肿瘤坏死因子相关细胞凋亡诱导配体受体-4在人胰腺癌组织中的表达

目的：通过检测肿瘤坏死因子相关细胞凋亡诱导配体受体-4(TRAIL-R4)在胰腺癌组织中的表达，探讨胰腺癌细胞抵抗细胞凋亡的机理。方法：应用mRNA印迹法(Northern blotting)、蛋白质印迹法(Western blotting)和免疫组织化学技术，定性、定位分析TRAIL-R4在正常胰腺组织和胰腺癌组织中的表达。结果：TRAIL-R4 mRNA和蛋白在正常胰腺组织中呈弱表达或不表达，而在胰腺癌组织中呈高表达；免疫组织化学检测显示，在胰腺癌细胞中TRAIL-R4蛋白呈强染色。结论：TRAIL-R4表达水平在正常胰腺组织与胰腺癌组织中存在显著差异，提示胰腺癌细胞中可能存在对TRAIL介导的细胞凋亡抵抗新机理。     

P物质及其受体在慢性胰腺炎组织的表达和临床意义

目的 了解P物质及其受体NK－1R在正常胰腺和慢性胰腺炎中的表达，探讨它们与慢性胰腺炎时疼痛发生的关系。方法 25个慢性胰腺炎标本取自慢性胰腺炎手术，男性18例，女性7例，正常胰腺组织取自20个器官捐献者，男性11例，女性9例。应用实时定量逆转录整合酶链反应（RT－PCR）技术，检测正常胰腺和慢性胰腺炎组织中P物质和NK－1R的mRNA水平，应用Western blot技术检测NK－1R的蛋白水平，应用免疫组织化学方法进行NK－1R的组织学定位。将P物质及其受体NK－1R mRNA水平与疼痛的程度，发作频率和病程进行分析，寻找其中的相关性。结果 与正常胰腺相比，慢性胰腺炎组织中P物质和NK－1R mRNA和蛋白都过度表达，NK－1RmRNA水平与疼痛的程度，发作频率和病程明显相关。免疫组化检查显示，NK－1R的表达主要位于胰腺腺泡，胰腺导管，神经纤维和炎性细胞。结论 慢性胰腺炎组织中P物质和NK－1R的表达水平都明显上调，扰乱了神经激肽的作用环节，NK－1R的过度表达与疼痛发生有关。     

奥曲肽对大鼠急性胰腺炎腺泡死亡方式的影响

目的探讨奥曲肽对急性胰腺炎(Acute Pancreatitis,AP)腺泡细胞死亡方式的影响。方法使用奥曲肽对急性胰腺炎大鼠模型进行治疗,采用原位TUNEL及RT-PCR等技术,观察各组胰腺组织内Bax mRNA变化及胰腺腺泡细胞凋亡情况、胰腺病理学改变及组织学评分变化情况。结果大鼠胰腺细胞凋亡指数与胰腺组织病理学评分呈负相关;奥曲肽可使AP模型的胰腺组织内Bax mRNA表达增加,诱导胰腺腺泡细胞凋亡增加,使胰腺病理学改变及组织学评分改善。结论奥曲肽可能诱导AP腺泡细胞的凋亡,减轻胰腺炎的严重程度。     

