Significant association between high serum CCL5 levels and better disease‐free survival of patients with early breast cancer

Analysis of anticancer immunity aids in assessing the prognosis of patients with breast cancer. From 250 operated breast cancers, we focused on serum levels of C‐C motif chemokine ligand 5 (CCL5), which is involved in cancer immune reactions. Serum levels of CCL5 were measured using a cytometric bead‐based immunoassay kit and CCL5 expression in cancer cells was determined using immunohistochemical staining. In addition, mRNA in cancer and stromal cells was analyzed by microdissection and comparison with the public dataset. Disease‐free survival (DFS) of patients with high CCL5 levels (cut‐off, 13.87 ng/mL; n = 192) was significantly better than those with low CCL5 levels (n = 58; hazard ratio, 0.20; 95% confidence interval, 0.10‐0.39; P < .0001). An improved overall survival was observed in patients with high CCL5 levels compared to those with low CCL5 levels (P = .024). On the contrary, high immunohistochemical expression of CCL5 in cancer cells was significantly associated with decreased DFS. As serum CCL5 levels did not correlate with CCL5 expression in cancer cells and the relative expression of mRNA CCL5 was elevated in stromal cells in relation to cancer cells, serum CCL5 might be derived not from cancer cells, but from stromal cells. Expression of CCL5 in serum, but not in cancer cells, might contribute to improved patient prognosis mediating through not only immune reaction, but through other mechanisms. Determination of circulating CCL5 levels could be useful for predicting patient prognosis.     

Spontaneous Regression of Metastatic Renal Cell Carcinoma after SARS-CoV-2 Infection: A Report of Two Cases

Spontaneous regression of metastatic renal cell carcinoma (mRCC) is a rare event, often associated with an activation of innate immunity by various triggers. SARS-CoV-2 infection induces a strong inflammatory response in some patients and a cytokine storm is one of the main causes of severe morbidity and mortality associated with the virus. Here, we describe two cases of patients with histologically and radiologically proven mRCC whose treatment was delayed due to COVID-19 and who experienced spontaneous tumour regression following the infection. Both patients reported here had predominantly pulmonary and mediastinal involvement and underwent nephrectomy. The interval between the diagnosis of COVID-19 and the detection of tumour regression was 3 and 4 months, respectively. Although approved vaccines and other measures are clearly the best way to prevent COVID-19-associated morbidity and mortality in cancer patients, we hypothesize that innate immunity activation by the infection can contribute to tumour regression in special circumstances.     

Gastric cancer cells exploit CD4+ cell-derived CCL5 for their growth and prevention of CD8+ cell-involved tumor elimination

The level of serum CCL5, a C-C chemokine, is reportedly correlated with tumor progression in several cancers. We herein investigated the mechanisms by which CCL5 might contribute to tumor progression in gastric cancer. Serum CCL5 levels significantly correlated with tumor progression and prognosis in patients with gastric cancer. Immunohistochemistry showed that tumor-infiltrating lymphocytes expressed CCL5, while the tumor cells expressed the CCL5 receptors. Fluorescent double staining showed that tumor-infiltrating CD4+ cells rather than CD8+ cells preferentially expressed CCL5. Using gastric cancer cell lines (MKN45, KATO III), we examined CCL5 production by coculturing whole peripheral blood mononuclear cells (PBMCs), CD4+ cells, or CD8+ cells, with tumor cells. CD4+ cells cocultured with tumor cells remarkably enhanced CCL5 production in a direct cell-cell contact manner over other cocultured PBMCs, including CD8+ cells. Gastric cancer cell lines expressed CCL5 receptors and augmented their proliferation in response to CCL5 stimulation. Furthermore, we examined the effect of CCL5-treated cancer cells on the cocultured PBMCs, focusing on the CD4+/CD8+ proportion and apoptosis. Coculture of CCL5-treated gastric cancer cells with PBMCs resulted in a significant decrease in the proportion of CD8+ cells but not CD4+ cells, suggesting Fas-FasL-mediated apoptosis in CD8+ cells. In immunodeficient mice coinjected with KATO III and PBMCs, neutralization of CCL5 significantly suppressed tumor progression, resulting in a favorable outcome. In conclusion, gastric cancer cells might thus induce CD4+ T cells to secrete CCL5 and exploit it for their progression, as well as to aid in the prevention of CD8+ T cell-involved tumor elimination.     

