不同制作工艺的复方颗粒剂对乳腺癌小鼠瘤体生长及PI_(3)K和Akt表达水平的影响

目的探索不同制作工艺的复方颗粒剂对乳腺癌小鼠瘤体生长及磷脂酰肌醇-3激酶(PI_(3)K)和蛋白激酶B(Akt)表达水平的影响。方法以BALC乳腺癌小鼠为模型,采用1×10^(7)细胞/ml乳腺癌细胞4T1原位移植多选择小鼠乳腺脂肪垫内方式造模,将造模成功组分成煎药剂组(A组)、配方颗粒剂组(B组)、生理盐水组(C组)及模型组(D组),每组各15只,同时另选15只作为空白对照组(E组),仅进行正常条件性饲养。给药21 d后检测各组BALC乳腺癌小鼠的瘤质量、脾脏指数、胸腺指数及卵巢雌激素、孕激素、PI_(3)K和Akt,探讨不同工艺复方颗粒治疗乳腺癌的疗效和作用机制。结果A组和B组小鼠瘤体质量明显低于C组和D组小鼠(P<0.05),A组与B组瘤体质量和抑瘤率比较差异无统计学意义(P>0.05),C组与D组瘤体质量比较差异无统计学意义(P>0.05),E组小鼠均未见瘤块;与E组相比,A组、B组、C组和D组小鼠脾脏指数明显提高(P<0.05);A组、B组小鼠脾脏指数较C组、D组明显降低(P<0.05);与E组相比,A组、B组、C组和D组小鼠胸腺指数均降低(P<0.05),A组、B组较C组、D组小鼠胸腺指数升高(P<0.05);B组、C组和D组小鼠血清雌二醇和孕酮水平明显高于E组(P<0.05),A组与E组小鼠血清雌二醇和孕酮水平差异无统计学意义(P>0.05),A组、B组小鼠血清雌二醇和孕酮水平明显低于C组和D组(P<0.05),且A组小鼠血清雌二醇和孕酮水平低于B组(P<0.05);A组、B组、C组和D组小鼠PI_(3)K和Akt蛋白水平明显高于E组小鼠(P<0.05),A组和B组小鼠PI_(3)K和Akt蛋白水平明显低于C组和D组小鼠(P<0.05),并且A组小鼠PI_(3)K和Akt蛋白水平明显低于B组(P<0.05)。结论黄精覆盆子复方颗粒的加工工艺仅在抑制血清雌二醇、孕酮水平和抑制PI_(3)K和Akt表达等方面差异有统计学意义,但对瘤质量及瘤质量抑制率差异无统计学意义,煎制工艺和制粒工艺对黄精覆盆子复方颗粒的疗效影响不显著。

不同浓度复方夏枯草制剂对人非小细胞肺癌细胞移植裸鼠的瘤体生长影响及机制探讨

目的观察不同浓度复方夏枯草制剂对人非小细胞肺癌细胞(NCI-H460)移植裸鼠瘤体生长的影响,并探讨其可能机制。方法取SPF级裸鼠36只,将0.2 mL的NCI-H460细胞悬液注射到裸鼠右后肢皮下制备移植瘤模型,将肿瘤体积长到60～80 mm3的30只裸鼠(其余6只剔除实验)分为高剂量组、中剂量组、低剂量组、阳性组、模型组各6只,另取6只正常裸鼠作为对照组,高剂量组、中剂量组、低剂量组分别以2.4、1.2、0.6 g/kg的复方夏枯草制剂灌胃,阳性组注射0.025 g/kg的环磷酰胺,对照组和模型组灌胃等体积蒸馏水;阳性组隔两天给药1次,其他组每天1次。停药次日,测量移植瘤体积,观察瘤组织病理变化;免疫组化法检测瘤组织Bcl-2、Bax、Caspase-3。结果与模型组比较,高剂量组、阳性组给药后瘤体积、瘤重减小(P均<0.05)。模型组癌细胞紧密,核仁体积大;阳性组和复方夏枯草制剂低、中、高剂量组细胞有不同程度坏死,癌细胞数目明显减少,且大小不一,胞质破裂,完整性不好。与模型组比较,高剂量组、中剂量组、低剂量组、阳性组Bax阳性率升高,高剂量组、中剂量组、阳性组Caspase-3阳性率升高(P均<0.05)。结论复方夏枯草制剂对NCI-H460细胞移植裸鼠瘤体生长有抑制作用,高剂量浓度效果最好,其作用机制可能与上调Bax、Caspase-3表达有关。