大黄素对大鼠急性胰腺炎的治疗作用

目的 探讨大黄素诱导细胞凋亡对大鼠急性胰腺炎(acute pancreatitis,AP)的治疗作用.方法 45只SD大鼠分为对照组、胰腺炎组、治疗组,每组15只.观察胰腺组织内腺泡细胞凋亡指数、NF-κB mRNA、Bax mRNA、外周血中中性粒细胞(polymorphonuclear neutrophii,PMN)凋亡指数及天冬氨酸特异性半胱氨酸蛋白酶(caspase-3、caspase-8)的变化情况.结果 与胰腺炎组比较,治疗组腺泡细胞和PMN凋亡指数及胰腺组织内NF-κB mRNA、Bax mRNA、PMN caspase-3与caspase-8表达均明显增加(F=853.199,327.126,143.586,48.857,231.750,96.552,P＜0.05).治疗组中,胰腺组织病理学评分与胰腺腺泡细胞凋亡指数、PMN凋亡指数均呈负相关(r=-0.96,-0.94,P＜0.05);胰腺腺泡细胞凋亡指数与胰腺组织内NF-κB mRNA、Bax mRNA表达呈正相关(r=0.73,0.76,P＜0.05);胰腺组织内NF-κB mRNA与Bax mRNA表达呈正相关(r=0.94,P＜0.05);PMN凋亡指数与PMN caspase-3、caspase-8表达均呈正相关(r=0.99,0.99,P＜0.05).结论 大黄素能有效治疗AP,其机制是通过Bax途径诱导胰腺腺泡细胞凋亡,并通过caspase途径来诱导外周血中PMN凋亡,从而明显减轻AP病情程度.     

细胞分裂周期蛋白CDC25家族在人胰腺导管腺癌中的表达及意义

目的 探讨CDC25在胰腺导管腺癌（PDAC）中的表达及意义。方法 分别收集8例手术切除的人胰腺癌、慢性胰腺炎、正常胰腺以及肝和（／或）淋巴结转移组织，采用Affymetrix公司的GeneChip HG-U95Av2 eDNA芯片初步筛查CDC25家族三个成员（CDC25A、B和C）在这些组织中的表达情况，然后通过定量PCR方法对基因芯片结果进行再验证分析。结果 基因芯片结果显示与慢性胰腺炎或正常胰腺组织比较，胰腺癌组织中CDC25B／mRNA的表达水平分别增加了1．4倍和1．9倍，而CDC25A和CDC25C mRNA水平在胰腺癌、慢性胰腺炎和正常胰腺组织中差异无统计学意义；定量PCR检测结果表明在胰腺癌组织中CDC25B／mRNA的平均表达水平分别比正常胰腺和慢性胰腺炎高7．5倍和3．9倍。结论CDC25B在胰腺癌细胞周期调控中起着重要作用，可能参与了胰腺癌的发生、发展和演进过程，CDC25B有可能成为胰腺癌早期诊断和治疗的一个靶点。     

胰腺癌中血管形成因子和细胞粘附分子的表达研究

目的　探讨CD3 4 和血管内皮生长因子 (VEGF)、细胞间粘附分子 (ICAM 1)在胰腺癌(pancreaticadenocarcinoma ,PAC)组织、慢性胰腺炎组织 (chronicpancreatitis ,CP)中的表达及病理意义 ,明确血管形成在胰腺癌演化过程中所起的重要作用。方法　应用免疫组化Envission方法对 2 4例胰腺癌组织、2 4例慢性胰腺炎组织、7例正常胰腺组织 ,进行了CD3 4 、VEGF、ICAM 1的表达情况的检测。对CD3 4 阳性血管进行MVD计数 ,并结合胰腺癌的病理特征进行分析。结果　癌组织 (4 7 2±9 4 )和慢性胰腺炎组织 (4 0 8± 7 93)中微血管密度明显高于对照组 (9 85± 2 86 ) (P <0 0 1)。VEGF在正常胰腺组织中不表达 ,在胰腺癌组织中VEGF主要表达于肿瘤细胞和导管细胞的胞质中 ,在慢性胰腺炎组织中VEGF在叶间及叶内导管细胞均高表达。细胞间粘附分子ICAM 1在正常对照胰腺组织中未见表达 ,仅见于某些内皮细胞着色 ,在胰腺癌组织及慢性胰腺炎组织中 ,除内皮细胞高表达外 ,肿瘤细胞阳性表达亦较高 ,慢性胰腺炎中ICAM 1亦在叶间及小叶内导管细胞中高表达。结论　我们发现微血管形成及其调控因子、细胞粘附分子与慢性胰腺炎、胰腺癌的生物学行为密切相关 ,在胰腺癌的演变中亦起了不可低估的作用 ,抗血管形成治疗无论是对胰腺癌抑     

