基于轻量化YoloV5s的血癌细胞检测

为了解决人工检测血癌细胞耗费人力,且容易出现漏检、误检的情况,提出一种新型的检测血癌细胞检测算法——YoloV5s-FasterNet。该算法在原本的YoloV5s框架上,通过将主干网络中的C3检测层改进为FasterNet轻量化网络用来提取特征信息,降低整体网络模型的复杂程度,并在主干网络中增加坐标注意力(coordinate attention, CA)机制模型更好的定位和识别目标信息来提高检测精度。通过在血癌数据集上进行大量实验结果表明:与原模型相比,改进的模型平均精度提升2.2%,参数量减少25.7%,检测速度提高15%,实验结果良好,证明该算法对血癌细胞检测具有实用性。

螺旋藻藻蓝蛋白对人血癌细胞株HL-60,K-562和U-937的生长影响

运用半固体琼脂培养法和MTT检测法测定了螺旋藻藻蓝蛋白对人血癌细胞株HL-60，K-562和U-937生长的影响。体外培养条件下用不同浓度的螺旋藻藻蓝蛋白处理这3种肿瘤细胞，结果显示螺旋藻藻蓝蛋白对这三种肿瘤细胞均有不同程度的抑制作用，并存在浓度剂量效应，高浓度抑制作用强。

台大发现调控慢性骨髓血癌细胞新机制

据“中央社”报道，台湾大学生化暨分子生物研究所发现可促成慢性骨髓血癌（CML）细胞凋亡的新机制；若可借由该机制筛选适合药物，将有机会找出治疗CML的新疗法。

大蒜素对肝癌细胞血道转移的影响

目的:探讨大蒜素对肝癌小鼠模型肿瘤细胞经血道转移的影响及相关机理。方法:取昆明小鼠36只,尾静脉接种H22肝癌细胞悬液后用不同浓度的大蒜素溶液干预1周,处死小鼠,取肺组织观察肺部转移瘤生长情况,取脾和胸腺称重后分别计算脾指数和胸腺指数。结果:实验组小鼠脾指数明显增高且具较明显的剂量效应关系,胸腺指数有一定程度的增高,各实验组均表现出一定程度的肿瘤抑制作用,高浓度组(F组)最明显。结论:大蒜素能显著促进脾的生长,且能一定程度促进胸腺的生长,从而提高机体免疫力;较高浓度的大蒜素具有抑制H22肝癌血道转移模型肺转移作用。

小细胞肺癌免疫磁性微珠的构建及鉴定

目的 :构建能特异地与靶细胞结合并赋有磁响应性的小细胞肺癌免疫磁性微珠 ,检验其在分离微量癌细胞中的效率。方法 :将微量小细胞肺癌H12 8细胞加入到外周血单个核细胞悬液中混匀 ,再通过特异性单抗包被的免疫磁性微珠吸附、富集、免疫细胞化学鉴定。最后 ,计算癌细胞的回收率和检测敏感性。结果 :包被的小细胞肺癌免疫磁性微珠与H12 8能敏感而特异地结合。与免疫细胞化学方法结合可检出 5 4 .4 %混入外周血单个核细胞中的微量癌细胞 ,未有假阳性。结论 :免疫磁性微珠能有效地从外周血单个核细胞中分离出微量肺癌细胞 。

结肠癌病人手术前后血中CK-20 mRNA检测的临床意义

目的探讨结肠癌病人手术前后外周血中CK-20 mRNA水平变化的情况,从而判断肿瘤微转移情况。方法采用逆转录多聚酶链式反应方法(RT-PCR方法),以CK-20 mRNA为靶基因,检测了38例结肠癌病人手术前后CK-20mRNA表达情况。结果结肠良性疾病组CK-20 mRNA表达均为阴性。结肠癌组(38例)术前CK-20 mRNA阳性率为23.7%(9/38),术后阳性率为37%(14/38),术后明显高于术前(P<0.05)。A组(术中先结扎回流静脉及切断相应系膜)术前术后阳性率为30%(6/20),B组(不结扎回流静脉及不切断相应系膜)术前阳性率为35%(7/20),术后阳性率为50%(19/20),B组术后阳性率明显高于术前(P<0.05)。结论结肠癌病人(B期、C期)术前已有部分病人血中存在游离癌细胞,手术中的牵拉刺激可能增加癌细胞扩散的可能性,术中先结扎回流静脉及切断相应系膜可起到阻止癌细胞血行播散的可能性。

