结合CT影像学及临床病理学特征评估直肠癌术前N分期

目的探讨影响直肠癌N分期的CT影像学及临床病理学特征及其结合评估直肠癌术前N分期的作用。 方法回顾性收集四川大学华西医院胃肠外科2010年7月至2013年7月间行直肠癌根治性切除术的300例中低位直肠癌患者的临床资料,根据术后病理将患者分为淋巴结阴性组（164例）和淋巴结阳性组（136例）,分析影响淋巴结分期的CT影像学及临床病理特征,并分析其结合评估直肠癌术前N分期的作用。 结果与淋巴结阴性组比较,淋巴结阳性组CEA较高（Z=-3.636,P<0.001）、肿瘤大小较大（t=-4.460,P<0.05）,并且T分期较晚（Z=-4.895,P<0.05）、分化程度较低（Z=-4.861,P<0.05）;两组间性别、年龄、CA199、肿瘤位置、手术方式、肿瘤分型的差异无统计学意义（P>0.05）;此外淋巴结阳性组CT片淋巴结数目较多（Z=-5.134,P<0.001）,平均长径（t=-6.462,P<0.05）、平均短径（t=-6.900,P<0.05）、最长长径（Z=-4.128,P<0.001）、最长短径（t=-7.183,P<0.05）以及CT值（Z=-6.560,P<0.001）均较大;淋巴结位置两组间差异有统计学意义（χ²=8.202,P<0.05）。多因素分析显示只有T分期、分化程度是淋巴结分期的独立影响因素。CT片指标与CEA、T分期、或分化程度结合可提高诊断特异性至80%以上。 结论T分期与分化程度是淋巴结分期的独立影响因素,CT片指标与CEA、T分期、或分化程度结合可提高诊断特异性至80%以上,但是敏感性和准确性仍较低,需要研究发现其他新的淋巴结分期方法。     

RhoGDI2蛋白的高表达与结直肠癌侵袭和转移的相关性分析

目的通过检测RhoGTP酶解离抑制因子2（RhoGTPase dissociation inhibitor 2,RhoGDI2）在结直肠癌和癌旁组织中的表达并结合临床病理特点进行分析,探讨RhoGDI2的蛋白表达水平与结直肠癌侵袭转移的关系及在肿瘤发生发展中的作用。 方法选取山东省医学科学院附属医院2012年07月至2014年07月采取手术切除的153例结直肠癌病例,采用免疫组织化学检测153例肿瘤组织标本和癌旁标本中RhoGDI2蛋白的表达水平。 结果RhoGDI2蛋白在结肠癌组织中呈阳性表达,且主要在胞浆中表达;但在癌旁正常组织中无阳性表达（57.5% vs 0.00%）。结直肠癌组织中RhoGDI2蛋白的表达在低分化组显著高于高中分化组（χ²=2.090,P<0.05）。RhoGDI2的阳性表达与结直肠肿瘤的大小呈正相关,肿瘤越大阳性表达率越高（χ²=4.293,P<0.05）,并随着肿瘤浸润深度阳性表达率增加（χ²=1.711,P<0.05）,其在有淋巴结转移者表达显著高于无淋巴结转移者（χ²=5.925,P<0.05）、有远处转移者显著高于无远处转移者（χ²=5.519,P<0.05）,并且与临床分期密切相关,分期较晚的显著高于分期较早的（χ²=5.683,P<0.05）。RhoGDI2在结直肠癌中的阳性表达与年龄（<60 years vs ≥60 years）（χ²=0.054,P>0.05）,性别（χ²=0.037,P>0.05）无相关性。 结论RhoGDI2在结直肠癌中高表达,并且与结直肠癌的局部侵袭和远处转移呈正相关。RhoGDI2可能在结直肠的发生发展和侵袭转移过程中起着重要的作用。     