Dynamics of T‐cell infiltration during the course of ovarian cancer: The gradual shift from a Th17 effector cell response to a predominant infiltration by regulatory T‐cells

The type of immune cells that are present within the tumor microenvironment can play a crucial role in the survival of patients. However, little is known about the dynamics of the tumor‐infiltrating immune cells during disease progression. We studied the immune cells that infiltrated the tumor tissues of ovarian cancer patients at different stages of disease. The early stages of development of ovarian carcinomas were characterized by a strong Th17 immune response, whereas in stage II patients, recruitment of high numbers of Th1 cells was observed. In disseminated tumors (Stages III–IV), we detected a dominant population of Helios⁺ activated regulatory T cells (Tregs) along with high numbers of monocytes/macrophages and myeloid dendritic cells (mDCs). Tumor‐infiltrating Tregs had markedly lower expression of CCR4 than circulating Tregs, and the numbers of tumor‐infiltrating Tregs significantly correlated with the levels of CCL22 in ovarian tumor cell culture supernatants, suggesting their recruitment via a CCR4/CCL22 interaction. CCL22 was mainly produced by tumor cells, monocytes/macrophages and mDCs in the primary ovarian tumors, and its expression markedly increased in response to IFNγ. Taken together, the specific recruitment of Tregs, probably triggered by inflammatory stimuli, leads to a significant immune suppression in the advanced stages of ovarian cancer.     

Inflammation in gastric cancer: Interplay of the COX‐2/prostaglandin E2 and Toll‐like receptor/MyD88 pathways

Cyclooxygenase‐2 (COX‐2) and its downstream product prostaglandin E₂ (PGE₂) play a key role in generation of the inflammatory microenvironment in tumor tissues. Gastric cancer is closely associated with Helicobacter pylori infection, which stimulates innate immune responses through Toll‐like receptors (TLRs), inducing COX‐2/PGE₂ pathway through nuclear factor‐κB activation. A pathway analysis of human gastric cancer shows that both the COX‐2 pathway and Wnt/β‐catenin signaling are significantly activated in tubular‐type gastric cancer, and basal levels of these pathways are also increased in other types of gastric cancer. Expression of interleukin‐11, chemokine (C‐X‐C motif) ligand 1 (CXCL1), CXCL2, and CXCL5, which play tumor‐promoting roles through a variety of mechanisms, is induced in a COX‐2/PGE₂ pathway‐dependent manner in both human and mouse gastric tumors. Moreover, the COX‐2/PGE₂ pathway plays an important role in the maintenance of stemness with expression of stem cell markers, including CD44, Prom1, and Sox9, which are induced in both gastritis and gastric tumors through a COX‐2/PGE₂‐dependent mechanism. In contrast, disruption of Myd88 results in suppression of the inflammatory microenvironment in gastric tumors even when the COX‐2/PGE₂ pathway is activated, indicating that the interplay of the COX‐2/PGE₂ and TLR/MyD88 pathways is needed for inflammatory response in tumor tissues. Furthermore, TLR2/MyD88 signaling plays a role in maintenance of stemness in normal stem cells as well as gastric tumor cells. Accordingly, these results suggest that targeting the COX‐2/PGE₂ pathway together with TLR/MyD88 signaling, which would suppress the inflammatory microenvironment and maintenance of stemness, could be an effective preventive or therapeutic strategy for gastric cancer.     