微波消融与手术切除治疗原发性小肝癌对癌细胞播散入血的影响

目的对比研究微波消融与手术切除治疗原发性小肝癌(PHC)对癌细胞播散入血及外周血细胞免疫功能的影响。方法将符合条件的40例患者,分为微波组19例,手术组21例。于治疗前、治疗后30min、1d及7d采静脉血,实时定量巢式RTPCR检测外周血甲胎蛋白(AFP)mRNA,并检测CD3、CD4、CD8、CD4/CD8及肝功能。结果手术组和微波组患者术后血清ALT及AST均升高,手术组升高较微波组显著;与术前相比,微波组患者术后7d内CD3、CD4、CD8和CD4/CD8无明显变化(P>0.05),手术组CD3、CD4和CD4/CD8较术前降低;实时定量巢式RTPCR检测两组患者外周血标本,治疗前67.5%(27/40)患者可检测出AFPmRNA拷贝数,治疗后表达量增高,两组之间比较,差异无统计学意义。随访患者1～16个月,其外周血中AFPmRNA持续表达者,复发转移的可能性大。结论微波消融或手术切除原发性小肝癌,可造成患者外周血中脱落肝癌细胞增多。患者外周血细胞免疫功能手术后降低,而微波消融后得以很好保护。微波消融对肝功能的损伤较小,此方法治疗PHC有一定的临床应用价值。

血小板与癌症转移

血小板与癌症转移文张彦龙癌症被称为人类生命和健康的第一杀手，其危害的关键在于它的转移。研究发现．人体内具有凝血作用的血小板，在癌症的转移过程小，却与癌细胞相互“勾结”、“助纣为虐”，成为癌症转移的“帮凶”。癌症的转移是从原发肿瘤组织上的癌细胞脱落开始...

Role of AFP mRNA expression in peripheral blood as a predictor for postsurgical recurrence of hepatocellular carcinoma: A systematic review and meta-analysis

AIM:To identify the role of alpha-fetoprotein (AFP) mRNA expression in peripheral blood one week after surgery as a predictor for recurrence of hepatocellular carcinoma (HCC). METHODS: Published studies fulfilling the selection criteria were identified by searching several databases online. After a methodology assessment using a quality scale designed by European Lung Cancer Working Party, data in each research were aggregated by means of meta-analysis. RESULTS: Altogether 368 cases were included in the 9 selected studies, which fulfilled the selection criteria. The quality scores ranged from 35% to 84% with a median score of 55%. The 'design' subscore had the lowest median value (38%). By aggregating the data, a high x2 value (77.576) was presented. The fail-safe number was 136 and 64 for P= 0.05 and 0.01, respectively. CONCLUSION: AFP mRNA expression in peripheral blood 1 wk after surgery correlated with the recurrence of HCC and was a good predictor for tumor recurrence.

RNA interference-mediated gene silencing of vascular endothelial growth factor in colon cancer cells

AIM： TO inhibit the expression of vascular endothelial growth factor （VEGF） in colon cancer cell line by RNA interference （RNAi）.METHODS： Followed the service of E-RNAi, we designed and constructed two kinds of shRNA expression vectors aiming at the VEGF gene, then transfected them into colon cancer HT29 cells by lipofectamineTM 2000. The level of VEGF mRNA was investigated by RT-PCR and Northern blotting. The protein expression of VEGF was observed by immunofluoresence staining and Western blotting.RESULTS： We got two kinds of VEGF specific shRNA expression vectors which could efficiently inhibit the expression of VEGF in HT29 cells. RT-PCR, Northern blotting, immunofluoresence staining and Western blotting showed that inhibition rate for VEGF expression was up to 42%, 89%, 73% and 82%, respectively.CONCLUSION： The expression of VEGF can be inhibited by RNA interference in HT29 cells.