慢性胰腺炎胰腺纤维化发病机制及其治疗的研究进展

慢性胰腺炎胰腺纤维化是指慢性胰腺炎时胰腺组织呈现胰腺实质纤维化、腺泡细胞萎缩以及炎症细胞浸润等现象。其中,胰腺的纤维化是慢性胰腺炎发病的重要病理生理过程。在这一过程中,正常胰腺组织被大量富含连接组织的     

大黄素诱导细胞凋亡对不同类型急性胰腺炎腺泡死亡方式的影响

目的 探讨大黄素(emodin)诱导细胞凋亡对不同类型急性胰腺炎(AP)腺泡细胞死亡方式影响及其可能机制.方法 制作大鼠急性水肿型胰腺炎(AEP)与急性坏死型胰腺炎(ANP)模型.使用大黄素进行治疗.采用原位TUNEL及RT-PCR等技术,观察胰腺组织内细胞凋亡、NF-κBmRNA、Bax mRNA及TNF-α mRNA等变化情况.结果 各组大鼠胰腺细胞凋亡指数与胰腺组织病理学评分呈负相关;大黄素治疗可诱导各型AP模型腺泡细胞凋亡,胰腺病理学改变及组织学评分改善,胰腺组织内NF-κB mRNA及Bax mRNA表达增加.结论 诱导不同类型AP胰腺细胞凋亡可明显减轻AP病情.大黄素为治疗AP的有效药物,可能通过影响NF-κB活化及Bax的表达来诱导AP时腺泡细胞的凋亡,减轻胰腺炎的严重程度.     

Rho/Rho激酶信号通路与胰腺疾病

Rho/Rho激酶信号通路是真核细胞内广泛存在的一条信号通路,参与多种生物学行为.研究表明,Rho/Rho激酶在胰腺腺泡细胞、导管细胞及内分泌细胞均见表达,并与胰腺内、外分泌功能以及胰腺癌、胰腺炎和糖尿病的发生、发展密切相关.     

胰腺癌中雌激素受体和雌激素诱导基因的表达

有关胰腺癌表达雌激素受体的问题迄未阐明，作者采用RNA印迹法、原位杂交和免疫组织化学观察正常人体和胰腺癌组织的雌激素受体表达．同时也测定了雌激素诱导蛋白、孕激素受体、pS_2和ERD_5，结果如下：1二雌激素受体RNA印迹分析测定胰腺癌、胰腺炎和正常胰腺标本，可见6．2kb转录物，其大小与MCF7乳腺癌细胞所表达的相同。经激光密度计读数校正后在癌肿和正常组织中的雌激素受体mRNA表达无数量上差异。雌激素受体的原位杂交和免疫组化技术均未能定位雌激素受体表达。胰腺癌的平均雌激素受体值为0．5fmol／mg，而正常胰腺组织则为1．…     

Phospholipase A2 isoforms are altered in chronic pancreatitis.

