Risk of malignancy in resected cystic tumors of the pancreas < or =3 cm in size: is it safe to observe asymptomatic patients? A multi-institutional report.

Recent international consensus guidelines propose that cystic pancreatic tumors less than 3 cm in size in asymptomatic patients with no radiographic features concerning for malignancy are safe to observe; however, there is little published data to support this recommendation. The purpose of this study was to determine the prevalence of malignancy in this group of patients using pancreatic resection databases from five high-volume pancreatic centers to assess the appropriateness of these guidelines. All pancreatic resections performed for cystic neoplasms < or =3 cm in size were evaluated over the time period of 1998-2006. One hundred sixty-six cases were identified, and the clinical, radiographic, and pathological data were reviewed. The correlation with age, gender, and symptoms (abdominal pain, nausea and vomiting, jaundice, presence of pancreatitis, unexplained weight loss, and anorexia), radiographic features suggestive of malignancy by either computed tomography, magnetic resonance imaging, or endoscopic ultrasound (presence of solid component, lymphadenopathy, or dilated main pancreatic duct or common bile duct), and the presence of malignancy was assessed using univariate and multivariate analysis. Among the 166 pancreatic resections for cystic pancreatic tumors < or =3 cm, 135 cases were benign [38 serous cystadenomas, 35 mucinous cystic neoplasms, 60 intraductal papillary mucinous neoplasms (IPMN), 1 cystic papillary tumor, and 1 cystic islet cell tumor], whereas 31 cases were malignant (14 mucinous cystic adenocarcinomas and 13 invasive carcinomas and 4 in situ carcinomas arising in the setting of IPMN). A greater incidence of cystic neoplasms was seen in female patients (99/166, 60%). Gender was a predictor of malignant pathology, with male patients having a higher incidence of malignancy (19/67, 28%) compared to female patients (12/99, 12%; p < 0.02). Older age was associated with malignancy (mean age 67 years in patients with malignant disease vs 62 years in patients with benign lesions (p < 0.05). A majority of the patients with malignancy were symptomatic (28/31, 90%). Symptoms that correlated with malignancy included jaundice (p < 0.001), weight loss (p < 0.003), and anorexia (p < 0.05). Radiographic features that correlated with malignancy were presence of a solid component (p < 0.0001), main pancreatic duct dilation (p = 0.002), common bile duct dilation (p < 0.001), and lymphadenopathy (p < 0.002). Twenty-seven of 31(87%) patients with malignant lesions had at least one radiographic feature concerning for malignancy. Forty-five patients (27%) were identified as having asymptomatic cystic neoplasms. All but three (6.6%) of the patients in this group had benign disease. Of the patients that had no symptoms and no radiographic features, 1 out of 30 (3.3%) had malignancy (carcinoma in situ arising in a side branch IPMN). Malignancy in cystic neoplasms < or =3 cm in size was associated with older age, male gender, presence of symptoms (jaundice, weight loss, and anorexia), and presence of concerning radiographic features (solid component, main pancreatic duct dilation, common bile duct dilation, and lymphadenopathy). Among asymptomatic patients that displayed no discernable radiographic features suggestive of malignancy who underwent resection, the incidence of occult malignancy was 3.3%. This study suggests that a group of patients with small cystic pancreatic neoplasms who have low risk of malignancy can be identified, and selective resection of these lesions may be appropriate.

Interleukin-1 beta and interferon-gamma regulate interleukin-6 production in cultured human intestinal epithelial cells.

Recent studies suggest that interleukin-6 (IL-6) is produced in the intestinal mucosa during sepsis and endotoxemia and that the enterocyte may be a source of IL-6 in these conditions. The regulation of IL-6 production in the enterocyte is not fully understood. We tested the hypothesis that IL-6 production in the enterocyte is regulated by proinflammatory cytokines. This was done by treating cultured Caco-2 cells, a transformed human intestinal epithelial cell line, with different concentrations of tumor necrosis factor-alpha (TNF-alpha), IL-1 beta, IL-6 or interferon-gamma (IFN-gamma). IL-6 production by the Caco-2 cells was determined by ELISA. The expression of IL-6 mRNA was determined by reverse-transcriptase polymerase chain reaction. IL-6 was not produced in unstimulated Caco-2 cells. Treatment of the Caco-2 cells with IL-1 beta resulted in a dose- and time-dependent stimulation of IL-6 production with a maximal effect noted at an IL-1 beta concentration of .5 ng/mL at 24 h. IFN-gamma alone did not stimulate IL-6 production but potentiated the effect of IL-1 beta in a synergistic fashion. Treatment of the Caco-2 cells with IL-1 beta induced expression of IL-6 mRNA with a response noticed after 30 min. TNF-alpha and IL-6 did not influence the production of IL-6 in the Caco-2 cells. The results suggest that enterocyte IL-6 production is stimulated by IL-1 beta and that this effect is potentiated by IFN-gamma. The regulation of IL-6 production in the enterocyte may be specific for IL-1 beta, since neither TNF nor IL-6 stimulated IL-6 production.