平消胶囊对小鼠肾包膜下移植人肺癌瘤体生长的影响

目的 研究平消胶囊对人肺癌瘤体的作用。方法 移植人肺癌瘤块于小鼠肾包膜下 ,观察药物对肿瘤生长的影响。结果 平消胶囊在 0 1、0 3g/kg剂量 ,连用 7天对SRC人肺癌小鼠体重无明显影响 ,提示该药对SRC小鼠无明显性毒性 ,可明显抑制小鼠肾包膜下移植的人肺癌瘤体的生长。

鼻咽纤维血管瘤12例围手术期护理体会

鼻咽纤维血管瘤为良性肿瘤，生长部位隐蔽，瘤体生长迅速，易向鼻窦、眼眶及颅内扩展，瘤体内血管丰富，以男性青少年为主。手术是首选治疗方法，但术中极易出血，手术难度大，手术对患者的心理及生理创伤都很大。做好护理工作显得尤为重要。我科自2003年以来共收治12例鼻咽纤维血管瘤患者，经手术治疗后效果满意，现将护理体会报道如下。

听神经瘤的生长分型及显微外科手术策略

目的对听神经瘤的患者的临床瘤体生长分型和显微外科手术的相应策略进行研究分析。方法抽取来本院就诊的102例听神经瘤临床确诊患者,对这些患者的瘤体生长分型情况进行研究,并根据不同分型采取相应的显微外科手术策略。结果经研究发现,该类患者的瘤体可以分为原位型、小脑型、脑干型、三叉神经型、乳突型等5种类型。治疗后患者病情显著改善。结论对不同类型的听神经瘤患者采用不同的手术方式进行治疗,可以使临床治疗的针对性更强,手术的效果更加理想。

体表及软组织常见肿瘤的诊治

肿瘤通常表现为肿块,根据肿瘤发展速度和对人体器官结构与功能影响的不同,临床将其分为良性与恶性两种。①良性肿瘤：瘤体生长较慢,呈膨胀性生长,可推开,根据生长部位可挤压邻近组织器官。肿瘤周围有结缔组织增生,形成包膜,与周围组织之间界限明显,肿体多呈圆形或椭圆形。②恶性肿瘤：生长快,呈浸润性生长,可破坏邻近组织或器官,没有包膜,周围组织分界不清,不容易推动,表面不平,硬度不均,质脆;由于发展较快,血液供应不足,瘤中央易发生坏死、溃烂和出血,并具有转移特点。以下概要介绍一些常见体表及软组织肿瘤的诊治。

扶正增效方放射增敏与肿瘤细胞内O^6-甲基鸟嘌呤DNA甲基转移酶的关系

目的探讨扶正增效方放射增敏与肿瘤细胞内 O^6-甲基鸟嘌呤 DNA 甲基转移酶(O^6-MT)关系。方法建立裸鼠人肺腺癌 PAa 模型,分为6组,从接种日始,Ⅱ、Ⅳ、Ⅵ组裸鼠每天灌服0.6g 扶正增效方水煎剂,Ⅰ、Ⅲ组灌服等量无菌生理盐水,35天Ⅴ、Ⅵ组腹腔注射2mg STZ,36天予Ⅲ、Ⅳ、Ⅴ、Ⅵ组瘤体10Gy X 线照射,测瘤体直径、O^6-MT 含量、MGMT 染色及细胞病理学镜检。结果 6组中O^6-MT 含量工组最高,Ⅵ组最少,Ⅳ、Ⅴ、Ⅵ组与Ⅰ组相比差异显著,Ⅳ、Ⅵ组相比差异也显著;MGMT 染色强度变化与 O^6-MT 含量一致。瘤体生长Ⅰ、Ⅱ组瘤体放疗第4天起明显增大,Ⅲ组第6天明显增大,与Ⅰ、Ⅱ组相比增长减慢;Ⅳ、Ⅴ、Ⅵ组瘤体在第4天明显减少,以第Ⅵ组最明显;病理学镜检Ⅲ组见小的散在坏死灶,Ⅳ、Ⅴ组坏死区域较Ⅲ组增加,Ⅳ组与Ⅴ组相似;Ⅵ组坏死区域明显增多增大。通过对 O^6-MT 活性、MGMT 染色强度与病理学镜检、瘤体大小对比,细胞内 O^6-MT 含量与放射敏感性密切相关,O^6-MT 含量低组别放疗效果好。结论 O^6-MT含量决定其放射敏感性,据 O^6-MT 活性高低预测其放射敏感性;扶正增效方放射增敏一个重要途径是抑制 DNA 甲基转移酶活性而实现的。

