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PubMed1973

Pain from distension of the pelvic colon by inflating a balloon in the irritable colon syndrome.

The effects of inflating a balloon introduced through a sigmoidoscope to 35 cm in the pelvic colon have been observed and compared in 67 patients with the irritable colon syndrome and in 16 normal and constipated subjects acting as controls. Inflation to 60 ml caused pain in 6% of the controls at a mean diameter of 3.8 cm and in 55% of patients with the irritable colon syndrome (diameter 3.4 cm). An estimate of gut wall tension at this volume of inflation showed it to be normal in patients with the irritable colon syndrome; the incidence of pain in relation to wall tension was increased nearly tenfold in the irritable colon group. Inflation of the balloon to different volumes was normally painless to a maximum acceptable diameter which remained constant for each study under constant conditions; continued inflation eventually gave rise to pain without increasing the diameter. The pain was felt in the hypogastrium in 40%, in one or both iliac fossae in 31%, and in the rectum in 21%; the other 8% felt pain in the back or elsewhere and there were no significant differences between clinical groups. Exceptionally, in 6% of the controls, and in 52% of patients with the irritable colon syndrome, pain occurred at balloon diameters that could still be increased by 10% or more with further inflation. This was probably the outcome of a low threshold for visceral pain in the section of bowel in contact with the balloon. Colonic hyperalgesia of this kind, possibly a random occurrence, may be an important contributory factor in the aetiology of the irritable colon syndrome.

Anthropometry↗

PubMed2000

Segmental wall thickening in the colonic loop distal to colonic carcinoma at CT: importance and histopathologic correlation.

PURPOSE: To determine the importance of the finding of segmental wall thickening in the colonic loop distal to colonic carcinoma at computed tomography (CT) by means of histopathologic correlation. MATERIALS AND METHODS: Thirteen consecutive patients whose helical CT scans showed segmental wall thickening (>1 cm in maximal width, >5 cm in length) in the colonic loop distal to colonic carcinoma were included. The thickness and length of an involved segment, location, morphologic tumor type, CT patterns of wall thickening, and pericolic changes were evaluated. Surgical pathologic findings in all 13 patients were correlated with CT findings. RESULTS: The involved segment distal to the colonic carcinoma showed circumferential wall thickening with a preserved wall layer pattern at CT. Pericolic changes of varying degrees were seen in 10 patients. Histopathologic examination revealed submucosal and subserosal edema (n = 6), chronic inflammation and fibrosis (n = 5), or both (n = 1), and no histopathologic alteration (n = 1). The tumors were mostly fungating (n = 11), larger than 5 cm in the greatest dimension (n = 12), located in the ascending colon (n = 10), and extended to pericolic adipose tissue (n = 11). CONCLUSION: Colonic carcinoma, especially a large fungating type involving the ascending colon with pericolic infiltration, can produce segmental wall thickening in the distal segment at CT, which represents edema or colitis at histopathologic examination.

Adult↗

PubMed2004

Influence of the surgical manipulation of the colon in colonic induced carcinogenesis in rats.

AIM: to investigate the influence of different experimental manipulations in a model of colonic experimental carcinogenesis with pharmacological induction in the rat. EXPERIMENTAL DESIGN: a total of 90 Sprague-Dawley male rats, divided into three groups, were used: non-surgical (n = 30); surgical with colonic trauma (n = 20), and surgical with colo-colonic anastomosis (n = 40). Carcinogenic induction was carried out with 1-2 dimethylhydrazine dihydrochloride. Colonic adenocarcinomas were identified and the number of tumors, as well as tumoral surface and percentage of tumoral surface was established. One-way ANOVA and Chi-square were employed for the statistical analysis. RESULTS: the number of tumors was greater in the surgical group than in the control group, and tumors preferentially developed around the manipulated colon. Surface and tumoral percentage were greater in the surgical group than in the control group, being also greater in the anastomosis group than in the group with colonic trauma. Within anastomosis groups, a greater tumor surface and percentage was found in the group with titanium than in the group with reabsorbable material. CONCLUSIONS: the experimental manipulation of the colon in rats enhances drug-induced colon carcingenesis. The creation of an anastomosis further increases the carcinogenic process compared with simulated anastomosis. This process is also enhanced by the quantity of suture material included in the anastomosis, and by the non-reabsorbable nature of the materials used in the anastomotic line.