Interleukin-1beta induces complement component C3 and IL-6 production at the basolateral and apical membranes in a human intestinal epithelial cell line.

In previous studies, stimulation of cultured enterocytes with IL-1beta resulted in production of IL-6 and complement component C3. The cellular mechanisms of these responses in the enterocyte are not fully understood. We tested the hypothesis that IL-1beta-induced C3 and IL-6 production is differentially regulated at the apical and basolateral membranes of the enterocyte. Caco-2 cells (a transformed human colonic carcinoma cell line) were grown in a 2-chamber system to full differentiation. The cells were treated with IL-1beta either at the apical or basolateral membrane, and C3 and IL-6 mRNA levels and release of C3 and IL-6 into the apical and basal chambers were determined. The release of C3 was greatest into the basal chamber regardless of whether the cells were stimulated at the apical or basolateral membrane. In contrast, the production of IL-6 was greatest at the cell membrane that was stimulated with IL-1beta. Stimulation of the Caco-2 cells with IL-1beta resulted in increased mRNA levels for C3 and IL-6 with no major differences noted when the cells were treated at the apical or basolateral membrane. The results suggest that enterocyte production and release of at least some acute phase proteins and cytokines are differentially regulated at the apical and basolateral membrane of the enterocyte after stimulation with IL-1beta.

IL-1beta induction of NF-kappaB activation in human intestinal epithelial cells is independent of oxyradical signaling.

IL-1beta stimulation of cultured epithelial cells induces the degradation of IkappaBalpha and the consequent nuclear translocation of NF-lambdaB, a critical proinflammatory transcription factor in the mucosal host immune response. The role of reactive oxygen intermediates, serine protease activity, and tyrosine kinase activity in the activation of NF-kappaB is weakly conserved across various cell lineages and has not been defined in human enterocytes, a major target of oxidant stress in sepsis, thermal injury, and hemorrhagic shock. We report here that in Caco-2BBe cells, a transformed human colon cancer cell line with features of small intestinal epithelial cells in culture, exposure to oxidant stress (hydrogen peroxide 1-10 mM) did not induce NF-kappaB activation. Similarly, scavenging of free radicals and oxidants by pyrrolidine dithiocarbamate and dimethyl sulfoxide did not block IL-1beta-induced IkappaBalpha degradation and NF-kappaB activation. Genistein, a nonspecific tyrosine kinase inhibitor, also had no effect on IL-1beta-mediated effects on NF-kappaB. Serine protease inhibition by tosyl-lysine-chloromethylketone and tosyl-phenylalanine-chloromethylketone inhibited IkappaBalpha degradation and NF-kappaB activation stimulated by IL-1beta. Our data highlight the strong divergence between epithelial and mononuclear cells in the signal transduction pathways relating IL-1beta stimulation and NF-kappaB nuclear translocation.

Complement C3 production in human intestinal epithelial cells is regulated by interleukin 1beta and tumor necrosis factor alpha.

BACKGROUND: Sepsis and endotoxemia are associated with increased mucosal production of complement component C3; the enterocyte may be a source of C3 in these conditions. OBJECTIVE: To test the hypothesis that interleukin 1beta (IL-1beta) and tumor necrosis factor alpha (TNF-alpha) regulate the production of C3 in the enterocyte at the transcriptional level and that this regulation is potentiated by interferon gamma (IFN-gamma). METHODS: Cultured Caco-2 cells, a human intestinal epithelial cell line, were treated with various concentrations of human recombinant IL-1beta (0.005-1.25 ng/mL) or TNF-alpha (1-1000 U/mL) with or without the addition of IFN-gamma (250 U/mL). C3 levels in the culture medium were measured by enzyme-linked immunosorbent assay and cellular messenger RNA levels by Northern blot analysis. RESULTS: Treatment of the Caco-2 cells with IL-1beta or TNF-alpha resulted in a time- and dose-dependent increase in C3 production. The use of IFN-gamma alone did not affect C3 production but potentiated the effect of IL-1beta and TNF-alpha in a synergistic manner. C3 messenger RNA levels were increased following stimulation with either cytokine. CONCLUSIONS: C3 production in the enterocyte is regulated by IL-1beta and TNF-alpha at the transcriptional level, and this response is potentiated by IFN-gamma. The results suggest that C3 production in the intestinal mucosa may be regulated locally by cytokines in a paracrine or autocrine manner.