乙肝表面抗原等因素对结直肠癌肝转移的影响

目的本研究将探讨乙肝表面抗原（HBsAg）等多项临床因素对结直肠癌肝转移的影响,为进一步治疗结直肠癌肝转移提供新的研究思路及方向。 方法回顾性分析青岛大学医学院附属医院2010年1月至2011年6月病理证明的结直肠癌患者892例。收集患者的相关临床资料（包括乙肝表面抗原、年龄、术前相关实验室检查、术后病理结果等）,研究是否会影响肝转移的发生。 结果结直肠癌是否发生肝转移两组患者在性别、年龄、肿瘤发生部位、大小、病理组织类型、是否造口、血清白蛋白、总胆红素及谷草转氨酶等方面相比,差异均无统计学意义（χ²=0.359,Z=-1.631,χ²=0.003,χ²=1.223,χ²=0.619,χ²=0.516,Z=-3.235,Z=-0.106,Z=-0.328;均P>0.05）。HBsAg阳性较阴性患者发生肝转移几率明显降低,差异有统计学意义（χ²=5.809,P<0.05）。另外,肝转移与分化水平（χ²=14.165,P<0.01）、浸润程度（χ²=17.808,P<0.01）以及淋巴结转移数目（χ²=41.798,P<0.01）有关,差异均有统计学意义。多因素logistic回归分析结果表示乙肝病毒表面阳性患者肝转移发生低,而低分化、浸润程度高、淋巴结转移多者肝转移率高。 结论乙型肝炎病毒表面抗原阳性会降低肝转移的发生几率。分化程度越低、浸润程度越高、淋巴结转移数多,越容易发生肝转移。     

结直肠锯齿状病变的微卫星状态研究

目的 比较结直肠锯齿状病变与传统腺瘤、腺癌的微卫星状态的差异,以期间接验证传统型锯齿状成瘤通路的存在.方法 收集北京军区总医院病理科保存的75例大肠息肉及肿瘤组织蜡块标本,其中锯齿状腺癌(Sca)15例,非锯齿状腺癌(N-Sca)20例,传统型锯齿状腺瘤(TSA)20例,普通腺瘤20例.抽提基因组DNA,采用荧光标记引物扩增BAT25、BAT26两个位点,随后使用DNA自动测序仪检测其微卫星状态,并对实验结果进行统计学分析.结果部分标本扩增失败,对于成功扩增的68例标本:18例TSA中6例为高度微卫星不稳定型(MSI-H),12例为低度微卫星不稳定型(MSI-L)/微卫星稳定型(MSS);18例普通腺瘤均为MSS;13例Sca中3例为MSI-H,10例为MSI-L/MSS;19例N-Sca中仅1例为MSI-H,18例为MSI-L/MSS.统计学分析表明,普通腺瘤组、N-Sca组MSI-H发生率明显低于TSA组和Sca组(P<0.05),而后两组间差异无统计学意义(P>0.05).结论 与普通腺瘤、N-Sca相比,MSI-H更多见于TSA、Sca,由此推断存在一条有别于传统"腺瘤-癌"发生模式的传统型锯齿状成瘤通路,但尚需大规模前瞻性研究确认.     

结直肠癌中HMGA2表达的意义与微卫星不稳定性的关系

目的探讨高迁移率族蛋白(HMG) A2在结直肠癌组织中表达意义及与微卫星不稳定性(MSI)的关系。方法结直肠癌手术标本70例,采用免疫组化法检测微卫星不稳定四种相关蛋白MLH1、MSH2、MSH6、PMS2及HMGA2的表达情况,分为高频微卫星不稳定组(MSI-H)、低频微卫星不稳定(MSI-L)/微卫星稳定组(MSS)两组,研究HMGA2与MSI的相关性及与结直肠癌临床特征之间的关系,进一步用Western印迹法验证免疫组化结果。结果结直肠癌中HMGA2阳性率为65. 71%(46/70),与正常肠黏膜相比差异显著(P<0. 001),低分化癌组高于中、高分化癌组,差异有意义(P<0. 05); TNMⅢ+Ⅳ期明显高于Ⅰ+Ⅱ期(P<0. 05)。MSI-H发生率为17. 14%(12/70),右半结肠发生率高于左半结肠(P<0. 05),此外,MSI-H发生与患者年龄、肿瘤分化程度有关(P<0. 05)。MSI-H组、MSI-L/MSS组中HMGA2的表达差异无统计学意义(P>0. 05)。结论HMGA2高表达可能促进结直肠癌的发生与发展,作用机制与微卫星状态无关,需要进一步研究。     