苦参碱联合介入化疗栓塞治疗中晚期肝癌疗效观察

目的探讨苦参碱注射液联合介入化疗栓塞治疗中晚期肝癌的疗效。方法68例肝癌患者随机分成对照组:单用介入化疗栓塞33例;治疗组:苦参碱联合介入化疗栓塞35例。结果在临床症状改善、肝功能恢复、抑制瘤体生长、减轻介入化疗后毒副作用方面,治疗组明显优于对照组。结论苦参碱联合介入化疗栓塞治疗中晚期肝癌能明显提高疗效,改善生活质量、延长生存时间,值得推广应用。

Suppression of human colon tumor growth by adenoviral vector-mediated NK4 expression in an athymic mouse model

AIM： To investigate the suppressive effects of adenoviral vector-mediated expression of NK4, an antagonist of hepatocyte growth factor （HGF）, on human colon cancer in an athymic mouse model to explore the possibility of applying NK4 to cancer gene therapy. METHODS： A human colon tumor model was developed by subcutaneous implantation of tumor tissue formed by LS174T cells grown in athymic mice. Fifteen tumorbearing mice were randomized into three groups （n= 5 in each group） at d 3 after tumor implantation and mice were injected intratumorally with phosphate-buffered saline （PBS） or with recombinant adenovirus expressing 13-galactosidase （Ad-LacZ） or NK4 （rvAdCMV/NK4） at a 6-d interval for total 5 injections in each mouse. Tumor sizes were measured during treatment to draw a tumor growth curve. At d 26 after the first treatment, all animals were sacrificed and the tumors were removed to immunohistochemically examine proliferating cell nuclear antigen （PCNA）, microvessel density （represented by CD31）, and apoptotic cells. In a separate experiment, 15 additional athymic mice were employed to develop a tumor metastasis model by intraperitoneal injection （ip） of LS174T cells. These mice were randomized into 3 groups （n = 5 in each group） at d 1 after injection and were treated by ip injection of PBS, or Ad-LacZ, or rvAdCMV/NK4 at a 6-d interval for total two injections in each mouse. All animals were sacrificed at d 14 and the numbers and weights of disseminated tumors within the abdominal cavity were measured. RESULTS： Growth of significantly suppressed human colon tumors were in the athymic mice treatedwith rvAdCMV/NK4 （2537.4± 892.3 mm^3） compared to those treated by either PBS （5175.2 ± 1228.6 mm^3） or Ad-LacZ （5578.8± 1955.7 mm^3） （P 〈 0.05）. The tumor growth inhibition rate was as high as 51%. Immunohistochemical staining revealed a similar PCNA labeling index （75.1% ± 11.2% in PBS group vs 72.8% ± 7.6% in Ad-LacZ group vs 69.3% ± 9.4% in rvAdCMV/ NK4 group） in all groups, but significantly lower microvessel density （10.7 ± 2.4 in rvAdCMV/NK4 group vs 25.6 ± 3.8 in PBS group or 21.3 ± 3.5 in Ad-LacZ group, P 〈 0.05）, and a markedly higher apoptotic index （7.3% ± 2.4% in rvAdCMV/NK4 group vs 2.6 4, 1.1% in PBS group or 2.1% ± 1.5% in Ad-LacZ group, P 〈 0.05） in the rvAdCMV/NK4 group compared to the two control groups. In the tumor metastasis model, the number and weight of disseminated tumors of mice treated with rvAdCMV/NK4 were much lower than those of the control groups （tumor number： 6.2 ± 3.3 in rvAdCMV/ NK4 group vs 22.9 ± 7.6 in PBS group or 19.8 ± 8.5 in Ad-LacZ group, P 〈 0.05; tumor weight： 324 ± 176 mg in rvAdCMV/NK4 group vs 962 ± 382 mg in PBS group or 1116 ± 484 mg in Ad-LacZ group, P 〈 0.05）. CONCLUSION： The recombinant adenovirus, rvAdCMV/ NK4, can attenuate the growth of colon cancer in vivo, probably by suppressing angiogenesis and inducing tumor cell apoptosis, but not by direct suppression of tumor cell proliferation. Moreover, rvAdCMV/NK4 may inhibit peritoneal dissemination of colon cancer cells in a murine tumor metastasis model. These findings indicate that NK4 gene transfer may be an effective tool for the treatment of colon cancer.