OBJECTIVE: To determine if phospholipase A2 (PLA2) type II and type IV mRNA expression and protein are altered in chronic pancreatitis. SUMMARY BACKGROUND DATA: PLA2s have an important regulatory function in several signaling pathways, especially in inflammation. In this study, we examined the expression of three PLA2 isoforms (type I, type II, and type IV) in chronic pancreatitis. METHODS: The distribution of PLA2 was studied in 15 pancreas samples obtained from patients with chronic pancreatitis using immunohistochemical, Northern blot, and in situ hybridization techniques. Normal pancreas obtained from healthy organ donors served as control. RESULTS: Northern blot analysis revealed enhanced mRNA levels of PLA2 type II (5.7-fold) and type IV (5.1-fold) in chronic pancreatitis (p < 0.01) versus normal pancreas. In normal pancreas, intense PLA2 type I immunostaining was present in acinar cells, whereas PLA2 type II immunostaining was visible only in some acinar cells. In chronic pancreatitis, PLA2 type II immunostaining was present more frequently and with higher intensity in acinar cells. Furthermore, PLA2 type II immunoreactivity was more abundant in metaplastic ductal cells in the chronic pancreatitis samples. By in situ hybridization, areas with ductal metaplasia in chronic pancreatitis exhibited intense PLA2 type IV mRNA signals. All chronic pancreatitis tissues with concomitantly increased mRNA expression for PLA2 type II and type IV exhibited a higher degree of degeneration, ductal metaplasia, and fibrosis. CONCLUSIONS: Upregulation of PLA2 types II and IV in areas with more histologic damage suggests that these PLA2 isoforms might contribute to the morphologic changes that occur in chronic pancreatitis.     

Nerve growth factor and its high-affinity receptor in chronic pancreatitis

OBJECTIVE: To study the mechanisms that are involved in nerve growth and contribute to pain generation in chronic pancreatitis (CP). SUMMARY BACKGROUND DATA: Chronic pancreatitis is a painful disease associated with characteristic nerve changes, including an increase in nerve number and diameter. The mechanisms that influence nerve growth are not known. Nerve growth factor (NGF) and its high-affinity tyrosine kinase receptor A (TrkA) are involved in neural development and survival and growth of central and peripheral nerves. METHODS: Nerve growth factor and TrkA were investigated by Northern blot analysis, in situ hybridization, and immunohistochemical staining in the pancreases of 24 patients with CP, and the findings were correlated with clinical parameters. RESULTS: By Northern blot analysis, NGF and TrkA mRNA expression were increased in 42% (13.1-fold) and 54% (5.5-fold) of the CP samples (p < 0.01), respectively. In situ hybridization revealed that in CP, enhanced NGF mRNA expression was present in metaplastic ductal cells, in degenerating acinar cells, and in acinar cells dedifferentiating into tubular structures. TrkA mRNA was intensely present in the perineurium. Further, enhanced NGF and TrkA mRNA signals were also present in intrapancreatic ganglia cells in CP samples. Immunohistochemistry confirmed the in situ hybridization findings. Analysis of the molecular findings with clinical parameters revealed a significant relation (p < 0.05) between NGF mRNA levels and pancreatic fibrosis (r = 0.64) and acinar cell damage (r = 0.74) and between TrkA mRNA and pain intensity (r = 0.84). CONCLUSION: Activation of the NGF/TrkA pathway occurs in CP. It might influence neural morphologic changes and the pain syndrome in this disorder.     

A subgroup of patients with chronic pancreatitis overexpress the c-erb B-2 protooncogene.

OBJECTIVE: Chronic pancreatitis (CP) is a chronic condition associated with pancreatic fibrosis. A small subgroup of patients with CP develop enlargement of the head of the pancreas (EHP). This study examined some of the mechanisms that may lead to the development of EHP. SUMMARY BACKGROUND: The c-erb B-2 protooncogene encodes a 185-kDa transmembrane growth factor receptor (p185) that regulates cell growth and differentiation. METHODS: The authors analyzed c-erb B-2 expression in samples obtained from the head of the pancreas from 26 patients with CP (5 women, 21 men) using immunohistochemical and molecular technique. A diagnosis of CP with EHP was made when the vertical pancreatic head diameter was greater than 4 cm (14 patients), as determined by contrast-enhanced computed axial tomography scan. Pancreatic tissues from 15 healthy organ donors served as control subjects. RESULTS: In all patients without EHP and in the healthy control subjects, p185 immunoreactivity was present at low levels. In contrast, strong p185 immunoreactivity was observed in acinar and ductal cells in all patients with EHP. By in situ hybridization, c-erb B-2 messenger ribonucleic acid (mRNA) grains were expressed at high levels in patients with CP with EHP in both ductal and acinar cells. Northern blot analysis demonstrated a 4.5-fold increase (p < 0.001) in c-erb B-2 mRNA levels in patients with EHP compared with patients without EHP and healthy control subjects. Southern blot analysis did not reveal c-erb B-2 gene amplification or rearrangement. CONCLUSIONS: These findings indicate the c-erb B-2 is not overexpressed in most patients with CP. However, its overexpression in patients with CP with EHP suggest that c-erb B-2 may contribute to the pathophysiologic processes that lead to pancreatic head enlargement.     