College of American Pathologists Tumor Regression Grading System for Long-Term Outcome in Patients with Locally Advanced Rectal Cancer

BackgroundThe National Comprehensive Cancer Network''s Rectal Cancer Guideline Panel recommends American Joint Committee of Cancer and College of American Pathologists (AJCC/CAP) tumor regression grading (TRG) system to evaluate pathologic response to neoadjuvant chemoradiotherapy for locally advanced rectal cancer (LARC). Yet, the clinical significance of the AJCC/CAP TRG system has not been fully defined.Materials and MethodsThis was a multicenter, retrospectively recruited, and prospectively maintained cohort study. Patients with LARC from one institution formed the discovery set, and cases from external independent institutions formed a validation set to verify the findings from discovery set. Overall survival (OS), disease‐free survival (DFS), local recurrence‐free survival (LRFS), and distant metastasis‐free survival (DMFS) were assessed by Kaplan‐Meier analysis, log‐rank test, and Cox regression model.ResultsThe discovery set (940 cases) found, and the validation set (2,156 cases) further confirmed, that inferior AJCC/CAP TRG categories were closely /ccorrelated with unfavorable survival (OS, DFS, LRFS, and DMFS) and higher risk of disease progression (death, accumulative relapse, local recurrence, and distant metastasis) (all p < .05). Significantly, pairwise comparison revealed that any two of four TRG categories had the distinguished survival and risk of disease progression. After propensity score matching, AJCC/CAP TRG0 category (pathological complete response) patients treated with or without adjuvant chemotherapy displayed similar survival of OS, DFS, LRFS, and DMFS (all p > .05). For AJCC/CAP TRG1–3 cases, adjuvant chemotherapy treatment significantly improved 3‐year OS (90.2% vs. 84.6%, p < .001). Multivariate analysis demonstrated the AJCC/CAP TRG system was an independent prognostic surrogate.ConclusionAJCC/CAP TRG system, an accurate prognostic surrogate, appears ideal for further strategizing adjuvant chemotherapy for LARC.Implications for PracticeThe National Comprehensive Cancer Network recommends the American Joint Committee of Cancer and College of American Pathologists (AJCC/CAP) tumor regression grading (TRG) four‐category system to evaluate the pathologic response to neoadjuvant treatment for patients with locally advanced rectal cancer; however, the clinical significance of the AJCC/CAP TRG system has not yet been clearly addressed. This study found, for the first time, that any two of four AJCC/CAP TRG categories had the distinguished long‐term survival outcome. Importantly, adjuvant chemotherapy may improve the 3‐year overall survival for AJCC/CAP TRG1–3 category patients but not for AJCC/CAP TRG0 category patients. Thus, AJCC/CAP TRG system, an accurate surrogate of long‐term survival outcome, is useful in guiding adjuvant chemotherapy management for rectal cancer.     

Molecular detection of p16 promoter methylation in the serum of recurrent colorectal cancer patients

We previously proved that p16 promoter methylation present in the tumors of colorectal cancer patients can be detected in the serum of those same patients using methylation-specific PCR (MSP). To seek the possibility that this technique could be applied to the monitoring of cancer recurrence, we examined the p16 methylation using MSP. We detected tumor DNA in the serum of 31 of 45 (69%) patients with recurrent colorectal cancer. No methylation was found in serum DNA of 50 patients with colorectal cancers whose corresponding tumor DNA had no methylation in p16 promoter. These results suggested that MSP might be a sensitive and useful method to detect recurrent colorectal cancer in serum.     