结直肠癌AIM2和血清CEA表达水平及其临床意义

目的探讨结直肠癌患者黑色素瘤缺乏因子2（AIM2）和血清癌胚抗原（CEA）表达水平及其临床意义。 方法收集辽宁省肿瘤医院2010年1月~2013年3月118例结直肠癌患者的肿瘤组织标本及其50例癌旁正常组织标本,采用免疫组织化学法测定组织中AIM2的表达,回顾性搜集患者临床病理参数及术前通过电化学发光法（ECUA）测定的血清CEA水平。通过相关性分析癌组织中AIM2表达水平和血清CEA水平的相关性,分析两种指标与临床病理参数的关系。采用Kaplan-Meier法对不同AIM2、CEA水平组别进行生存分析。 结果118例肿瘤组织中有42例AIM2呈高表达,有39例癌旁正常组织呈高表达,差异具有统计学意义（χ²=25.295,P<0.001）;结直肠癌患者术前血清CEA阳性率为44.07%（52/118）。Spearman等级相关性分析结果显示,结直肠癌组织AIM2和血清CEA表达呈负相关（r=-0.660,P<0.001）。肿瘤的浸润深度、TNM分期以及淋巴结转移是影响癌组织AIM2表达水平的相关因素（χ²=4.847,7.794,3.961;均P<0.05）;肿瘤大小、TNM分期以及分化程度是影响患者术前血清CEA水平的相关因素（χ²=17.14,5.779,5.293;均P<0.05）。K-M生存分析显示,AIM2高表达组生存时间明显长于低表达组,术前CEA阴性组生存时间明显长于阳性组,AIM2高表达联合CEA阴性患者生存时间明显长于AIM2低表达联合CEA阳性患者,差异具有统计学意义。 结论结直肠癌患者AIM2和血清CEA表达可能与结直肠癌的进展有关,联合分析两个指标有助于评估结直肠癌患者预后。     

老年结直肠癌的临床和病理特点及其预后分析

目的探讨老年结直肠癌患者的临床、病理及预后特点。 方法收集2005年1月至2009年12月间于湖南中医药大学第一附属医院普外科诊断为结肠癌且接受手术治疗的患者的完整资料,进行生存分析和预后的多因素分析。共选取84例老年患者,其中男性48例,女性36例,平均年龄71.38岁,与同期75例中青年结肠癌患者的临床和病理资料进行比较。应用SPSS 19.0统计学软件进行数据分析,以P<0.05有统计学意义。各组间相关因素比较采用χ²检验,应用Kaplan-Meier法进行生存分析,多因素分析采用Cox风险比例回归模型计算。 结果84例老年结直肠癌患者中,患者临床表现以血便为主。直肠是最常见出血部位。病理组织类型以腺癌为主(占86.90%)。多因素分析结果显示,年龄、手术方式、病理分型、组织学分化程度、TNM分期、化疗是影响预后重要的独立因素。与中青年结肠癌患者(年龄<65岁)相比,肿瘤大体分型(χ²＝10.652,P＝0.005)、组织学类型(χ²＝29.466,P<0.001)、分化程度(χ²＝26.806,P＝0.033)、淋巴结转移(χ²＝6.963,P＝0.031)、肿瘤浸润深度(χ²＝7.983,P＝0.018)、TNM分期(χ²＝9.720,P＝0.021)及远处转移方面(χ²＝5.165,P＝0.023),差异有统计学意义。 结论老年直肠癌患者的病程发展缓慢、肿瘤分化程度较高,早期根治性手术治疗可以取得较好的疗效及预后,化疗是保护性因素,早期诊疗是提高结直肠癌患者总体生存率的关键。     

老年高血压合并糖尿病患者服药依从性的影响因素

目的 分析老年高血压合并糖尿病患者服药依从性的影响因素。方法 选取2018年3月至2021年3月收治的老年高血压合并糖尿病患者300例为受试者,采用Morisky测评表进行问卷调查,调查老年高血压合并糖尿病患者服用降压药和降糖药的依从性。采用多因素logistic回归分析服药依从性的影响因素。结果 本次研究纳入的受试者中服药依从性良好者114例(38.0%),服药依从性差者186例(62.0%)。与服药依从性差的患者相比,服药依从性良好者的血压控制达标率更高(89.6%比12.9%,χ²=170.12,P<0.001)。服药依从性差和良好组的年龄(χ²=6.007,P=0.014)、文化程度(χ²=7.212,P=0.007)、居住地区(χ²=13.197,P<0.001)、高血压(χ²=20.259,P<0.001)及糖尿病病程(χ²=12.262,P=0.002)、服药种类(χ²=4.285,P=0.038)及家...     