1,2-Dimethylhydrazine↗

PubMed1991

Heterogenicity of ornithine decarboxylase during mouse colon carcinogenesis and in human colon tumors.

Ornithine decarboxylase (ODC) was separated, using diethylamino-ethyl ion-exchange chromatography, into multiple peaks of activity. We investigated the isoforms of ODC during 1,2-dimethylhydrazine-induced colon carcinogenesis and in human colon tumors. ODC in both mouse and human normal-appearing colonic mucosa was consistently separated into two active peaks by diethylaminoethyl-Sepharose CL-6B column chromatography. The major peak (Peak I) contained about 75% of the mouse and 72% of the human colonic mucosal ODC activity. During and after 10 weekly injections of 1,2-dimethylhydrazine (20 mg/kg, i.p.), colonic ODC activity was significantly enhanced with induction of both peaks but with a more significant increase in Peak II. ODC activity in both 1,2-dimethylhydrazine-induced and human colon tumors was significantly higher compared with the normal colon mucosa. The chromatographic profile of tumors showed the predominance of the second peak. Furthermore, the chromatographic profile of ODC after alkaline phosphatase treatment yielded an elution of only one peak coincident with the Peak I and the disappearance of Peak II. The second peak of ODC (the phosphorylated form) may be a specific isoform associated with colon tumorigenesis and tumor growth.

Alkaline Phosphatase↗

PubMed1987

Analysis of pp60c-src in human colon carcinoma and normal human colon mucosal cells.

The tyrosine-specific protein kinase activity of pp60c-src molecules obtained from RIPA buffer lysates of human colon tumor-derived cell lines is elevated over that found in lysates from normal human colon mucosa cells. The elevation of pp60c-src kinase activity in the lysates of the cultured colon tumor cells does not appear to be the result of pp60c-src overexpression suggesting that the specific activity of the pp60c-src phosphotransferase may be enhanced. Cell-free translation of c-src mRNA from colon tumor cells and normal colon mucosa cells yielded pp60c-src molecules with similar levels of in vitro protein kinase activity suggesting that pp60c-src kinase activity in these cells may be regulated differently at a post-translational level. Analysis of pp60c-src molecules from normal colon and colon carcinoma cells revealed that they possessed indistinguishable sites and quantities of phosphorylated serine and tyrosine residues and were not detectably complexed with other cellular proteins. The activation of pp60c-src kinase activity in the colon tumor cells is associated with an apparent increase in the turnover rate of tyrosine-phosphates within the carboxyl terminal portion of the pp60c-src molecules from these tumor derived cell lines.

Colon↗

PubMed1987

Expression of cloned sequences in biopsies of human colonic tissue and in colonic carcinoma cells induced to differentiate in vitro.

A computer-based scanning and image-processing system has been developed to quantitate the relative level of expression of each of 4000 cloned complementary DNA sequences in small biopsies routinely removed from the mucosa of normal and neoplastic human large intestine. Individuals have been studied from well-defined population groups in which colonic epithelial cells have progressed to increasingly advanced stages of neoplastic transformation. Comparison of normal colonic mucosa to colonic carcinomas demonstrated alterations in expression of approximately 7% of the cloned sequences; fewer changes were found between benign colonic adenomas and either normal colonic mucosa or carcinomas. A subset of the sequences which change in expression during progression from normal mucosa, to adenoma, to carcinoma showed complementary changes when colon carcinoma cells were induced to differentiate in vitro with sodium butyrate; quantitative correlations between in vivo and in vitro results were highly significant. Comparison of normal colonic mucosa with mucosa from patients with the autosomal dominant disease familial polyposis revealed more extensive alterations in gene expression involving approximately 25% of the clones screened. Flat colonic mucosa in familial polyposis is therefore markedly aberrant and may be highly dedifferentiated, suggesting several possible mechanisms for the very high incidence of cancer that develops in this epithelium.

Adenoma↗

PubMed1994

Effect of caloric restriction on colonic proliferation in obese persons: implications for colon cancer prevention.