Detection of aberrant methylation of HOXA9 and HIC1 through multiplex MethyLight assay in serum DNA for the early detection of epithelial ovarian cancer

Accumulated evidence revealed that aberrant CpG island hypermethylation plays an important role in carcinogenesis which can serve as a promising target for molecular detection in body fluids. Despite a myriad of attempts to diagnose ovarian cancer (OC) at an early stage, this clinical aim remains a major challenge. To date, no single biomarker is able to accurately detect early OC in either tissue or body fluid. Aberrant DNA methylation patterns in circulating DNA provide highly specific cancer signals. In our study, we establish a novel panel of methylation-specific genes for the development of a TaqMan based qPCR assay to quantify methylation levels. We analyzed promoter methylation of homeobox A9 (HOXA9) and hypermethylated in cancer 1 (HIC1) quantitatively in 120 tissue samples and in 70 matched serum cell-free DNA (CFDNA) of cancerous and noncancerous samples by MethyLight assay. HOXA9 and HIC1 methylation occurred in 82.3 and 80.0% of OC tissue samples in singleplex assay, thereby confirming that methylation was highly cancer-specific. When either or both gene promoter showed methylation, the sensitivity was 88.2% with a specificity of 88.6% in tissue samples. The combined sensitivity for this novel marker panel in serum CFDNA was 88.9% (area under the curve [AUC] = 0.95). In contrast, no hypermethylation was observed in serum from matched cancer-free control women. Our results confirm the elevated performance of novel epigenetic marker panel (HOXA9 and HIC1) when analyzed in tissue and matched serum samples. Our findings reveal the potential of this biomarker panel as a suitable diagnostic serum biomarker for early screening of OC.     

Molecular sputum analysis for the diagnosis of lung cancer

Lung cancer is the leading cause of cancer mortality rate worldwide, mainly because of the presence of metastatic disease at the time of diagnosis. Early detection of lung cancer improves prognosis, and towards this end, large screening trials in high-risk individuals have been conducted since the past century. Despite all efforts, the need for novel (complementary) lung cancer diagnostic and screening methods still exists. In this review, we focus on the assessment of lung cancer-related biomarkers in sputum in the past decennium. Besides cytology, mutation and microRNA analysis, special attention has been paid to DNA promoter hypermethylation, of which all available literature is summarised without time restriction. A model is proposed to aid in the distinction between diagnostic and risk markers. Research on the use of sputum for non-invasive detection of early-stage lung cancer has brought new insights and advanced molecular techniques. The sputum shows a promising potential for routine diagnostic and possibly screening purposes.     

胰腺癌Panc-1细胞TFPI-2基因甲基化状态与其体内体外侵袭能力的关系

目的：探讨甲基化酶抑制剂5-氮杂-2＇-脱氧胞苷（5-aza-2-deoxycytidine,5-Aza-dC）对胰腺癌Panc-1细胞体内体外侵袭能力及裸鼠皮下移植肿瘤组织TFPI-2基因甲基化状态及表达的影响。方法：用不同浓度的5-Aza-dC处理胰腺癌Panc-1细胞。Transwell法测定各组Panc-1细胞的体外侵袭能力。将用药物处理过的各组Panc-1细胞分别接种于裸鼠皮下,观察各组成瘤率及肿瘤大小。用MSP及RT-PCR检测裸鼠移植瘤组织TFPI-2基因甲基化状态及TFPI-2基因mRNA表达情况。结果：与对照组相比,药物处理组Panc-1细胞体外侵袭能力明显下降,裸鼠成瘤率明显降低,第八周时,肿瘤体积明显低于对照组（P〈0.05）。与对照组相比,TFPI-2基因异常甲基化状态在药物处理组裸鼠移植瘤组织中得到逆转,药物处理组移植瘤TFPI-2基因mRNA重新表达,并呈剂量依赖性（P〈0.05）。结论：甲基化酶抑制剂5-氮杂-2＇-脱氧胞苷可能在一定程度上抑制人胰腺癌Panc-1细胞系的体内体外侵袭和生长能力,其机制可能与逆转TFPI-2基因高甲基化状态从而恢复其表达有关。     

