瘤多以皮肤症状为首发,具有独特的临床病理特点,诊断依靠组织学及免疫表型,目前尚无有效的治疗方案且预后差。