胃肠道外间质瘤预后因素分析

目的探讨胃肠道外间质瘤（EGIST）的临床特征及影响预后的因素。 方法回顾性分析2006年11月至2017年5月间辽宁省肿瘤医院收治的首次进行外科治疗且经病理证实的47例胃肠道外间质瘤患者的临床及随访资料,与本中心的254例胃肠间质瘤（GIST）患者资料进行对比。 结果EGIST与GIST患者在年龄（χ²=6.394,P<0.011）,肿瘤大小（χ²=60.941,P<0.001）,组织学类型（χ²=30.081,P<0.001）,CD117表达（χ²=52.99,P<0.001）,CD34表达（χ²=37.21,P<0.001）、Dog-1表达（χ²=24.57,P<0.001）,是否坏死（χ²=10.38,P=0.006）、改良NIH危险度分级（χ²=56.12,P<0.001）之间差异有统计学意义。EGIST患者1、2、3年生存率分别为84.6%、78.3%、63.4%;接受R0切除的EGIST患者25例（53.2%）。R0切除患者的生存率明显高于非R0切除患者（χ²=5.104,P=0.024）。其中,25例R0切除的患者中显示不同核分裂像、不同肿瘤直径大小、是否伴坏死与EGIST患者的预后未体现统计学意义（χ²=2.067,P=0.151;χ²=1.355,P=0.244;χ²=0.912,P=0.34）。 结论EGIST患者症状隐匿,不易早诊断,首次就诊时肿瘤体积往往较大。是否R0切除关系到患者的预后。     

HBV相关慢加急性肝衰竭TBil水平的合理界值分析

目的 探讨HBV相关慢加急性肝衰竭（HBV-ACLF）患者的合理胆红素诊断阈值,以期更为精准地早期诊断。方法回顾性分析解放军总医院第五医学中心2008年9月—2018年9月收治的1232例HBV-ACLF患者,根据基线血清TBil水平分为A组（TBil<205.2μmol/L）和B组（TBil≥205.2μmol/L）,比较2组患者临床特征及28 d、90 d、1年及3年生存情况。计量资料两组间比较采用t检验或Mann-Whitney U秩和检验。计数资料组间比较采用χ²检验。使用Kaplan-Meier法分析2组患者的生存率,并应用log-rank检验进行比较。结果 2组间年龄（t=3.188,P=0.001）、男性（χ²=33.833,P<0.001）、肝衰竭分型（χ²=39.987,P<0.001）、WBC（Z=6.586,P<0.001）、HGB（Z=4.272,P<0.001）、PLT（Z=3.680,P<0.001）、Cr（Z=4.505,P<0.001）、TC（Z=...     

I~III期结直肠癌淋巴结转移比率与预后关系

目的评价I~III期结直肠癌淋巴结转移比率与患者预后的关系。 方法回顾性分析中山大学附属第一医院胃肠胰腺外科2004年6月至2008年11月间446例行根治性切除的结直肠癌患者临床病理数据,探讨结直肠癌预后相关危险因素,评估结直肠癌淋巴结转移比率与患者预后的关系。 结果446例结直肠癌I、II、III期患者的5年总体生存率分别约为87.4%,83.1%和64.8%（Log-rank检验,P<0.001）。我们根据淋巴结转移比率（metastatic lymph node ratio, mLNR）将CRC患者分为三组：A组：mLNR为0;B组：mLNR为>0%~14%;C组：mLNR为>14%。A、B、C组三组患者的5年总体生存率分别约为84.3%、79.6%和49.1%（Log-rank检验,χ²=55.959,P<0.001）。就直肠癌患者而言,A、B、C三组5年生存率分别为79.0%、73.5%和43.2%（Log-rank检验,χ²=26.332,P<0.001）。而对于结肠癌患者来说三组的5年生存率分别为87.1%,80.8%和55.5%（Log-rank检验,χ²=21.214,P<0.001）。单因素和多因素Cox分析均显示,mLNR是结直肠癌独立的预后危险因素,随着mLNR的上升,结直肠癌患者的预后变差。 结论淋巴结转移比率（mLNR）是结直肠癌患者预后的独立危险因素,与N分期类似,但更有优势,可作为评估结直肠癌患者预后的指标之一。     

Molecular profiling of the colon cancer in South-Eastern Romania: Results from the MERCUR study