Blunt carotid artery injuries.

BACKGROUND: Blunt carotid artery trauma remains a rare but potentially devastating injury. Early detection and treatment remain the goals of management. Our objective was to identify patients sustaining blunt carotid injuries at a regional trauma center and report on the incidence, demographics, diagnostic workup, management, and outcome. STUDY DESIGN: A retrospective chart review was performed of patients sustaining blunt carotid artery injury between 1990 and 1996. RESULTS: Twenty patients were identified during the 7-year period. All patients suffered blunt trauma, with motor vehicle accidents being the most common mechanism, and the internal carotid the most frequently injured vessel. Associated injuries were present in all patients, with head (65%) or chest (65%) injuries being the most common. The combination of head and chest trauma (45%) was found to be associated with a 14-fold increase in the likelihood of carotid injury. Cerebral angiography was diagnostic in all patients and the majority were treated nonoperatively with anticoagulation. Twenty percent of patients were discharged with a normal neurologic exam, while 45% left with a significant neurologic deficit. Overall mortality was 5%. CONCLUSIONS: Blunt carotid injuries are rare but are associated with significant morbidity and mortality. The combination of craniofacial and chest wounds should raise the index of suspicion for blunt carotid injury. Anticoagulation was associated with the least morbidity.

Conductive hearing loss following retrolabyrinthine surgery.

BACKGROUND: Conductive hearing loss can occur following neuro-otological procedures due to bony ossicular fixation resulting from viable bone dust remains. OBJECTIVE: To highlight the frequency and features of the complication of conductive hearing loss following retrolabyrinthine surgery. DESIGN: In a review of 77 retrolabyrinthine neuro-otological procedures, 3 cases (3.9%) of postoperative conductive hearing loss were encountered. RESULTS: Bone dust can cause a postoperative conductive hearing deficit that becomes apparent 6 months following surgery, and progressive deterioration can occur up to 18 months. The anatomical areas of ossicular fixation are the incudomalleal joint in the attic and around the stapes in the oval window niche. Excision of these bony accumulation particles does not revert the conductive hearing loss. CONCLUSIONS: We advocate the use of occlusive material in the aditus during temporal bone surgery to prevent bone dust accumulation in the attic and middle ear. In the event of such a complication, an incus transposition ossiculoplasty is recommended.

Vestibular nerve section following previous mastoidectomy.

Vestibular neurectomy is an effective procedure in the management of vertigo due to active labyrinthine disease. Various approaches have been developed for selectively sectioning the vestibular nerve, in order to preserve serviceable hearing and avoid facial nerve injury. In patients who have a mastoid cavity, from previous surgery for chronic otitis media, the approach to the vestibular nerve has to be modified. Considerations taken into account are cavity infection, hearing status, and the presence of associated loud tinnitus. Vestibular or vestibulo-cochlear nerve section has been undertaken, by the senior author, in eight patients with a mastoid cavity from previous surgery for chronic otitis media. Translabyrinthine, retrosigmoid and middle fossa approaches have all been used; strategies for selection of each specific technique are considered, and the aetiology of post-chronic suppurative otitis media (CSOM) peripheral vestibular disease discussed.

Subtotal petrosectomy with external canal overclosure in the management of chronic suppurative otitis media.

Subtotal petrosectomy with external canal overclosure has been used in the management of 10 patients with chronic suppurative otitis media in the past four years. These patients fall into two categories. One group consisted of patients with end-stage chronically discharging mastoid cavities, despite aggressive medical therapy. The other group comprised patients who had developed disabling peripheral vestibular symptoms and had a mastoid cavity from past surgery for chronic otitis media. In both groups the affected ear had absent or poor auditory function. In the second group, a translabyrinthine section of the vestibular and/or cochlear nerves was performed in conjunction with subtotal petrosectomy. The procedure has been very successful in relieving the persistent otorrhoea, giving the patient an ear without a cavity that would need regular care. No restriction on swimming and participation in other water sports is an additional advantage. Illustrative cases are used to discuss the technique and indications.