Effect of antidepressants on body weight, ethology and tumor growth of human pancreatic carcinoma xenografts in nude mice

AIM: To investigate the effects of mirtazapine and fluoxetine, representatives of the noradrenergic and specific serotonergic antidepressant (NaSSA) and se- lective serotonin reuptake inhibitor (SSRI) antidepres- sant respectively, on body weight, ingestive behavior, locomotor activity and tumor growth of human pancre- atic carcinoma xenografts in nude mice. METHODS: A subcutaneous xenograft model of hu- man pancreatic cancer cell line SW1990 was estab- lished in nude mice. The tumor-bearing mice were ran- domly divided into mirtazapine group [10 mg/(kg·d)], fluoxetine group [10 mg/(kg·d)] and control group (an equivalent normal saline solution) (7 mice in each group). Doses of all drugs were administered orally, once a day for 42 d. Tumor volume and body weight were measured biweekly. Food intake was recorded once a week. Locomotor activity was detected weekly using an open field test (OFT). RESULTS: Compared to the fluoxetine, mirtazapine significantly increased food intake from d 14 to 42 and attenuated the rate of weight loss from d 28 to 42 (t = 4.38, P < 0.05). Compared to the control group, food intake was significantly suppressed from d 21 to 42 and weight loss was promoted from d 35 to 42 in the fluoxetine group (t = 2.52, P < 0.05). There was a significant difference in body weight of the mice after removal of tumors among the three groups. The body weight of mice was the heaviest (13.66 ± 1.55 g) in the mirtazapine group and the lightest (11.39 ± 1.45 g) in the fluoxetine group (F(2,12) = 11.43, P < 0.01). The behavioral test on d 7 showed that the horizontal and vertical activities were significantly increased in the mirtazapine group compared with the fluoxetine and control groups (F(2,18) = 10.89, P < 0.01). These effects disappeared in the mirtazapine and fluoxetine groups during 2-6 wk. The grooming activity was higher in the mirtazapine group than in the fluoxetine group (10.1 ± 2.1 vs 7.1 ± 1.9 ) (t = 2.40, P < 0.05) in the second week. There was no significant difference in tumor vol- ume and tumor weight of the three groups. CONCLUSION: Mirtazapine and fluoxetine have no effect on the growth of pancreatic tumor. However, mirtazapine can significantly increase food intake and improve nutrition compared with fluoxetine in a pan- creatic cancer mouse model.

EFFECT OF PREOPERATIVE USE OF LONG-ACTING OCTREOTIDE ON GROWTH HORMONE SECRETING PITUITARY ADENOMA AND TRANSSPHENOIDAL SURGERY

Objective To investigate whether somatostatin analog octreotide long acting release (LAR) shrinks growth hormone (GH) secreting adenomas, and improves the results of subsequent transsphenoidal surgery. Methods Seventeen previously untreated active acromegalic patients with pituitary adenomas were treated with LAR (30 mg intramuscular injection every 28 days) for 3 months prior to transsphenoidal surgery. Clinical reaction, mean GH secretion, and tumor volume were measured under basal conditions and after LAR treatment. Results Presurgical treatment improved acromegaly symptoms and induced a significant reduction of GH under the 5 ng/mL limit in microadenoma (P < 0.05), while only 18.2% (2/11) in macroadenoma. Meanwhile, tumor shrinkage occurred in 58.8% (10/17) patients, with 1 case in the microadenoma group. All marked shrinkage (> 25%) occurred in the macroadenoma group. Statistical analysis showed tumor shrinkage caused by LAR was greater in macroadenoma group than that in microadenoma group (P < 0.05). During operation, adenoma was soft in 15 cases, with the exception of 2 cases in which the soft tumor was divided by fibrous septa, but all tumor removal was smooth. Conclusions A short term administration of preoperative LAR may induce a significant decrease in GH-secretion level and adenoma volume. Presurgical use of octreotide LAR improves surgical results especially in macroadenomas.