Dietary intervention to prevent colon cancer is a major health issue. At present it is not clear which dietary factors modify colon cancer risk. Caloric restriction reduces the incidence of many spontaneous and carcinogen-induced tumors in rodents, but its role in human carcinogenesis is unknown. The relationships of body mass index (BMI), body composition, and resting metabolic rate (RMR) to colon cancer risk are also undefined. In this study involving obese persons, we measured the effect of reducing caloric intake on rectal cell proliferation, a biomarker in colon carcinogenesis, and studied the relation of BMI, body composition, and RMR to rectal cell proliferation. Colonic cell proliferation was measured in rectal biopsies from persons weighing more than 130% of ideal body weight. Follow-up biopsies were performed in patients who enrolled in and completed a 16-week behavior modification weight-reduction program in which caloric intake was reduced. Baseline measurements included body composition by total body electrical conductance, RMR, and BMI. Rectal biopsies were processed for autoradiography following incubation with [3H]thymidine. Epithelial proliferation measurements were evaluable in 35 persons at baseline and in 8 persons before and after caloric restriction. Before caloric restriction, mean (+/- SD) BMI was 38 +/- 4 kg/m2 and percentage of body fat 41 +/- 2%. Subjects reduced their caloric intake by a mean of 34 +/- 4% and their weight by 8.6 +/- 1%. Caloric restriction resulted in a 39% reduction in whole-crypt labeling index (P < 0.001) and a 57% reduction in upper crypt labeling index (P < 0.05) without reduction in crypt depth. Labeling index was unrelated to BMI, RMR, or body composition. We conclude that caloric restriction reduced rectal cell proliferation measurements--intermediate biomarkers related to colon carcinogenesis. BMI, RMR, and body composition were unrelated to colonic proliferation. Caloric restriction may have a role in colon cancer prevention.

Adult↗

PubMed1998

Frequent nitric oxide synthase-2 expression in human colon adenomas: implication for tumor angiogenesis and colon cancer progression.

An increased expression of nitric oxide synthase (NOS) has been observed in human colon carcinoma cell lines as well as in human gynecological, breast, and central nervous system tumors. This observation suggests a pathobiological role of tumor-associated NO production. Hence, we investigated NOS expression in human colon cancer in respect to tumor staging, NOS-expressing cell type(s), nitrotyrosine formation, inflammation, and vascular endothelial growth factor expression. Ca2+-dependent NOS activity was found in normal colon and in tumors but was significantly decreased in adenomas (P < 0.001) and carcinomas (Dukes' stages A-D: P < 0.002). Ca2+-independent NOS activity, indicating inducible NOS (NOS2), is markedly expressed in approximately 60% of human colon adenomas (P < 0.001 versus normal tissues) and in 20-25% of colon carcinomas (P < 0.01 versus normal tissues). Only low levels were found in the surrounding normal tissue. NOS2 activity decreased with increasing tumor stage (Dukes' A-D) and was lowest in colon metastases to liver and lung. NOS2 was detected in tissue mononuclear cells (TMCs), endothelium, and tumor epithelium. There was a statistically significant correlation between NOS2 enzymatic activity and the level of NOS2 protein detected by immunohistochemistry (P < 0.01). Western blot analysis of tumor extracts with Ca2+-independent NOS activity showed up to three distinct NOS2 protein bands at Mr 125,000-Mr 138,000. The same protein bands were heavily tyrosine-phosphorylated in some tumor tissues. TMCs, but not the tumor epithelium, were immunopositive using a polyclonal anti-nitrotyrosine antibody. However, only a subset of the NOS2-expressing TMCs stained positively for 3-nitrotyrosine, which is a marker for peroxynitrite formation. Furthermore, vascular endothelial growth factor expression was detected in adenomas expressing NOS2. These data are consistent with the hypothesis that excessive NO production by NOS2 may contribute to the pathogenesis of colon cancer progression at the transition of colon adenoma to carcinoma in situ.

Adenoma↗

PubMed1996

Colonization of human lung grafts in SCID-hu mice by human colon carcinoma cells.