Tetanus in a case of lepromatous leprosy.

A patient of Lepromatous Leprosy had neuropathic plantar ulcer of 6 months duration. He developed "Tetanus". We are reporting this case with review of literature, as there is dearth of published literature on this association of Leprosy and Tetanus.

Gastric duplication cyst masquerading as a mucinous pancreatic cyst: case report and literature review.

Gastric duplication cysts are rare cystic neoplasms that are often difficult to distinguish from other entities. We describe a healthy 44-year-old woman who presented with acute right lower quadrant abdominal and flank pain as well as chronic nausea and constipation. Her physical examination was unremarkable but contrasted computed tomography revealed a 6 cm cystic lesion between the stomach and body of the pancreas. Endoscopic ultrasonography and fluid analysis were consistent with a mucinous cyst with a markedly elevated fluid carcinoembryonic antigen level. The patient subsequently underwent a laparoscopic distal pancreatectomy, which was converted to an open procedure when the lesion was noted to be adherent to the coeliac axis. Intraoperative endoscopy revealed no abnormality. Final pathology revealed a gastric duplication cyst. The patient recovered well and was asymptomatic on follow-up. In this report, we discuss the incidence, natural history and management of this rare entity.

Pancreatic cancer: can we screen? How should we stage?

Pancreatic cancer remains a deadly disease, with few patients surviving 5 years following diagnosis. Surgical resection remains the only treatment associated with the potential for cure; however, most patients have locally advanced or metastatic disease at presentation and thus are not surgical candidates. Advances in imaging technologies, biochemistry, and molecular genetics have raised hopes of improving the outcome for patients with pancreatic cancer through earlier and more accurate diagnosis. As our knowledge of the genetics of pancreatic cancer has increased, the possibility of screening to identify patients at risk to develop the disease also holds promise. This review focuses on the utility of current modalities to screen for pancreatic cancer as well as the most accurate and expedient methods to stage the disease.

Barotraumatic fracture of the stapes footplate.

We present a rare case in which barotrauma led to fracture of the stapes footplate and perilymph fistula, resulting in sudden severe sensorineural hearing loss and tinnitus. Surgical repair in this case resulted in excellent hearing recovery. The aetiology and management of inner ear barotrauma and stapes injury is discussed. We believe that early exploration and repair of suspected perilymph fistulae optimises hearing recovery.

The burden of screening for acoustic neuroma: asymmetric otological symptoms in the ENT clinic.

The rising numbers of legal cases relating to delay in the diagnosis of acoustic neuroma, combined with the increasing availability of magnetic resonance, is increasing pressure on otologists to make an early definitive diagnosis of cerebellopontine angle tumours. Unilateral or asymmetrical otologic symptoms not explained by external or middle ear disease are elicited in 16.6% of 500 consecutive attenders to an otolaryngology clinic. An agreed policy of risk stratification of patients with unexplained asymmetric otological symptoms is required if expense is to be limited and litigation minimized.

IL-6 production in human intestinal epithelial cells following stimulation with IL-1 beta is associated with activation of the transcription factor NF-kappa B.

Recent studies suggest that interleukin-1 beta (IL-1 beta) stimulates interleukin-6 (IL-6) production in human intestinal epithelial cells, but the intracellular mechanisms of this response are not known. In other reports, the nuclear factor-kappa B (NF-kappa B) regulated IL-6 production in certain cell types. We tested the hypothesis that IL-6 production in the enterocyte is associated with activation of NF-kappa B. Caco-2 cells, a human intestinal epithelial cell line, were grown in tissue culture whereafter they were treated with IL-1 beta (0.5 ng/ml). Cells were preincubated with pyrrolidine dithiocarbamate (PDTC; 10-500 microM), tosyl-lys-chloromethylketone (TLCK; 10-500 microM), or genistein (25-75 microM), all of which are known inhibitors of NF-kappa B. IL-6 levels in the culture media were measured after 24 hr by enzyme-linked immunosorbent assay (ELISA) and IL-6 messenger RNA (mRNA) levels were determined after 4 hr by competitive reverse-transcriptase polymerase chain reaction (RT-PCR). NF-kappa B activity was determined by electrophoretic gel mobility shift assay (EMSA). PDTC, TLCK, and genistein each inhibited IL-1 beta-induced IL-6 production by the Caco-2 cells in a dose-dependent fashion. These responses were also associated with a decrease in IL-6 mRNA levels. There was no NF-kappa B activity in untreated cells, but the addition of IL-1 beta resulted in the activation of NF-kappa B as determined by EMSA. The results suggest that IL-1 beta-induced IL-6 production in the enterocyte is associated with activation of NF-kappa B. The inhibition of IL-6 production by the NF-kappa B inhibitors indicates that the IL-6 production is regulated by NF-kappa B, although further experiments are needed to test that hypothesis.