胰腺癌Panc-1细胞TFPI-2基因甲基化状态与其体内体外侵袭能力的关系

目的:探讨甲基化酶抑制剂5-氮杂-2'-脱氧胞苷(5-aza-2-deoxycytidine,5-Aza-dC)对胰腺癌Panc-1细胞体内体外侵袭能力及裸鼠皮下移植肿瘤组织TFPI-2基因甲基化状态及表达的影响.方法:用不同浓度的5-Aza-dC处理胰腺癌Panc-1细胞.Transwell法测定各组Panc-1细胞的体外侵袭能力.将用药物处理过的各组Panc-1细胞分别接种于裸鼠皮下,观察各组成瘤率及肿瘤大小.用MSP及RT-PCR检测裸鼠移植瘤组织TFPI-2基因甲基化状态及TFPI-2基因mRNA表达情况.结果:与对照组相比,药物处理组Panc-1细胞体外侵袭能力明显下降,裸鼠成瘤率明显降低,第八周时,肿瘤体积明显低于对照组(P<0.05).与对照组相比,TFPI-2基因异常甲基化状态在药物处理组裸鼠移植瘤组织中得到逆转,药物处理组移植瘤TFPI-2基因mRNA重新表达,并呈剂量依赖性(P<0.05).结论:甲基化酶抑制剂5-氮杂-2'-脱氧胞苷可能在一定程度上抑制人胰腺癌Panc-1细胞系的体内体外侵袭和生长能力,其机制可能与逆转TFPI-2基因高甲基化状态从而恢复其表达有关.     

Crucial involvement of the CCL3‐CCR5 axis‐mediated fibroblast accumulation in colitis‐associated carcinogenesis in mice

Patients with inflammatory bowel diseases often develop colon carcinoma. Combined treatment of azoxymethane (AOM) and dextran sulfate sodium (DSS) recapitulates colitis‐associated cancer in mice. AOM/DSS‐induced tumor formation was reduced in CCL3‐ or its specific receptor, CCR5‐deficient mice despite the presence of a massive infiltration of inflammatory cells. However, AOM/DSS‐induced type I collagen‐positive fibroblast accumulation in the colon was reduced in CCL3‐ or CCR5‐deficient mice. This was associated with depressed expression of heparin‐binding epidermal growth factor‐like growth factor (HB‐EGF), which is expressed mainly by fibroblasts. Moreover in vitro, CCL3 induced fibroblasts to proliferate and to enhance HB‐EGF expression. Furthermore, CCR5 blockade reduced tumor formation together with reduced fibroblast accumulation and HB‐EGF expression, even when administered after the development of multiple colon tumors. Thus, CCL3‐CCR5‐mediated fibroblast accumulation may be required, in addition to leukocyte infiltration, to induce full‐blown colitis‐associated carcinogenesis. Our studies shed light on a therapeutic potential of CCR5 antagonist for patients with colitis‐associated cancer.     

Application of Crossover Analysis-logistic Regression in the Assessment of Gene- environmental Interactions for Colorectal Cancer

Background: Analysis of gene-gene and gene-environment interactions for complex multifactorial humandisease faces challenges regarding statistical methodology. One major difficulty is partly due to the limitations ofparametric-statistical methods for detection of gene effects that are dependent solely or partially on interactionswith other genes or environmental exposures. Based on our previous case-control study in Chongqing of China,we have found increased risk of colorectal cancer exists in individuals carrying a novel homozygous TT at locusrs1329149 and known homozygous AA at locus rs671. Methods: In this study, we proposed statistical methodcrossoveranalysis in combination with logistic regression model, to further analyze our data and focus on assessinggene-environmental interactions for colorectal cancer. Results: The results of the crossover analysis showed thatthere are possible multiplicative interactions between loci rs671 and rs1329149 with alcohol consumption. Multifactoriallogistic regression analysis also validated that loci rs671 and rs1329149 both exhibited a multiplicativeinteraction with alcohol consumption. Moreover, we also found additive interactions between any pair of twofactors (among the four risk factors: gene loci rs671, rs1329149, age and alcohol consumption) through thecrossover analysis, which was not evident on logistic regression. Conclusions: In conclusion, the method basedon crossover analysis-logistic regression is successful in assessing additive and multiplicative gene-environmentinteractions, and in revealing synergistic effects of gene loci rs671 and rs1329149 with alcohol consumption inthe pathogenesis and development of colorectal cancer.     