Phosphatidylserine receptor in chronic pancreatitis: evidence for a macrophage independent role

OBJECTIVE: This study analyzes the role of phosphatidylserine receptor (PSR) in chronic pancreatitis. SUMMARY BACKGROUND DATA: In chronic pancreatitis, destruction of parenchyma comes along with infiltration of lymphocytes and macrophages. The phosphatidylserine receptor is expressed on the surface of macrophages and is crucial for the recognition and engulfment of apoptotic cells. In the present study, we investigated the role of this receptor and its relation to apoptosis in chronic pancreatitis. METHODS: The expression and localization of PSR were analyzed by Northern blot analysis, RT-PCR, Western blot analysis and immunohistochemistry. Apoptosis was detected by the TUNEL method, and the RNA protection assay (RPA) was used to compare activation of apoptosis with PSR mRNA expression levels. In addition, the molecular data were related to clinicopathological parameters. RESULTS: PSR mRNA expression was low to absent in normal pancreatic tissue samples. In human chronic pancreatitis, increased expression of PSR mRNA was present in 12 of 29 samples (41%). Up-regulation of PSR could be confirmed by Western blot analysis. In chronic pancreatitis tissue, PSR immunoreactivity was present in all islets, in some ductal cells and in macrophages. The RNA protection assay revealed high mRNA levels of the antiapoptotic genes bcl-2 and bfl-1 (P < 0.05) in chronic pancreatitis tissues with high PSR mRNA expression. The TUNEL apoptosis in situ detection method showed positive signals in some redifferentiating acinar cells and focally in acinar cells adjacent to stromal fibroblasts in chronic pancreatitis tissue samples. The distribution pattern of PSR on pancreatic cells in chronic pancreatitis corresponded to a great extent with regions of high apoptotic activity. CONCLUSIONS: We show for the first time the presence of PSR in chronic pancreatitis on pancreatic cells other than macrophages in regions with high apoptotic activity. The coexpression and colocalization of this gene with other apoptosis mediators suggest its involvement in apoptotic processes. However, in chronic pancreatitis PSR is not only involved in phagocytosis of apoptotic cells by macrophages.     

Overexpression of caspase-1 in pancreatic disorders: Implications for a function besides apoptosis

The caspases are known to play a crucial role in the triggering and execution of apoptosis in a variety of cell types. We assessed the expression of caspase-1 in 42 pancreatic cancer tissue samples, 38 chronic pancreatitis specimens, and nine normal pancreatic tissues by immunohistochemistry and Western blot analysis. We found a clear overexpression of caspase-1 in both disorders, but differences in the expression patterns in distinct morphologic compartments. Pancreatic cancer tissue showed a clear cytoplasmatic overexpression of caspase-1 in tumor cells in 71% of the tumors, whereas normal pancreatic tissue showed only occasional immunoreactivity. In chronic pancreatitis an overexpression of caspase-1 was found in atrophic acinar cells (89%), hyperplastic ducts (87%), and dedifferentiating acinar cells (84%). Although in atrophic cells a clear nuclear expression was found, hyperplastic ducts and dedifferentiating acinar cells showed clear cytoplasmic expression. Western blot analysis revealed a marked expression of the 45 kDa precursor of caspase-1 in pancreatic cancer and chronic pancreatitis (80% and 86%, respectively). Clear bands at 30 kDa, suggested to represent the pl0-p20 heterodimer of active caspase-1, were found in 60% of the cancer tissue and 14% of the pancreatitis tissue specimens. Since we found a highly significant correlation between cytoplasm overexpression of caspase-1 in pancreatic cancer and overexpression of the known prognostic factors cyclin D1, epidermal growth factor, and epidermal growth factor receptor, it is plausible that caspase-1 has a yet unknown function in proliferative processes in addition to its well-known role in the apoptotic pathway. Supported by Deutsche Krebshilfe Grant 10-1276-Gal (Drs. F. Gansauge and S. Gansauge). Presented in part at the Forty-First Annual Meeting of The Society for Surgery of the Alimentary Tract, May 2l–24, 2000, San Diego, Calif.     