The Inhibitory Effect of Oridonin on the Growth of Fifteen Human Cancer Cell Lines

OBJECTIVE To study the inhibitory effect of oridonin on the growth of cancer cells. METHODS Fifteen human cancer cell lines were subjected to various concentrations of oridonin in culture medium. The inhibitory rate of cell growth was measured by the MTT assay, and compared with a negative control and 5-Fu-positive control. RESULTS The 50% inhibiting concentration （IC50） and maximal inhibition （Imax） of oridonin shown by studying the growth of the cancer cell lines were as follows： leukemias （HL60 cells： 3.9 μg/ml and 73.8%, K562 cells： 4.3 μg/ml and 76.2%）; esophageal cancers（SHEEC cells： 15.4 μg/ml and 99.2%, Eca109 cells： 15.1 μg/ml and 84.6%, TEl cells： 4.0 μg/ml and 70.2%）; gastric cancers （BGC823 cells： 7.6 μg/ml and 98.7%, SGC7901 cells： 12.3 μg/ml and 85.7%）; colon cancers （HT29 cells： 13.6 μg/ml and 97.2%, HCT cells： 14.5 μg/ml and 96.5%）; liver cancers （Bel7402 cells： 15.2 μg/ml and 89.2%, HepG2 cells： 7.1 μg/ml and 88.3%）; pancreatic cancer （PC3 cells： 11.3 μg/ml and 68.4%）; lung cancer （A549 cells： 18.6 μg/ml and 98.0% ）; breast cancer （MCF7 cells： 18.4 μg/ml and 84.7%）; uterine cervix cancer （Hela cells： 13.7 μg/ml and 98.5%）. CONCLUSION Oridonin had a relatively wide anti-tumor spectrum, and a relatively strong inhibitory effect on the growth of the 15 human cancer cells. Inhibitory effects were concentration dependent.

Targeting key signalling pathways in oesophageal adenocarcinoma:A reality for personalised medicine?

Cancer treatments are rapidly changing.Curative treatment for oesophageal adenocarcinoma currently involves surgery and cytotoxic chemotherapy or chemoradiotherapy.Outcomes for both regimes are generally poor as a result of tumor recurrence.We have reviewed the key signalling pathways associated with oesophageal adenocarcinomas and discussed the recent trials of novel agents that attempt to target these pathways.There are many trials underway with the aim of improving survival in oesophageal cancer.Currently,phase 2 and 3 trials are focused on MAP kinase inhibition,either through inhibition of growth factor receptors or signal transducer proteins.In order to avoid tumor resistance,it appears to be clear that targeted therapy will be needed to combat the multiple signalling pathways that are in operation in oesophageal adenocarcinomas.This may be achievable in the future with the advent of gene signatures and a combinatorial approach.

Associations Between Epidermal Growth Factor Receptor Gene Mutation and Serum Tumor Markers in Advanced Lung Adenocarcinomas: A Retrospective Study

Objective To investigate the associations between epidermal growth factor receptor （EGFR） gene mutations and serum tumor markers in advanced lung adenocarcinomas. Methods We investigated the association between EGFR gene mutations and clinical features, including serum tumor marker levels, in 97 advanced lung adenocarcinomas patients who did not undergo the treatment of EGlaR tyrosine kinase inhibitors. EGFR gene mutation was detected by real-time PCR at exons 18, 19, 20, and 21. Serum tumor marker concentrations were analyzed by chemiluminescence assay kit at the same time. Results EGFR gene mutations were detected in 42 （43%） advanced lung adenocarcinoma patients. Gender （P=0.003）, smoking status （P=0.001）, and abnormal serum status of carcinoembryonic antigen （CEA, P=0.028） were significantly associated with EGFR gene mutation incidence. Multivariate analysis showed the abnormal CEA level in serum was independently associated with the incidence of EGFR gene mutation （P=0.046） with an odds ratio of 2.613 （95% Ch 1.018-6.710）. However, receiver operating characteristic （ROC） curve analysis revealed CEA was not an ideal predictive marker for EGFR gene mutation status in advanced lung adenocarcinoma （the area under the ROC curve was 0.608, P=0.069）. Conclusions EGFR gene mutation status is significantly associated with serum CEA status in advanced lung adenocarcinmoas. However, serum CEA is not an ideal predictor for EGFR mutation.