Human colon carcinoma cell lines were examined in a colonization assay using SCID-hu mice engrafted with human fetal lung (HFL) tissues. Cell lines SW620 and COLO 320DM, derived from metastatic tumors, colonized HFL grafts after i.v. injection into SCID-hu mice. Cell lines SW480 and T34 initiated from primary colon tumors were unable to colonize HFL grafts. The ability to colonize HFL grafts but not mouse lungs of SCID-hu-L mice correctly reflects the clinical origin of these human colon carcinoma cell lines. Expression of a number of cell adhesion molecules was examined on SW480, SW620 and in vivo selected highly aggressive variants of SW620. NCAM and integrin alpha 3 expressed on the surface of SW480 cells were lost from metastatic cells, while carbohydrate ligands sialyl Lewis x and a, previously shown to be upregulated in metastatic colorectal tumors, were expressed at higher levels on colonizing cells. Unlike SW480, SW620 and its in vivo selected variants expressed RNA for calcium binding protein calbindin-D28K, a neuroendocrine marker. Acquisition of neuroendocrine features might be of potential importance in the development of the metastatic phenotype.

Animals↗

PubMed2003

Age-dependent variations of human and rat colon myofibroblasts in culture: Influence on their functional interactions with colon cancer cells.

Epithelial-mesenchymal interactions play a pivotal role in colon cancer invasion and metastasis. We aimed at elucidating the impact of long-term cultivation on the phenotypic and functional characteristics of primary fibroblasts and their interaction with the human colon adenocarcinoma cell line LoVoC5. We used fibroblasts from human colon tumor tissue, normal human colon mucosa, rat normal colon and 2 rat colon-derived myofibroblast cell lines, MIC316 and MG. The following parameters were studied: cell shape and size, growth curve, intermediate filament expression and extracellular matrix synthesis. Coculture models with or without cell contacts were used to test the effects on LoVoC5 cell proliferation, spreading and adhesion. Irrespective of their origin, fibroblastic cells in primary cultures presented marked phenotypic and functional changes with time. Before passage 5, they presented as large, slow-growing cells expressing vimentin and alpha-smooth muscle actin; synthesizing laminin-1, fibronectin and collagens I and IV; and inducing LoVoC5 proliferation, spreading and adhesion. After passage 15, they presented as small, fast-growing cells inconstantly expressing alpha-smooth muscle actin and synthesizing mainly type I collagen. In coculture with or without cell contacts, they inhibited LoVoC5 proliferation and allowed only limited cell spreading and adhesion. Myofibroblastic cell lines presented as large, fast-growing cells expressing vimentin and alpha-smooth muscle actin and synthesizing mainly type I collagen. They had no significant effects on LoVoC5 proliferation, spreading and adhesion. Our results underline the importance of age-dependent variations in colon mesenchymal cells in culture and for the in vitro study of epithelial-mesenchymal interactions in colon cancer.

Actins↗

PubMed1984

Sodium absorption with bacterial fatty acids and bile salts in the proximal and distal colon as a guide to colonic resection.

Rates of sodium absorption in the presence of bacterial fatty acids and bile salts are unknown along the length of the colon. Such information may guide resection of colon with a view to leaving colon most optimal for ion absorption. Absorption of sodium and permeability of the colonic mucosa to 51Cr EDTA was measured in the proximal (PC) and distal colon (DC) instilled with NaCl (120 mM), n-butyrate (40 mM) and chenodeoxycholic acid (1 or 2 mM) in varying combinations. Sodium absorption in the PC was 123.6 +/- 19 (nmoles/min/cm2)(n = 7) with saline alone and was doubled (P less than .001) when 40 mM n-butyrate replaced chloride anions. Sodium absorption in the DC with saline alone was 106.9 +/- 18 without significant alteration by addition of n-butyrate. CDC (1 mM) diminished sodium absorption in the PC and DC. Diminished sodium absorption induced by bile salts was significantly reversed by n-butyrate in the PC but not DC. Permeability of 51Cr EDTA was greatest with 2 mM CDC in the distal colon. Mucosal function--sodium absorption with SCFAs, permeability changes, and protection by bacterial fatty acids from sodium losses due to bile salts--was superior in the PC compared with DC. Our results suggest that it may be preferable to preserve the proximal rather than distal colon in operations of the colon to secure optimal absorption of sodium.

Animals↗

PubMed1987

Effect of dietary fiber on colonic cell proliferation and its relationship to colon carcinogenesis.

