60例肺癌标本的体外抗癌药敏试验结果分析

６０例肺癌标本的体外抗癌药敏试验结果分析秦治明，李良彬，温剑虎，吴庆琛重庆医科大学临床学院胸外科（重庆６３００４２）近年来以抗癌药物治疗个体化为目的的抗癌药敏试验日益受到肿瘤研究者的青睐，它是肿瘤治疗个体化的实验基础。在体外抗癌药敏试验中，以人癌细胞...

江苏部分农村地区肺癌流行趋势及其与吸烟的关系

江苏部分农村地区肺癌流行趋势及其与吸烟的关系沈洪兵，徐耀初，沈靖，叶本法，刘伯齐近年来，对农村肺癌的研究报道较少。本文对江苏部分农村地区的肺癌流行趋势及其与吸烟的关系作以下分析。对象与方法１９８９年７月，在医科院肿瘤所的统一部署下，将启东、杨中、建湖...

降钙素与肺癌

降钙素(CT)是甲状腺C细胞分泌的一种可降低血浆钙离子的多肽激素。在病理状态下,肿瘤组织可异位产生CT,如甲状腺髓样癌及肺癌患者的血中CT可异常增高。因此,国外学者把CT作为癌标之一进行临床研究和应用。本文主要对CT在肺癌患者血中的生化特性、与临床的关系及其可能的来源加以综述。

安徽省肺癌死亡抽样调查资料分析

安徽省肺癌死亡抽样调查资料分析权循凤，汪义高，吕桦根据安徽省１９９０～１９９２年肺癌死亡回顾调查资料，本文对肺癌的死亡危害情况进行了分析，结果如下。一、资料来源及可靠性资料源于安徽省１９９０～１９９２年恶性肿瘤回顾抽样调查资料。调查地区为二市七县。调...

接触不同浓度沥青烟的油毡工人与肺癌关系的研究

Ｐ＜０．０１．－观察死亡数低于５人表４不同接触浓度水平的肺癌ＳＤＲ和ＳＭＲ（男性）△对照组（１）＊Ｐ＜０．０５Ｐ＜０．０１表５不同接触浓度的肺癌标化死亡率与吸烟和职业接触的析因分析注：△指对照组（１）吸烟接触组与吸烟对照组比较时，肺癌也有显著超出量，ＳＭＲ为２．５６（Ｐ＜０．０１）．食道癌也有明显超出，ＳＭＲ为２．０４（Ｐ＜０．０５）。非吸烟接触组与非吸烟对照组比较，肺癌超出量特别显著，ＳＭＲ为６．１６（Ｐ＜０．０１），显示职业因素和油毡工人肺癌超量有密切联系。吸烟和职业两因素的析因分析表明，吸烟使接触低、中、高浓度的油毡工人肺癌ＲＲ增加１．５２～３．６４倍，可见，吸烟对肺癌也有加强作用，见表５。吸烟ＲＲ：是指吸烟与非吸烟标化死亡的率（１／１０万）比；职业接触ＲＲ是指接触组不吸烟与对照组（１）不吸烟者标化死亡的率比；吸烟＋职业接触ＲＲ是指接触组吸烟与对照组不吸烟者标化死亡的率比。结论在回顾研究的基础上继续前瞻性研究的结果表明，油毡工人癌症是第一位死因，肺癌居全癌之首，男性肺癌标化死亡率（３４．９４／１０万）显著高于对照人群和全国城市居民肺癌死亡率。不同观察期和不同入厂接触年代肺癌均显示稳定的超出量。接触高、?

北京市房山县癌高发区健康人群头发中铜、锌水平分析

以房山县癌高发区、癌中等区及同县对照区三组人群，年龄在４０～６０岁长期居住无明显疾病史健康人群作研究对象，分析结果表明发铜值基本无变化，癌高发区、癌中等区发锌值明显低于对照区，与癌标化死亡率呈负相关趋势，铜锌比值高于对照区，发锌值随吸烟指数、经济水平憎加而增高，男性的发锌值高于女性。