启动子区5''CpG岛去甲基化对人肠癌RKO细胞生物学表型的影响

目的:探讨DNA启动子区5'CpG岛甲基化状态与人肠癌RKO细胞生物学特征的关系.方法:应用特异性DNA甲基转移酶抑制剂-5-氮-2'-脱氧胞苷(5-Aza-2'-deoxycytidine,5-Aza-CdR)处理肠癌RKO细胞72小时,甲基化特异性PCR(methylation-specific PCR,MSP)及DNA测序法分析p16/CDKN2抑癌基因5'CpG岛甲基化状态;MTT、FCM、荧光染色及透射电镜检测启动子区去甲基化后对细胞生长、形态和细胞周期凋亡的影响.结果:肠癌RKO细胞p16/CDKN2基因5'CpG岛呈高甲基化状态;DNA甲基转移酶抑制剂(5-Aza-CdR)能较好地逆转启动子区胞嘧啶甲基化状态;CpG岛去甲基化后能明显地抑制肠癌细胞的生长,增加细胞群体倍增时间(P＜0.01),诱导肠癌细胞凋亡,并呈良好的量效依赖关系.结论:通过逆转CpG岛高甲基化能有效地抑制肠癌细胞增殖,为临床治疗大肠癌提供新的作用靶点.     

Effects of Promoter Region 5＇CpG Island Demethylation on the Biological Behavior of Human Colorectal Cancer RKO Cells in Vitro

OBJECTIVE To explore the relationship between the methylation status of the promoter 5＇CpG island region and the biological behavior of human colorectal cancer RKO cells in vitro. METHODS RKO cells were treated with a selective DNA methyltransferase inhibitor-5-aza-2＇-deoxycytidine （5-aza-CdR） for 72 h. Methylationspecific PCR （MSP）, T-A cloning and DNA sequence analysis were used to determinate the 5＇CpG island methylation status of the p16/CDKN2 tumor suppressor gene. Cell growth, morphological changes and apoptosis were analyzed by the MTT assay, flow cytometry, fluorescence staining and electron microscopy. RESULTS The 5＇CpG island of the p16/CDKN2 tumor suppressor gene in RKO cells was a typically hypermethylated. The DNA methyltransferase inhibitor （5-Aza-CdR） effectively reversed the hypermethylation status of the promoter region. With demethylation, RKO cell growth was suppressed, the cells doubling times were prolonged （P〈0.01） and apoptosis was induced, which showed a relationship. CONCLUSION A selective DNA methyltransferase （DNMT） inhibitor can inhibit proliferation by demethylation in 5＇CpG islands, and may be a potential new therapy target for colorectal cancer.     

Comparison of the Performance of Log-logistic Regression nd Artificial Neural Networks for Predicting Breast Cancer elapse

Background: Breast cancer is the most common cancers in female populations. The exact cause is notknown, but is most likely to be a combination of genetic and environmental factors. Log-logistic model (LLM)is applied as a statistical method for predicting survival and it influencing factors. In recent decades, artificialneural network (ANN) models have been increasingly applied to predict survival data. The present research wasconducted to compare log-logistic regression and artificial neural network models in prediction of breast cancer(BC) survival. Materials and Methods: A historical cohort study was established with 104 patients sufferingfrom BC from 1997 to 2005. To compare the ANN and LLM in our setting, we used the estimated areas underthe receiver-operating characteristic (ROC) curve (AUC) and integrated AUC (iAUC). The data were analyzedusing R statistical software. Results: The AUC for the first, second and third years after diagnosis are 0.918, 0.780and 0.800 in ANN, and 0.834, 0.733 and 0.616 in LLM, respectively. The mean AUC for ANN was statisticallyhigher than that of the LLM (0.845 vs. 0.744). Hence, this study showed a significant difference between theperformance in terms of prediction by ANN and LLM. Conclusions: This study demonstrated that the abilityof prediction with ANN was higher than with the LLM model. Thus, the use of ANN method for prediction ofsurvival in field of breast cancer is suggested.     