Connective Tissue Growth Factor Is a Regulator for Fibrosis in Human Chronic Pancreatitis

OBJECTIVE: To evaluate the parameters that mediate fibrogenesis in chronic pancreatitis (CP). BACKGROUND: Connective tissue growth factor (CTGF), which is regulated by transforming growth factor beta (TGF-beta), has recently been implicated in skin fibrosis and atherosclerosis. In the present study, the authors analyzed the concomitant presence of TGF-beta1 and its signaling receptors-TGF-beta receptor I, subtype ALK5 (TbetaR-I(ALK5)), and TGF-beta receptor II (TbetaR-II)-as well as CTGF and collagen type I in the pancreatic tissue of patients undergoing surgery for chronic pancreatitis. PATIENTS AND METHODS: CP tissue samples were obtained from 40 patients (8 women, 32 men) undergoing pancreatic resection. Tissue samples of 25 previously healthy organ donors (12 women, 13 men) served as controls. The expression of TGF-beta1, TbetaR-I(ALK5), TbetaR-II, CTGF, and collagen type I was studied by Northern blot analysis. By in situ hybridization and immunohistochemistry, the respective mRNA moieties and proteins were localized in the tissue samples. RESULTS: Northern blot analysis showed that CP tissue samples exhibited concomitant enhanced mRNA expression of TGF-beta1 (38-fold), TbetaR-II (5-fold), CTGF (25-fold), and collagen type I (24-fold) compared with normal controls. In addition, TbetaR-I(ALK5) mRNA was increased in 50% of CP tissue samples (1.8-fold). By in situ hybridization, TGF-beta1, TbetaR-I(ALK5), and TbetaR-II mRNA were often seen to be colocalized, especially in the ductal cells and in metaplastic areas where atrophic acinar cells appeared to dedifferentiate into ductal structures. In contrast, CTGF was located in degenerating acinar cells and principally in fibroblasts surrounding these areas. Moreover, CTGF mRNA expression levels correlated positively with the degree of fibrosis in CP tissues. CONCLUSION: The concomitant overexpression of CTGF, collagen type I, TGF-beta1, and its signaling receptors in CP suggests that these proteins contribute to enhanced extracellular matrix synthesis and accumulation, resulting finally in the fibrogenesis observed in CP.     