人血清胃蛋白酶原含量的测定与胃癌的关系

胃癌是我国的主要恶性肿瘤之一。国外已有用放射免疫的方法检测人末稍血清中胃蛋白酶原Ⅰ型和Ⅱ型（ＰＧⅠ和ＰＧⅡ），用ＰＧⅠ及ＰＧⅡ的测值和ＰＧⅠ／ｐＧⅡ的比值预测胃癌和癌前病变。本研究是采用生物素、亲合素酶标的方法测定人末稍血中的ＰＧⅠ和ＰＧⅡ，并探讨用该方法预测胃癌和癌前病变的可能性。结果表明，ｐＧⅠ在胃癌和萎缩性胃炎组（包括胃粘膜上皮化生或不典型增生）中的平均值最低，慢性胃炎、胃十二指肠溃疡和胃息肉及其它病变者的均值偏高。各组中男女性别间均值差异没有显著性。ＰＧⅡ在胃癌组中的平均值最高，余者从高至低依次为胃十二指肠溃疡、萎缩性胃炎、慢性胃炎和胃息肉及其它病变者。各组中男女性别间均值差异没有显著性。ＰＧⅠ／ＰＧⅡ比值也是胃癌组和萎缩性胃炎组的最低。以病理学诊断的胃癌和萎缩性胃炎（包括胃粘膜上皮化生或不典型增生）为标准，以ｐＧⅠ／ＰＧⅡ≤３．Ｏ检出胃癌和萎缩性胃炎的灵敏度为６２．９６％，特异度为６２．００％，阳性预告值为４７．２２％，阴性预告值为７５．６１％，病理和胃蛋白酶原两种方法检查的一致率为６２．３１％，与胃镜检出的效果相接近。这种方法经济，便于基层应用，对胃癌和癌前病变的检测有意义。

肺癌与环境

近年来,肺癌发病率呈高发趋势,尤其是城市妇女肺癌升高更引人注目。南京医学院最近对江苏省6个县区的200万人次进行调查,肺癌死亡率逐年上升,年均增长率为7.48％。经过调查,人们发现包括环境污染因素在内的多种诱因促进肺癌发生。 1、吸烟和被动吸烟:上海肿瘤研究所曾对市区和郊县145541名40岁以上的居民作过调查,结果表明,吸烟者肺癌标化死亡率,男性为90.8/10万;女性为59.4/10万,分别为非吸烟者的3.96倍和4.6倍。在公共场所或家庭中。

Expression of the Glypican-3 Gene in α-fetoprotein-negative Human Hepatocellular Carcinoma

Objective： To investigate the expression of Glypican-3 gene in （α-fetoprotein （AFP）-negative hepatocellular carcinoma （HCC） and clarify whether Glypican-3 expression is a useful parameter for the diagnosis of hepatocelhllar carcinoma （HCC）, especially for AFP-negative ones. Methods： Forty-one specimens of AFP-negative hepatocellular carcinoma and para-carcimoma tissue were studied for the expression of Glypican-3 by Northern blot. The expression of Glypican-3 protein was detected immunohistochemically with specific polyclonal antibody. Results： Northern blot analysis indicated that the expression of Glypican-3 mRNA was intensively detected in 30 of 41 AFP-negative HCC （73.17%）. In contrast, Glypican-3 mRNA was only weakly detected in 4 of the surrounding non-tumor liver tissues. There was significant difference in the Glypican-3 mRNA expression in large tumors （〉5 cm） （79.31%） and in small tumors （〈5 cm） （41.67%） （P〈0.01）. Gypican-3 mRNA was more frequently overexpressed in poorly differentiated HCC than in well differentiated ones （76.47% vs. 42.86%, P〈0.05）. The Glypican-3 expression was not correlated with age. sex. ttbsAg seropositivity, fibroeapsule, portal venous embolus and intrahepatic metastasis. The overexpression of Glypican-3 protein in HCC was targeted in tumor cells, not in bile duct cells and other interstitial cells. Conclusion： Glypican-3 was specially overexpressed in AFP-negative HCC, and its expression was closely correlated with the tumor size and tumor grade. Glypican-3 gene may play important roles in hepatocareinogenesis, and can be used as a new biochemical marker of HCC, especially for AFP-negative HCC.

The Establishment and Characterization of a Continuous Cell Line of Mouse Cervical Carcinoma

OBJECTIVE To establish a murine uterine cervical cancer cell line and to define its biological characters. METHODS Transplanted tumor tissue was used for in vitro primary culture of U14 cervical carcinoma cells. After 20 passages, we examined its morphology, chromosomes, tumorigenicity and produced a growth curve. CK was detected by immunohistochemistry, the cell cycle determined by flow cytometry and the metastatic potential assessed in 615 and C57BL/c mice. We also transfected the cells with the pEGFP-N1 plasmid. RESULTS A newly established murine cell line was passaged 50 times over a period of 10 months. The cells grow as a partially suspended culture, and are immunohistochemically CK（＋）. The cell line is characterized by a hypotetraploid karyotype, a chromosomal number of 64-68 and a doubling time of 21.8 h. Exponential growth occurs by the third and forth day of culture. Cell cycle analysis showed G1 34%, G2 26%, and 40% in the S phase. The tumorigenicity was 100% upon implantation. No mycoplasma contamination was detected. A monoclonal continuous U14-GFP cell strain which was 100% GFP （＋） was also produced. CONCLUSION We successfully established a new murine cervical U14 carcinoma cell line and an U14-GFP monoclonal strain. These cell lines are ideal for combined in vivo and in vitro tumor research.