Interleukin-6 production in human intestinal epithelial cells increases in association with the heat shock response.

BACKGROUND: In recent studies, IL-1beta stimulated the production of IL-6 in human enterocytes. The heat shock response influences the production of inflammatory mediators in certain cell types. We tested the hypothesis that heat shock regulates IL-1beta-induced IL-6 production in human intestinal epithelial cells. MATERIALS AND METHODS: Cultured Caco-2 cells, a human intestinal epithelial cell line, were exposed to thermal heat shock at 43 degreesC for 1 h and recovered at 37 degreesC for 1 h. Cells were harvested for analysis of heat shock protein-70 (HSP-70) production by Western blotting. In other experiments, IL-1beta (0.5 ng/ml) was added following heat shock and recovery. IL-6 protein was measured in culture medium after 24 h by enzyme-linked immunosorbent assay and IL-6 messenger RNA (mRNA) levels were measured after 4 h by competitive reverse transcriptase polymerase chain reaction. RESULTS: Heat shock resulted in the production of HSP-70 and potentiated IL-1beta-induced IL-6 production. The response to heat shock was associated with increased IL-6 mRNA levels. CONCLUSIONS: The results suggest that IL-1beta-induced IL-6 production in human enterocytes is increased in association with the heat shock response. The biological role of heat shock-potentiated IL-6 production in the enterocyte remains to be determined.

Implementation of a clinical pathway decreases length of stay and cost for bowel resection.

OBJECTIVE: To examine the effect of a clinical pathway for small and large bowel resection on cost and length of hospital stay. SUMMARY BACKGROUND DATA: Clinical pathways are designed to streamline patient care delivery and maximize efficiency while minimizing cost. Theoretically, they should be most effective in commonly performed procedures, in which volume and familiarity are high. METHODS: A clinical pathway to assist in the management of patients undergoing bowel resection was developed by a multidisciplinary team and implemented. Data about length of stay and cost was collected for all patients undergoing bowel resection 1 year before and 1 year after pathway implementation. Three groups were compared: patients undergoing bowel resection in the year prior to pathway implementation (prepathway), patients in the year after pathway implementation but not included on the pathway (nonpathway), and patients included in the pathway (pathway). RESULTS: The mean cost per hospital stay was $19,997.35 +/- 1244.61 for patients in the prepathway group, $20,835.28 +/- 2286.26 for those in the nonpathway group, and $13,908.53 +/- 1113.01 for those in the pathway group (p < 0.05 vs. other groups). Mean postoperative length of stay was 9.98 +/- 0.62 days (prepathway), 9.68 +/- 0.88 days for (nonpathway), and 7.71 +/- 0.37 days (pathway) (p < 0.05 vs. other groups). CONCLUSIONS: Implementation of the pathway produced significant decreases in length of stay and cost in the pathway group as compared to the prepathway group. These results support the further development of clinical pathways for general surgical procedures.

Stress response decreases the interleukin-1beta-induced production of complement component C3 in human intestinal epithelial cells.