Ruptured high flow gastric varices with an intratumoral arterioportal shunt treated with balloon-occluded retrograde transvenous obliteration during temporary balloon occlusion of a hepatic artery

A patient presented with hematemesis due to gastric variceal bleeding with an intratumoral arterioportal shunt. Contrast-enhanced CT revealed gastric varices and hepatocellular carcinoma with tumor thrombi in the right portal vein. Angiography and angio-CT revealed a marked intratumoral arterioportal shunt accompanied with reflux into the main portal vein and gastric varices. Balloon-occluded retrograde venography from the gastro-renal shunt showed no visualization of gastric varices due to rapid blood flow through the intratumoral arterioportal shunt. The hepatic artery was temporarily occluded with a balloon catheter to reduce the blood flow through the arterioportal shunt, and then concurrent balloon-occluded retrograde transvenous obliteration （BRTO） was achieved. Vital signs stabilized immediately thereafter, and contrast-enhanced CT revealed thrombosed gastric varices. Worsening of hepatic function was not recognized. BRTO combined with temporary occlusion of the hepatic artery is a feasible interventional procedure for ruptured high flow gastric varices with an intratumoral arterioportal shunt.

New multi protein patterns differentiate liver fibrosis stages and hepatocellular carcinoma in chronic hepatitis C serum samples

AIM： To identify a multi serum protein pattern as well as single protein markers using surface-enhanced laser desorption/ionisation time-of-flight mass spectrometry （SELDI-TOF-MS） for detection and differentiation of liver fibrosis （F1-F2）, liver cirrhosis （F4） and hepatocellular carcinoma （HCC） in patients with chronic hepatitis C virus （HCV）. METHODS： Serum samples of 39 patients with F1/F2 fibrosis, 44 patients with F4 fibrosis, 34 patients with HCC were applied to CM10 arrays and analyzed using the SELDI-TOF ProteinChip System （PBS-Ⅱc; Ciphergen Biosystems） after anion-exchange fractionation. All patients had chronic hepatitis C and histologically confirmed fibrosis stage/HCC. Data were analyzed for protein patterns by multivariate statistical techniques and artificial neural networks. RESULTS： A 4 peptide/protein multimarker panel （7486, 12843, 44293 and 53598 Da） correctly identified HCCs with a sensitivity of 100% and specificity of 85% in a two way-comparison of HCV-cirrhosis versus HCV-HCC training samples （AUROC 0.943）. Sensitivity and specificity for identification of HCC were 68% and 80% for random test samples. Cirrhotic patients could be discriminated against patients with F1 or F2 fibrosis using a 5 peptide/protein multimarker pattern （2873, 6646, 7775, 10525 and 67867 Da） with a specificity of 100% and a sensitivity of 85% in training samples （AUROC 0.976） and a sensitivity and specificity of 80% and 67% for random test samples. Combination of the biomarker classifiers with APR/score and alfa-fetopotein （AFP） improved the diagnostic performance. The 6646 Da marker protein for liver fibrosis was identified as apolipoprotein C-I. CONCLUSION： SELDI-TOF-MS technology combined with protein pattern analysis seems a valuable approach for the identification of liver cirrhosis and hepatocellular carcinoma in patients with chronic hepatitis C. Host probably a combination of different serum markers will help to identify liver cirrhosis and early-stage hepatocellular carcinomas in the future.