The Prognostic Value of Pathological and Molecular Margins Marked by p53 and eIF4E in Laryngeal Carcinoma

Objective: To study the prognostic value of the pathological margin and molecular margin marked by eIF4E and P53 protein in laryngeal carcinoma. Methods: The prognostic value of pathological and molecular margin was studied in 253 cases and 67 cases respectively, the latter were pathological negative margin chosen from the former. Immunohistochemisty was used to detect the expression of eIF4E and p53 proteins. Results: The rate of pathological, p53 and eIF4E positive margins was 20.2%, 19.4% and 32.8% respectively. The recurrent rate of those with positive margins was higher than that of negative margins, which including pathological margin (70.6% vs 35.1%, P =0.0000), p53 margin (69.2% vs 33.3%, P =0.018) and eIF4E margin (63.6% vs 28.9%, P =0.018); The survival rate of those with negative margins was higher than those with positive margins, including pathological margin (the 5-year cumulative survival rate was 37.52% and 64.37% respectively, P =0.0023), p53 margin (the 5-year cumulative survival rate was 24.62% and 75.69% respectively, P =0.0012) and eIF4E margin (the 5-year cumulative survival rate was 43.31% and 77.52% respectively, P =0.0006). Conclusion: The prognosis of those with both pathological and molecular positive margins was worse than that of the negative margins; Both the eIF4E and p53 were useful markers to pick out the poor prognostic patients from those with pathological negative margin, and the former seemed to be more potential.

The prognostic molecular markers in hepatocellular carcinoma

The prognosis of hepatocellular carcinoma (HCC) still remains dismal, although many advances in its clinical study have been made. It is important for tumor control to identify the factors that predispose patients to death. With new discoveries in cancer biology, the pathological and biological prognostic factors of HCC have been studied quite extensively. Analyzing molecular markers (biomarkers) with prognostic significance is a complementary method. A large number of molecular factors have been shown to associate with the invasiveness of HCC, and have potential prognostic significance. One important aspect is the analysis of molecular markers for the cellular malignancy phenotype. These include alterations in DNA ploidy, cellular proliferation markers (PCNA, Ki-67, Mcm2, MIB1, MIA, and CSE1L/CAS protein), nuclear morphology, the p53 gene and its related molecule MD M2, other cell cycle regulators (cyclin A, cyclin D, cyclin E, cdc2, p27, p73), oncogenes and their receptors (such as ras, c-myc, c-fms, HGF, c-met, and erb-B receptor family members), apoptosis related factors (Fas and FasL), as well as telomerase activity. Another important aspect is the analysis of molecular markers involved in the process of cancer invasion and metastasis. Adhesion molecules (E-cadherin, catenins, serum intercellular adhesion molecule-1, CD44 variants), proteinases involved in the degradation of extracellular matrix (MMP-2, MMP-9, uPA, uPAR, PAI), as well as other molecules have been regarded as biomarkers for the malignant phenotype of HCC, and are related to prognosis and therapeutic outcomes. Tumor angiogenesis is critical to both the growth and metastasis of cancers including HCC, and has drawn much attention in recent years. Many angiogenesis-related markers, such as vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), platelet-derived endothelial cell growth factor (PD-ECGF), thrombospondin (TSP), angiogenin, pleiotrophin, and endostatin (ES) levels, as well as intratumor microvessel density (MVD) have been evaluated and found to be of prognostic significance. Body fluid (particularly blood and urinary) testing for biomarkers is easily accessible and useful in clinical patients. The prognostic significance of circulating DNA in plasma or serum, and its genetic alterations in HCC are other important trends. More attention should be paid to these two areas in future. As the progress of the human genome project advances, so does a clearer understanding of tumor biology, and more and more new prognostic markers with high sensitivity and specificity will be found and used in clinical assays. However, the combination of some items, i.e., the pathological features and some biomarkers mentioned above, seems to be more practical for now.