Interleukin-1beta (IL-1beta) increases the production of complement component C3 in enterocytes. Heat shock regulates the response to cytokines and other inflammatory mediators in various cell types. We tested the hypothesis that the heat-shock response regulates IL-1beta-induced C3 production in the enterocyte. Cultured Caco-2 cells, a human intestinal epithelial cell line, were treated with sodium arsenite (10-500 microM) for 1 h or subjected to hyperthermia (43 degrees C) for 1-4 h, and allowed to recover for 1 h. The cells were then treated with IL-1beta (0.5 ng/ml) for up to 24 h, whereafter C3 levels were measured by ELISA and C3 mRNA by Northern blot analysis. Heat-shock protein of 72 kDa (hsp72) was determined by Western blot analysis. Treatment of the cells with sodium arsenite or subjecting them to hyperthermia induced the expression of hsp72. The IL-1beta-induced expression of C3 mRNA and C3 production were down-regulated by hyperthermia and sodium arsenite in a dose-dependent fashion. The results suggest that the stress response induced by hyperthermia or sodium arsenite decreases IL-1beta-induced C3 production in human enterocytes.

Complement component C3 production in IL-1beta-stimulated human intestinal epithelial cells is blocked by NF-kappaB inhibitors and by transfection with ser 32/36 mutant IkappaBalpha.

BACKGROUND: Recent studies suggest that interleukin-1beta (IL-1beta) stimulates the production of the acute phase protein complement component C3 in human intestinal epithelial cells. The transcription factor NF-kappaB activates different genes involved in the response to cytokines. It is not known if IL-1beta-induced C3 production in the enterocyte is regulated by NF-kappaB. MATERIALS AND METHODS: Cultured Caco-2 cells, a human intestinal epithelial cell line, were treated with one of the NF-kappaB inhibitors, tosyl-lys-chloromethylketone (TLCK), genistein, or pyrrolidine dithiocarbamate (PDTC), or with N-acetyl-leu-leu-norleucinal (LLnL), a proteasome inhibitor known to block the degradation of Ikappabeta, the cytosolic inhibitor of NF-kappaB. Following this treatment, the Caco-2 cells were stimulated with IL-1beta, and C3 levels in the culture medium were measured after 24 h by ELISA. C3 mRNA levels were determined after 4 h by Northern blot analysis. In other experiments, Caco-2 cells were transfected with a mutant IkappaBalpha in which serines 32 and 36 were substituted by alanine. This mutation prevents IkBalpha phosphorylation and subsequent NF-kappaB nuclear translocation. After transfection, the cells were stimulated with IL-1beta, and C3 levels in the culture medium were measured after 24 h. Cytosolic IkappaBalpha was determined by Western blot analysis. RESULTS: TLCK, genistein, and LLnL each inhibited IL-1beta-induced C3 production in a dose-dependent fashion. These responses were associated with decreased C3 mRNA levels. In contrast, PDTC did not influence C3 production or C3 mRNA in the Caco-2 cells. Transfection of the Caco-2 cells with the Ser 32/36 mutant IkBalpha resulted in maintained IkappaBalpha levels and decreased IL-beta-induced C3 production. CONCLUSIONS: IL-1beta-stimulated C3 production in the enterocyte may be regulated by NF-kappaB.

Angiopoietin-1 inhibits tumour growth and ascites formation in a murine model of peritoneal carcinomatosis.

Angiopoietin-1 is an important regulator of endothelial cell survival. Angiopoietin-1 also reduces vascular permeability mediated by vascular endothelial growth factor. The effects of angiopoietin-1 on tumour growth and angiogenesis are controversial. We hypothesised that angiopoietin-1 would decrease tumour growth and ascites formation in peritoneal carcinomatosis. Human colon cancer cells (KM12L4) were transfected with vector (pcDNA) alone (control) or vector containing angiopoietin-1 and injected into the peritoneal cavities of mice. After 30 days, the following parameters were measured: number of peritoneal nodules, ascites volume, and diameter of the largest tumour. Effects of angiopoietin-1 on vascular permeability were investigated using an intradermal Miles assay with conditioned media from transfected cells. Seven of the nine mice in the pcDNA group developed ascites (1.3+/-0.5 ml (mean+/-s.e.m.)), whereas no ascites was detectable in the angiopoietin-1 group (0 out of 10) (P<0.01). Number of peritoneal metastases (P<0.05), tumour volume, (P<0.05), vessel counts (P<0.01), and tumour cell proliferation (P<0.01) were significantly reduced in angiopoietin-1-expressing tumours. Conditioned medium from angiopoietin-1-transfected cells decreased vascular permeability more than did conditioned medium from control cells (P<0.05). Our results suggest that angiopoietin-1 is an important mediator of angiogenesis and vascular permeability and thus could theoretically serve as an anti-neoplastic agent for patients with carcinomatosis from colorectal cancer.