Relationship between P-glycoprotein and CD44 expression in esophageal carcinoma

Objective： To investigate the relationship between P-glycoprotein （P-gp） and adhesion molecule CD44 expression as well as their clinical significance in esophageal carcinoma. Methods： To examine the expressed level of P-gp and CD44 by flow cytometry （FCM） in the operated samples of 70 cases with esophageal carcinoma and their normal mucosa of esophageal incision, and to evaluate their relationship with clinicopathological factors. Results： Among the 70 cases with esophageal carcinoma, the expression of P-gp in the 27 cases （38.6%） was negative （positive cells 〈25%）; 11 cases （15.7%） were 25%-40% expression of P-gp positive cells; 14 cases （20%） were 41%-60% expression of P-gp positive cells; 18 cases （25.7%） were the high expression （positive cells 〉60%） of P-gp. Of the cases with the tumor sizes being more than 4 cm, the expression of CD44 showed a significant difference （P〈0.05） in 25 cases with P-gp positive, compared with 19 cases with P-gp negative. Of the cases with high-mild differentiated esophageal carcinoma, the expression of CD44 showed a significant difference （P〈0.05） in 22 cases with P-gp positive, compared with 17 cases with P-gp negative. Of the cases with clinical Ⅲ-Ⅳ stage, the expression of CD44 showed a significant difference （P〈0.05） in 26 cases with P-gp positive, compared with 10 cases with P-gp negative. Of the cases with lymph node metastasis, the CD44 expression showed a significant difference （P=0.050） in 27 cases with P-gp positive, compared with 11 cases with P-gp negative. Of the cases of the patients＇ age being more than 56 years, the expression of CD44 showed a significant difference （P〈0.01） in 27 cases with P-gp positive, compared with 12 cases with P-gp negative. When the P-gp and CD44 expression were positive, the clinical Ⅱ stage and Ⅲ-Ⅳ stage in esophageal carcinoma was showed a significant difference （P〈0.05）. Conclusion： When the CD44 and P-gp both have the positive high expression, it will be significantly associated with the esophageal carcinoma progression and metastasis, so both were a positive expression in esophageal carcinoma, it might suggest a poor and unfavorable prognosis result.

Hepatocellular carcinoma masquerading as a bleeding gastric ulcer: A case report and a review of the surgical management

Hepatocellular Carcinoma (HCC) is a common malignancyworldwide. While bleeding from the gastrointestinal tract(BGIT) has a well known association with HCC, suchcases are mainly due to gastric and esophageal varices.BGIT as a result of invasion of the gastrointestinal tractby HCC is extremely rare and is reportedly associatedwith very poor prognosis. We describe a 67-year-oldmale who presented with BGIT. Endoscopy showed thesite of bleeding to be from a gastric ulcer, but endoscopictherapy failed to control the bleeding and emergencysurgery was required. At surgery, the ulcer was found tohave arisen from direct invasion of the gastrointestinaltract by HCC of the left lobe. Control of the bleedingwas achieved by surgical resection of the HCC en-bloc with the lesser curve of the stomach. The patientremains alive 33 mo after surgery. Direct invasion of thegastrointestinal tract by HCC giving rise to BGIT is veryuncommon. Surgical resection may offer significantlybetter survival over non-surgical therapy, especially if thepatient is a good surgical candidate and has adequatefunctional liver reserves. Prognosis is not uniformly grave.

Genistein inhibits invasive potential of human hepatocellular carcinoma by altering cell cycle, apoptosis, and angiogenesis

AIM： To study the in vitro and in vivo inhibitory effects of genistein on invasive potential of Bel 7402 hepatocellular carcinoma （HCC） cells and to explore the underlying mechanism. METHODS： Bel 7402 HCC cells were exposed to genistein. The invasive activity of tumor cells was assayed in transwell cell culture chamber, p125^FAK expression and cell cycle were evaluated by a functional assay. Cell apoptosis analysis was performed with TUNEL method. In addition, bilateral subrenal capsule xenograft transplantation of HCC was performed in 10 nude mice. Genistein was injected and the invasion of HCC into the renal parenchyma was observed. Nicrovessels with immunohistochemical staining were detected. RESULTS： Genistein significantly inhibited the growth of Bel 7402 cells, the inhibitory rate of tumor cells was 26 -42%. The invasive potential of Bel 7402 cells in vitro was significantly inhibited, the inhibitory rate was 11- 28%. Genistein caused G2/M cell cycle arrest, S phase decreased significantly. The occurrence of apoptosis in genistein group increased significantly. The expression of p125^FAK in 5 μg/mL genistein group （15.26±0.16%） and 10 μg/mL genistein group （12.89±0.36%） was significantly lower than that in the control group （19.75± 1.12%, P〈0.05）. Tumor growth in genistein-treated nude mice was significantly retarded in comparison to control mice, the inhibitory rate of tumor growth was about 20%. Genistein also significantly inhibited the invasion of Bel 7402 cells into the renal parenchyma of nude mice with xenograft transplant. The positive unit value of microvessels in genistein-treated group （10.422 ±0.807） was significantly lower than that in control group （22.330 ± 5.696, P〈 0.01）. CONCLUSION： Genistein can effectively inhibit the invasive potential of Bel 7402 HCC cells by altering cell cycle, apoptosis and angiogenesis, inhibition of focal adhesion kinase may play a significant role in this process.