Colorectal cancer is a heterogeneous disease with multiple epigenetic alterations and different molecular features. The molecular classification is based on 2 major distinct pathways: microsatellite stable pathway and the microsatellite instability pathway. Molecular profiling of colorectal cancer provides important information regarding treatment and prognosis. Aim of the study was to assess the frequency of microsatellite instability in colon cancer and the clinicopathological characteristics of the tumors with high level of microsatellite instability (MSI-H) in our region. The secondary outcome was to assess the frequency of v-raf murine sarcoma viral oncogene homolog B1 (BRAF) mutations in colon cancer.The study included 129 patients with colon cancer fit for surgery. Demographic data, clinical and pathological data, immunohistochemistry staining pattern (4 mismatch repair proteins were investigated), and BRAF gene mutations were assessed. According to microsatellite instability status by polymerase chain reaction, patients were divided into 3 groups: microsatellite stable (MSS) = 108 patients, high level of microsatellite instability (MSI-H) = 15 patients and low level of microsatellite instability (MSI-L) = 6 patients. Different clinicopathological comparisons between MSS and MSI-H patients, and between MSS and MSI-L patients were performed.Microsatellite instability was found in 16.3% patients: 11.6% had MSI-H and 4.7% had MSI-L. Significantly more patients in the MSI-H group than in the MSS group were female (P = .01) and had a family history of colon cancer (P < .001). MSI-H and MSI-L groups were associated with the ascending colon location of the tumors, were mostly type G3, T2, and stage I whereas MSS tumors were mostly G2, pT3, and stage III. Overall, BRAF mutations were identified in 18/129 patients (13.9%). BRAF mutant tumors were predominantly associated with MSI-H and MSI-L tumors. Immunohistochemistry had a sensitivity of 76% and a specificity of 89% in detecting MSI tumors and an accuracy of 87.6%.The frequency of microsatellite instability in our study was 16.3%. MSI-H is a distinct molecular phenotype of colon cancer with particular features: female gender, family history of colorectal cancer, a predilection for the ascending colon, poorly differentiated, predominantly T2, and stage I. The frequency of BRAF mutations was 13.9% and mutations were more often present in the MSI tumors.     

Microsatellite Instability of Gastric and Colorectal Cancers as a Predictor of Synchronous Gastric or Colorectal Neoplasms

Background/Aims

Microsatellite instability (MSI) plays a crucial role in gastrointestinal carcinogenesis. The aim of this study was to clarify whether MSI is a useful marker for predicting synchronous gastric and colorectal neoplasms.

Methods

Consecutive patients who underwent both esophagogastroduodenoscopy and colonoscopy before the resection of gastric or colorectal cancers were included. MSI was analyzed using two mononucleotide and three dinucleotide markers.

Results

In total, 434 gastric cancers (372 microsatellite stability [MSS], 21 low incidence of MSI [MSI-L], and 41 high incidence of MSI [MSI-H]) and 162 colorectal cancers (138 MSS, 9 MSI-L, and 15 MSI-H) were included. Patients with MSI gastric cancer had a higher prevalence of synchronous colorectal cancer, colorectal adenoma, and gastric adenoma than those with MSS gastric cancers (4.8% vs 0.5%, p=0.023; 11.3% vs 3.2%, p=0.011; 3.2% vs 1.2%, p=0.00, respectively). The prevalence of synchronous colorectal adenomas was highest in MSI-L gastric cancers (19.0%), compared with MSI-H (7.3%) or MSS (3.2%) gastric cancers (p=0.002). In addition, there were no significant differences in the prevalence rates of synchronous colorectal adenoma among the MSI-H (13.3%), MSI-L (11.1%), and MSS (12.3%) colorectal cancers (p=0.987).

Conclusions

The presence of MSI in gastric cancer may be a predictor of synchronous gastric and colorectal neoplasms, whereas MSI in colorectal cancer is not a predictor of synchronous colorectal adenoma.     

Low-level microsatellite instability colorectal carcinomas: do they really belong to a "gray zone" between high-level microsatellite instability and microsatellite-stable cancers?