Phospholipase A2 isoforms in acute pancreatitis

OBJECTIVE: To assess phospholipase A2 isoforms during human and experimental acute necrotizing pancreatitis. Phospholipase A2 isoforms (group I, II, and IV) were examined in acute pancreatitis tissues in humans and rats to determine whether the exocrine pancreas itself is a source of these mediators. SUMMARY BACKGROUND DATA: Phospholipase A2 has important regulatory functions, especially in inflammation. METHODS: Using Northern blot analysis and immunohistochemistry, the expression and localization of phospholipase A2 isoforms were analyzed in pancreatic tissue obtained from 21 patients with acute necrotizing pancreatitis and in pancreatic tissues of rats with acute edematous and necrotizing pancreatitis. Rat samples were examined daily for 1 week. RESULTS: In human acute pancreatitis, phospholipase A2-I mRNA expression was 8.9-fold decreased. By contrast, phospholipase A2-II (7.8-fold) and phospholipase A2-IV (8.1-fold) mRNA levels were increased. By in situ hybridization, phospholipase A2-IV was found to be expressed in remaining acinar and ductal cells adjacent to the necrotic areas. Immunostaining revealed moderate to intense phospholipase A2-II immunoreactivity in remaining acinar and ductal cells next to the necrosis. In rat pancreatitis, phospholipase A2-II mRNA levels in the pancreas were unchanged in the early phase (8 hours) but markedly increased after 24 hours, with a fluctuating pattern until day 7. CONCLUSIONS: Enhanced expression of phospholipase A2-II and A2-IV isoenzymes in human and experimental acute pancreatitis suggests that these enzymes play a role in modulating the inflammatory reaction in the pancreas. Because phospholipase A2-II and A2-IV mRNA was strongly present in remaining viable pancreatic acinar and ductal cells, the pancreas itself seems to be at least partly a source and a regulator of phospholipase A2-II- and A2-IV-dependent inflammatory reactions in acute pancreatitis.     

Identification of Disease-specific Genes in Chronic Pancreatitis Using DNA Array Technology

OBJECTIVE: To use DNA arrays to analyze the differential gene expression patterns in the normal pancreas and in pancreatic diseases. SUMMARY BACKGROUND DATA: Genome-wide gene expression analysis will provide new insights into gene function and cause of disease. METHODS: RNA was extracted from eight normal pancreatic specimens, eight specimens with chronic pancreatitis (CP), and eight pancreatic cancer (PCa) tissues. Poly A(+) RNA was purified, reverse-transcribed, and converted into cRNA using biotinylated nucleotides. The HuGeneFL DNA array containing 5,600 full-length human genes was used for analysis. RESULTS: First, normal pancreatic tissues were analyzed in comparison with a panel of other normal tissues (colon, liver, prostate, lung, lymph node). This analysis revealed 11 signature genes that were selectively expressed in the pancreas (e.g., pancreatic elastase-IIA). Comparison of the expression of 5,600 genes between the normal pancreas, CP, and PCa specimens showed that the expression of 34 genes was decreased in CP tissues compared with normal pancreatic tissues, and that the expression of all of these genes was simultaneously decreased in PCa. In addition, the expression of 157 genes was increased in CP tissues compared with the normal pancreas. Of those, 152 genes were simultaneously increased in PCa. Thus, only 5 of 5,600 genes were significantly overexpressed in CP compared with both normal pancreas and PCa. CONCLUSIONS: The majority of alterations observed in CP are present in PCa, and the number of genes whose expression is selectively deregulated in CP is surprisingly small. These results may provide new insight into the pathobiology of CP and help identify certain molecular alterations that might serve as targets for new diagnostic tools and disease-specific therapy.     

胰液中端粒酶及亚单位检测对胰腺癌的诊断价值

目的　探讨检测胰液中端粒酶逆转录酶 (hTERT)mRNA表达和端粒酶活性对胰腺癌的诊断与鉴别诊断价值。方法　对比分析 2 4例胰腺癌和 14例慢性胰腺炎患者胰液中的hTERTmRNA和端粒酶活性的检测结果。结果　hTERTmRNA在胰腺癌中表达阳性率为 87.5 % ( 2 1/ 2 4) ;慢性胰腺炎中阳性率为 2 1.4% ( 3 / 14 ) (P <0 .0 0 1)。胰腺癌与慢性胰腺炎胰液中端粒酶阳性检出率分别为83 .3 % ( 2 0 / 2 4) ,2 8.6% ( 4 / 14 ) (P <0 .0 0 1)。结论　胰液中检测hTERTmRNA表达和端粒酶活性对胰腺癌诊断与鉴别诊断有一定价值。