影响结直肠癌患者预后的病理因素——应用电子计算机的多因素逐步回归分析

应用电子计算机及多因素逐步回归分析方法,对80例不同预后(术后生存时间<5年或≥5年)的结直肠癌患者的3个临床病理指标和5个计量病理指标进行分析,结果显示,临床病理指标组织学分级和临床分期,计量病理指标DNA含量和核浆比,4个指标与预后关系密切。用它们建立回归方程,区分术后生存时间<5年组和≥5年组,两组差别显著(P相似文献   

Investigating the Incidence of Prostate Cancer in Iran 2005 -2008 using Bayesian Spatial Ecological Regression Models

Background: Prostate cancer is the most commonly diagnosed form of cancer and the sixth leading cause ofcancer-related deaths among men in the entire world. Reported standardized incidence rates are 12.6, 61.7, 11.9and 27.9 in Iran, developed countries, developing countries and the entire world, respectively. The present studyinvestigated the relative risk of PC in Iran at the province level and also explored the impact of some factors bythe use of Bayesian models. Materials and Methods: Our study population was all men with PC in Iran from2005 to 2008. Considered risk factors were smoking, fruit and vegetable intake, physical activity, obesity andhuman development index. We used empirical and full Bayesian models to study the relative risk in Iran atprovince level to estimate the risk of PC more accurately. Results: In Iran from 2005 to 2008 the total numberof known PC cases was 10,361 with most cases found in Fars and Tehran and the least in Ilam. In all modelsjust human development index was found to be significantly related to PC risk Conclusions: In the unadjustedmodel, Fars, Semnam, Isfahan and Tehran provinces have the highest and Sistan-and-Baluchestan has theleast risk of PC. In general, central provinces have high risk. After adjusting for covariates, Fars and Zanjanprovinces have the highest relative risk and Kerman, Northern Khorasan, Kohgiluyeh Boyer Ahmad, Ghazvinand Kermanshah have the lowest relative risk. According to the results, the incidence of PC in provinces withhigher human development index is higher.     

顺铂、5-氟尿嘧啶持续动脉灌注化疗对口腔癌患者免疫功能的影响

目的 研究顺铂、5-氟尿嘧啶持续动脉灌注化疗对口腔癌患者免疫功能的影响.方法 选取30例口腔癌患者为治疗组,选取30例健康志愿者为对照组,给予治疗组顺铂、5-氟尿嘧啶持续动脉灌注化疗,观察治疗组化疗前后T淋巴细胞各亚群的改变、T细胞表型表达特点、细胞因子水平改变.结果 30例健康志愿者T淋巴细胞各表型占总细胞数的比例处于正常范围,化疗前治疗组CD3+、CD4+、CD4+/CD8+较对照组低(P<0.05),CD8+较对照组高(P<0.05),化疗后治疗组CD4+/CD8+较化疗前升高(P<0.05),CD8+较化疗前降低(P<0.05);化疗前治疗组CD4+/INF-y+INF-y+低于对照组(P<0.05),化疗后治疗组INF-y+较化疗前升高,且高于对照组(P<0.05),化疗后治疗组CD4+/INF-y+INF-y+较化疗前升高,但仍低于对照组(P<0.05);化疗前治疗组CD4+/IL-2+IL-2+低于对照组(P<0.05),化疗后治疗组CD4+/IL-2+IL-2+与化疗前比较有所上升,但仍低于对照组(P<0.05).结论 给予口腔癌患者手术治疗的同时,进行顺铂、5-氟尿嘧啶持续动脉灌注化疗,能够改善患者的免疫功能,有利于患者的预后.