Usefulness of serum des-γ-carboxy prothrombin in detection of hepatocellular carcinoma

AIM： To evaluate whether DCP is better than AFP for differentiating HCC from nonmalignant liver disease and further evaluate the usefulness of DCP in early diagnosis of small HCC. METHODS： Serum DCP and AFP levels were determined in 127 patients. Among these patients, 32 were with noncirrhotic chronic hepatitis, 34 were with compensated cirrhosis, and 61 were with HCC. The cut-off value for the DCP and AFP were set as 40 mAU/mL and 20 ng/mL, respectively. To compare the diagnostic value of DCP and AFP in distinguishing HCC from nonmalignant chronic liver disease, receiver operating characteristic （ROC） curves were constructed for each assay. RESULTS： The accuracy, sensitivity, and specifidty of DCP were higher than AFP in detecting HCC （81.9%, 77%, and 86.4% vs 68.5%, 59%, and 77.3%, respectively）. The area under the ROC （AUROC） curves revealed that DCP had a better accuracy than AFP in diagnosis of HCC （0.85 [95%CI, 0.78-0.91] vs 0.73 [95%CI, 0.65-0.81], P= 0.013）. In 39 patients with solitary HCC, the positive rates of DCP were 100% in patients with tumor size larger than 3 cm, 66.7% in patients with tumor size 2-3 cm and 50% in patients with tumor size less than 2 cm. The positive rates of AFP in patients with tumor size larger than 3 cm, 2-3 crn and less than 2 cm were 55.6%, 50%, and 33.3%, respectively. The median level of DCP in HCC patients with tumor size larger than 3 cm was significantly higher than those with tumor size 2-3 cm and those with the size of less than 2 cm. CONCLUSION： Our study indicates that DCP has a better diagnostic value than AFP in differentiating HCC from nonmalignant chronic liver disease. DCP has not only a stronger correlation with HCC than AFP in tumor size but also more effectiveness than AFP in detecting small size of HCC.

Serum chromogranin-A in hepatocellular carcinoma: Diagnostic utility and limits

AIM: The utility of serum alpha-fetoprotein (α-FP) for the detection of hepatocellular carcinoma (HCC) is questionable. High serum levels of chromogranin-A (CgA) have recently been reported in HCC. Impaired hepatic, renal, and heart functions influence circulating CgA. The aim of this study was to assess sensitivity and specificity of serum CgA as a marker of HCC in patients with liver cirrhosis (LC). METHODS: Serum CgA levels were measured by RIA in 339 patients of which 54 HCC, 132 LC, 45 chronic hepatitis (CH), 27 chronic heart failure (CHF), 36 chronic renal failure (CRF), 45 chronic inflammatory bowel disease (IBD) as disease controls and in 75 healthy controls. Patients with liver disease or IBD and concomitant renal and/or heart failure were excluded. Pearson correlation, non-parametric combination test and confidence interval analysis were used for statistical analysis. RESULTS: Serum CgA above normal values (100 ng/mL) were found in 83% of HCC patients, in 48% of LC patients, in 20% of CH patients, in 33% of IBD patients, in 92% of CRF patients, in 100% of CHF patients, and in none of the healthy controls. The mean CgA values in HCC (769±1046), in LC (249±369), in CH (87±94), in CRF (1390±1401), in CHF (577±539), in IBD (146±287) were significantly higher than those in healthy controls (48±18). HCC patients had higher CgA values (P<0.01) than LC, CH, and IBD patients but did not differ from those with CRF or CHF. The 95% CI for the mean (250-1289 ng/mL) in HCC patients was selected as a CgA range and the lower value of such range was assumed as cut-off. Sensitivity and specificity of CgA, calculated in relation to the cut-off in patients with cirrhosis and HCC, were respectively 61% (CI 48-73%) and 82% (CI 75-88%). Serum a-FP values were >200 ng/mL in 21% of the HCC patients and in none of the LC patients. No significant correlation was found between a-FP and CgA in patients with HCC and in patients with cirrhosis. CONCLUSION: When HCC is suspected and a-FP is normal or <200 ng/mL, CgA serum values represent a complementary diagnostic tool, unless kidney or heart failure is present.