DEC1 nuclear expression:A marker of differentiation grade in hepatocellular carcinoma

AIM: To investigate the expression patterns of human differentiated embryo chondrocyte 1 (DEC1) in hepatocellular carcinoma (HCC) and corresponding adjacent non-tumor and the normal liver tissues, the association between DEC1 expression and histopathological variables and the role of DEC1 in hepatocarcinogenesis. METHODS: The expression of DEC1 was detected immunohistochemically in 176 paraffin-embedded sections from 63 patients with HCC and 50 subjects with normal liver tissues. RESULTS: DEC1 protein was persistently expressed in the cytoplasm of hepatocytes in normal liver and HCC tissues. Compared with adjacent non-tumor liver tissues, HCC tissues showed high nuclear expression of DEC1 protein. However, high DEC1 nuclear expression was more frequently detected in well-differentiated (83.3%) than in moderately (27.3%) and poorly differentiated HCC (16.7%). Low DEC1 expression was associated with poor histological differentiation and malignancy progression. A correlation was found between the nuclear expression of DEC1 protein and histological differentiation (r = 0.376, P = 0.024). CONCLUSION: DEC1 is expressed in the cytoplasm of hepatocytes and because nuclear DEC1 expression is decreased with decreasing differentiation status of HCC, nuclear DEC1 might be a marker of HCC differentiation.

The Expression and Clinical Significance of Fas and FasL in Lung Cancer

Objective: To investigate the expression and clinical significance of Fas andFasL in lung cancer. Methods: SP immunohistochemical technique was used to detect the expression ofFas and FasL in 46 cases of lung cancer and 30 cases of adjacent non-neoplastic tissue. Results:Down-regulation, of Fas and up-regulation of FasL were found in lung carcinoma. The levels of Fasexpression in squamous cell carcinoma, adenocarcinoma and SCLC were significantly lower than that ofadjacent normal tissues (P<0. 01) , while the expression levels of FasL were the opposite (P< 0.05). Fas expression was associated with high histological grade and no metastasis (P<0. 05). FasLexpression was related to histological grade, late clinical stage and metastasis (P<0. 05). BothFas and FasL expression was not related to the histological type of lung cancer (P>0. 05). Thelevel of Fas expression was negatively related to that of FasL (P<0. 05). Conclusion:Down-regulation of Fas and up-regulation of FasL may work in coordination with the occurrence,development and metastasis of lung cancer. Fas or FasL can be used as one of markers in earlydiagnosis of lung cancer. Therefore, the combined assay may be helpful in predicting the grade ofmalignancy and the prognosis of patients with lung cancer.

Colorectal cancer screening by non-invasive metabolic biomarker fecal tumor M2-PK

AIM: To evaluate the utility of the innovative fecal tumor M2-Pyruvate kinase (M2-PK) test in our daily clinical routine, as a marker for the pre-selection of patients who should subsequently undergo colonoscopy for the diagnosis or exclusion of colorectal cancer. METHODS: Fecal tumor M2-PK was measured in stool samples of 96 study participants (33 patients with colorectal cancer, 21 patients with rectal carcinoma and 42 controls) who all underwent total colonoscopy. RESULTS: In 39 of 42 individuals in the control group, fecal tumor M2-PK was below 4.0 kU/L (93% specificity). Colorectal tumors were accompanied by a highly significant increase (P < 0.001) in fecal tumor M2- PK levels (median: colon carcinoma, 23.1 kU/L; rectal carcinoma, 6.9 kU/L; colorectal carcinoma, 14.7 kU/L), which correlated with Duke’s staging and T-classification. The overall sensitivity was 78% for colorectal cancer, increasing from 60% for stage T1 to 100% for stage T4 and from 60% for Duke’s A to 90% for Duke’s D tumors. CONCLUSION: Fecal tumor M2-PK is an appropriately sensitive tool to pre-select those patients requiring colonoscopy for the further diagnostic confirmation or exclusion of colorectal cancer.