Characterization of FGFR signaling pathway as therapeutic targets for sarcoma patients

The fibroblast growth factor receptor(FGFR) family plays important roles in regulating cell growth, proliferation, survival,differentiation and angiogenesis. Deregulation of the FGF/FGFR signaling pathway has been associated with multiple development syndromes and cancers, and thus therapeutic strategies targeting FGFs and FGFR in human cancer are currently being explored.However, few studies on the FGF/FGFR pathway have been conducted in sarcoma, which has a poor outcome with traditional treatments such as surgery, chemotherapy, and radiotherapy. Hence, in the present review, we provide an overview of the role of the FGF/FGFR pathway signal in sarcoma and FGFR inhibitors, which might be new targets for the treatment of sarcomas according to recent research.

血管瘤裸鼠移植模型生物学特性的动态观察

目的建立能客观、真实地反映人血管瘤的临床发展过程的稳定的血管瘤裸鼠移植模型,动态观察其生物学特性的变化。方法以裸小鼠为载体,选取1例2月龄婴儿增生期毛细血管瘤,将瘤体组织转种于裸小鼠皮下,动态观察瘤体生长情况及组织学变化,检测不同时期移植血管瘤糖皮质激素受体、血管内皮细胞生长因子、Ki67的表达。结果血管瘤组织移植后3～4周内,瘤体基本上无明显变化,40d后,大多数瘤体开始生长,60d左右达到最大,90d时可见部分瘤体颜色变浅,质地较前变硬,90～120d时部分瘤体仅有少许残留组织。糖皮质激素受体、血管内皮细胞生长因子、Ki67在增生期移植血管瘤中高表达,而在退化期移植血管瘤中表达极弱。糖皮质激素受体与Ki67、血管内皮细胞生长因子的表达正相关,Ki67与血管内皮细胞生长因子表达正相关。结论将人体血管瘤皮下部分移植于裸鼠所建立的人血管瘤动物模型,能较真实地反映人血管瘤的发展过程,是研究血管瘤的较理想的平台。糖皮质激素受体、血管内皮细胞生长因子与移植血管瘤的演变过程有着密切的关系。

Effect of breast-cancer metastasis suppressor 1 (BRMS1) on growth and metastasis of human gastric cancer cells in vivo

Objective： The aim of the study was to investigate inhibitory effects of breast-cancer metastasis suppressor 1 protein （BRMS1） on primary tumor growth and metastasis of human gastric cancer （GC） cells in nude mice. Methods： We compared the expression of BRMS1 in the primary gastric tumor and metastatic gastric tumor by immunohistochemistry. Expression of BRMS1 also was detected in the GC cells by RT-PCR and Western blot. Three groups of cultured human GC cell line SGC-7901, were maintained： transfected cells with pcDNA3.1（-）B/myc-BRMS1; negative control cells with pcD- NA3.1/myc-his（-）B; and blank control ceils without any transfection. Histologically intact samples of the cells, maintained by passage in the subcutis of nude mice, were transplanted orthotopically into stomach walls of nude mice to establish a nude mouse model of human gastric carcinoma. Their primary tumor growth and metastasis were then observed. Results： The expression of BRMS1 was markedly stronger in the primary gastric tumor compared with metastatic gastric tumor. We also detected BRMS1 gene and protein in the gastric cancer cell tines. Numbers of metastasis tumors significantly differed among mice infected with transfected cells, with negative controls and with blank controls （4.38 ± 0.60, 7.75 ± 0.59, and 7.63± 0.65, respectively; P 〈 0.05）. However, there were no significant differences in the size of orthotopic tumors among mice infected with transfected, negative control and blank control cells [（12.02 ± 0.70）, （12.71 ± 0.63） and （12.89 ± 0.71） mm, respectively; P 〉 0.05]. Conclusion： BRMS1 suppresses metastasis of GC cells, but does not inhibit growth of gastric tumors.

A “false positive” octreoscan in ileal Crohn’s disease

We present a case report of a patient with a suspicious ileal carcinoid tumour. Clinical examination as well as computer tomograghy (CT) scan suggested a tumour. Octeotride scan showed uptake in the same bowel loop reported as pathological in CT. The patient underwent surgery and biopsy which reported Crohn’s disease (CD). The interest in the case is due to the fact that this is, to the best of our knowledge, the second report of Crohn’sdisease as a cause of false positive octeotride scan. Unfortunately, no somatostatin recptors could be found in the sample, so further studies should be performed.