New insights into the role of PML in tumour suppression

The PML gene is involved in the t（15;17） translocation of acute promyelocytic leukaemia （APL）, which generates the oncogenic fusion protein PML （promyelocytic leukaemia protein）-retinoic acid receptor alpha. The PML protein localises to a subnuclear structure called the PML nuclear domain （PML-ND）, of which PML is the essential structural component. In APL, PML-NDs are disrupted, thus implicating these structures in the pathogenesis of this leukaemia. Unexpectedly, recent studies indicate that PML and the PML-ND play a tumour suppressive role in several different types of human neoplasms in addition to APL. Because of PML＇s extreme versatility and involvement in multiple cellular pathways, understanding the mechanisms underlying its function, and therefore role in tumour suppression, has been a challenging task. In this review, we attempt to critically appraise the more recent advances in this field and propose new avenues of investigation.

Effect of non-anticoagulant N-desulfated heparin on expression of vascular endothelial growth factor, angiogenesis and metastasis of orthotopic implantation of human gastric carcinoma

AIM： To investigate the effect of N-desulfated heparin on tumor metastasis and angiogenesis, and expression of vascular endothelial growth factor （VEGF） of orthotopic implantation of human gastric carcinoma in male severe combined immune deficiency （SCID） mice. METHODS： Human gastric cancer SGC-7901 cells were orthotopically implanted into the stomach of SC/D mice. The mice were randomly divided into normal saline group and N-desulfated heparin group. One week after operation, the mice in N-desulfated heparin group reo ceived i.v. injections of N-desulfated heparin （Shanghai Institute of Cell Biology, Chinese Academy of Sciences, 10 mg/kg.d） twice weekly for 3 wk. The mice in normal saline group received i.v. injections of normal saline （100 μL） twice weekly for 3 wk. The mice were sacrificed six weeks after implantation. Tumor metastasis was evaluo ated histologically for metastasis under microscope. Intratumoral microvessel density （MVD） and VEGF expression were evaluated immuohistochemically. VEGF mRNA expression in gastric tissue of SC/D mice was detected by real time PCR. RESULTS： The tumor metastasis rate was 80% in normal saline group and 20% in N-desulfated heparin group （P 〈 0.05）. MVD was 8.0 ± 3.1 in normal saline group and 4.3 ± 1.8 in N-desulfated heparin group （P 〈 0.05）. VEGF positive immunostaining was found in cytoplasm of cancer cells. The rate of VEGF positive expression was higher in normal saline group than in N-desulfated hepa- rin treated group （90% vs 20%, P 〈 0.05）. VEGF mRNA expression was significantly inhibited by N-desulfated heparin and was higher in normal saline group than in N-desulfated heparin group （Ct value 19.51 ± 1.01 vs 22.55± 1.36, P 〈 0.05）. N-desulfated heparin significantly inhibited the expression of VEGF mRNA in cancer cells. No bleeding occurred in N-desulfated heparin group. CONCLUSION： N-desulfated heparin can inhibit metastasis of gastric cancer by suppressing tumor VEGF expression and tumor angiogenesis, but has no obvious anticoagulant activity.