Comparison of Milan and UCSF criteria for liver transplantation to treat hepatocellular carcinoma

AIM:To assess the validity of the Milan and University of California San Francisco(UCSF) criteria and examine the long-term outcome of orthotopic liver transplantation(OLT) in patients with hepatocellular carcinoma(HCC) in a single-center study.METHODS:This study is a retrospective review of prospectively collected data.Between 1998 and 2009,56 of 356 OLTs were performed in patients with HCC.Based on pathological examination of liver explants,patients were retrospectively categorized into 3 groups:Milan +(n = 34),Milan-/UCSF +(n = 7) and UCSF-(n = 14).RESULTS:Median follow-up period was 39.5(1-124) mo.The 5-year overall survival rates in the Milan +,Milan-/UCSF + and UCSF-groups were 87.7%,53.6% and 33.3%,respectively(P < 0.000).Within these groups,tumor recurrence was determined in 5.8%,14.3% and 40% of patients,respectively(P < 0.011).Additionally,the presence of microvascular invasion within the explanted liver had a negative effect on the 5-year disease free survival(74.7% vs 46.7%,P < 0.044).CONCLUSION:The Milan criteria are reliable in the selection of suitable candidates for OLT for the treatment of HCC.For cases of OLT involving living donors,the UCSF criteria may be applied.

Study of Helicobacter pylori genotype status in saliva,dental plaques,stool and gastric biopsy samples

AIM:To compare genotype of Helicobacter pylori(H.pylori) isolated from saliva,dental plaques,gastric biopsy,and stool of each patient in order to evaluate the mode of transmission of H.pylori infection.METHODS:This cross-sectional descriptive study was performed on 300 antral gastric biopsy,saliva,dental plaque and stool samples which were obtained from patients undergoing upper gastrointestinal tract endoscopy referred to endoscopy centre of Hajar hospital of Shahrekord,Iran from March 2010 to February 2011.Initially,H.pylori strains were identified by rapid urease test(RUT) and polymerase chain reaction(PCR) were applied to determine the presence of H.pylori(ureC) and for genotyping of voculating cytotoxin gene A(vacA) and cytotoxin associated gene A(cagA) genesin each specimen.Finally the data were analyzed by using statistical formulas such as Chi-square and Fisher's exact tests to find any significant relationship between these genes and patient's diseases.P < 0.05 was considered statistically significant,RESULTS:Of 300 gastric biopsy samples,77.66% were confirmed to be H.pylori positive by PCR assay while this bacterium were detected in 10.72% of saliva,71.67% of stool samples.We were not able to find it in dental plaque specimens.The prevalence of H.pylori was 90.47% among patients with peptic ulcer disease(PUD),80% among patients with gastric cancer,and 74.13% among patients with none ulcer dyspepsia(NUD) by PCR assay.The evaluation of vacA and cagA genes showed 6 differences between gastric biopsy and saliva specimens and 11 differences between gastric and stool specimens.94.42% of H.pylori positive specimens were cagA positive and all samples had amplified band both for vacA s and m regions.There was significant relationship between vacA s1a/m1a and PUD diseases(P = 0.04),s2/m2 genotype and NUD diseases(P = 0.05).No statically significant relationship was found between cagA status with clinical outcomes and vacA genotypes(P = 0.65).The evaluation of vacA and cagA genes showed 6 differences between gastric biopsy and saliva specimens and 11 differences between gastric and stool specimens,CONCLUSION:Regard to high similarity in genotype of H.pylori isolates from saliva,stomach and stool,this study support the idea which fecal-oral is the main route of H.pylori transmission and oral cavity may serve as a reservoir for H.pylori,however,remarkable genotype diversity among stomach,saliva and stool samples showed that more than one H.pylori genotype may exist in a same patient.

Developments in metastatic pancreatic cancer:Is gemcitabine still the standard?

In the past 15 years, we have seen few therapeutic advances for patients with pancreatic cancer, which is the fourth leading cause of cancer-related death in the United States. Currently, only about 6% of patients with advanced disease respond to standard gemcitabine therapy, and median survival is only about 6 mo. Moreover, phase Ⅲ trials have shown that adding various cytotoxic and targeted chemotherapeutic agents to gemcitabine has failed to improve overall survival, except in cases in which gemcitabine combined with erlotinib show minimal survival benefi t. Several metaanalyses have shown that the combination of gemcitabine with either a platinum analog or capecitabine may lead to clinically relevant survival prolongation, especially for patients with good performance status. Meanwhile, many studies have focused on the pharmacokinetic modulation of gemcitabine by fi xed-dose administration, and metabolic or transport enzymes related to the response and toxicity of gemcitabine. Strikingly, a phase Ⅲ trial in 2010 showed that, in comparison to gemcitabine alone, the FOLFIRINOX regimen in patients with advanced disease and good performance status, produced better median overall survival, median progression-free survival, and objective response rates. This regimen also resulted in greater, albeit manageable toxicity.