BACKGROUND AND AIMS: Colorectal carcinomas demonstrating low-level microsatellite instability (MSI-L) may form a distinct group differing both from high-level MSI (MSI-H) and microsatellite-stable (MSS) tumors. MATERIALS AND METHODS: In a retrospective series of 172 colorectal carcinomas the microsatellite status was examined based on DNA extracted from archival blocks. Three groups - MSS ( n=100), MSI-L ( n=37), MSI-H ( n=35) - were compared with respect to clinical data, stage, histology, and immunoexpression of Ki-67, and P53. RESULTS: Compared to MSS and MSI-H carcinomas the MSI-L tumors were exceptionally rarely right-sided, and demonstrated the lowest proliferation fraction. There was a trend for less frequent high-grade histology, more frequent intermediate P53 expression, and prominent mucinous histology. CONCLUSION: Features of MSI-L colorectal carcinomas are not necessarily located between their MSS and MSI-H counterparts. The MSI-L category may contain a group of tumors belonging to a distinct carcinogenetic pathway.     

IL-1β and IL-8, matrix metalloproteinase 3, and pepsinogen secretion before and after H. pylori eradication in gastroduodenal phenotypes

Background: Adenomatous polyposis coli (APC) and β -catenin (encoded by CTNNB1 ) are important components in the WNT signalling pathway, a pathway altered in nearly all colorectal tumours. Conflicting results are reported on whether APC mutations are less common in tumours with a high degree of microsatellite instability (MSI-H) than in microsatellite stable (MSS) ones, and whether mutations in the regulatory domain of CTNNB1 substitute for APC mutations in the MSI-H tumours. Methods: A consecutive series of 218 primary colorectal carcinomas, stratified by MSI status, were analysed for mutations in the APC gene (by the protein truncation test) and in the CTNNB1 gene (by single-strand conformation polymorphism). Results: APC mutations detected in 66% of the patients were significantly more frequent in the MSS and MSI-L (low) tumours than in the MSI-H tumour group ( P < 0.001). The MSI-H tumours tended to have more frameshift mutations than the MSS/MSI-L tumours. The majority of the APC mutations were located in the mutation cluster region (MCR). Patients that had lost all β -catenin binding sites of the APC gene showed a shorter survival time than patients who retained some or all of these binding sites ( P = 0.045). Two mutations were found in the CTNNB1 gene, but neither of them was located in the regulatory domain in exon 3. Conclusion: This study confirms that APC mutations are less frequent in MSI-H tumours than in MSS and MSI-L tumours. However, CTNNB1 mutations do not substitute for APC mutations in MSI-H tumours in these Norwegian patients.     

Tumour infiltrating lymphocytes and apoptosis are independent features in colorectal cancer stratified according to microsatellite instability status

BACKGROUND: The presence of high level DNA microsatellite instability (MSI-H) in colorectal cancer is associated with an improved prognosis, as is the presence of tumour infiltrating lymphocytes (TILs). It is not clear if TILs contribute directly to the survival advantage associated with MSI-H cancers through activation of an antitumour immune response. AIMS: To correlate TIL and apoptosis rates in colorectal cancer stratified by MSI status. METHODS: The distribution of TILs was characterised and quantified in a selected series of 102 sporadic colorectal cancers classified according to levels of MSI as 32 MSI-H, 30 MSI-low (MSI-L), and 40 microsatellite stable (MSS). Archival blocks were immunostained using the T cell markers CD3 and CD8, and the B cell marker CD20. Apoptosis of malignant epithelial cells was quantified by immunohistochemistry with the M30 CytoDEATH antibody. RESULTS: Positive staining with anti-CD3 and negative staining with anti-CD20 identified virtually all TILs as T cells. The majority of CD3+ TILs (>75%) also stained with anti-CD8. TILs were most abundant in MSI-H colorectal cancers in which 23/32 (72%) scored as TIL positive. Only 5/40 (12.5%) MSS tumours and 9/30 (30%) MSI-L cancers were TIL positive (p<0.0001). MSI-H cancers showed a twofold higher rate of apoptosis (mean (SD) 3.52 (0.34)%) than the MSS cancers (1.53 (0.23)%) while the MSI-L subgroup had an intermediate level (2.52 (0.35)%) (p<0.0001). Overall, there was a small (r=0.347) but significant linear correlation between CD3+ and M30+ random apoptosis counts (p<0.001). However, TILs and apoptosis showed little colocalisation. CONCLUSIONS: While TILs might be expected to explain the increased apoptotic rate and improved prognosis of MSI-H cancers, it is likely that TILs and apoptosis are independent characteristics of MSI-H cancers.