The addition of specific fiber supplements to semipurified diets has been shown to stimulate large bowel cell proliferation in laboratory rodents. Relatively insoluble fibers such as cellulose, which is poorly fermented, the more-soluble oat bran, and inert bulking agents such as kaolin produce little or no effect on cell growth. On the other hand, wheat bran, pectin, guar gum, and degraded carageenan all stimulate large bowel cell proliferation, the greatest growth response tending to occur in the cecum or proximal colon. The proximal large bowel is also the major site for the intestinal fermentation of dietary fiber and any other nonabsorbed carbohydrates. The fermentation of fiber by colonic microorganisms results in the production of short-chain fatty acids and a lower pH of large bowel contents, metabolic events known to be associated with increased epithelial cell growth. In general, factors that stimulate cell growth also enhance tumor development, a concept that holds true in the colon even for dietary fibers such as pectin and guar gum. Wheat bran can also stimulate colon carcinogenesis when fed only during carcinogen exposure. Oat bran and corn bran may stimulate colon carcinogenesis by increasing fecal bile acid excretion, a feature of many soluble fibers, while the acidification of large bowel contents is associated with an increased frequency of chemically induced colonic cancers. A greater understanding of colonic metabolism and cell physiology is needed to define fully the mechanisms by which dietary fibers modify colon cancer development.

Animals↗

PubMed1999

Liver colonization by human colon cancer cells is reduced by antisense inhibition of MUC2 mucin synthesis.

BACKGROUND & AIMS: Alterations in the production of epithelial mucins have been correlated with advanced tumor stage in the colon, but direct evidence for a role of specific mucin genes in liver metastasis is lacking. The current study was designed to establish more directly the role of MUC2 in colon cancer metastasis. METHODS: MUC2 levels were manipulated in highly metastatic human colon cancer cells using eukaryotic expression constructs designed to express a portion of MUC2 complementary DNA in antisense orientation. To assess the effect of MUC2 levels on metastatic potential, liver colonization was assessed in athymic mice after splenic-portal inoculation. RESULTS: Stable integration of the MUC2 antisense construct into metastatic colon cancer cells (LS LiM6) resulted in an 80% reduction in MUC2-specific messenger RNA and a concomitant decrease in MUC2 apomucin protein. This reduction was associated with a 50% reduction in synthesis of mature glucosamine-labeled mucin, almost complete inhibition of secretion of sialyl-LeX and sialyl-Tn antigens, and a 40% decrease in binding of colon cancer cells to E-selectin. Reduction in MUC2 levels was associated with a marked decrease in liver colonization. CONCLUSIONS: This study provides direct evidence that MUC2 plays an important role in colon cancer metastasis.

Animals↗

PubMedDate not supplied

Comparison of drug transporter levels in normal colon, colon cancer, and Caco-2 cells: impact on drug disposition and discovery.

A critical step in early phase drug development is the determination of oral bioavailability. In part, the ability to predict whether a drug will be effectively transported across the gastrointestinal mucosa can be estimated from the physicochemical properties of the compound. Although advancements through rational drug design have more correctly predicted bioavailability, considerable variability remains to be explained. Transporter expression throughout the gastrointestinal tract may explain much of this variation. ATP-binding cassette (ABC) transporters were the first family of transporters identified to modify bioavailability. More recently, the solute carrier family has also been shown to alter the pharmacokinetic profile of drugs. Currently, the Caco-2 human colon carcinoma cell line is often used by the pharmaceutical industry to evaluate intestinal absorption of drugs; however, in vivo/in vitro permeabilities with carrier mediated drugs do not correlate well, suggesting that Caco-2 transporter expression varies from that of the small intestine. With this is mind, we integrated U133A GeneChip expression data from the NCBIs Gene Expression Omnibus (GEO) collection and then compared the expression pattern of Caco-2 cells to normal colon to determine if the Caco-2 cell line is a reliable model for colonic delivery. Furthermore, transporter expression of Caco-2 cells was compared to that of human colon tumors to assess whether this cell line could be useful to predict drug absorption for colon cancer. Our analysis shows that the expression pattern for Caco-2 cells closely resembles the gene expression profile of transporters within the normal colon, suggesting that this cell line may serve as an in vitro model of colonic drug adsorption. However, the molecular "fingerprint" of Caco-2 was distinctly different from tumor samples, indicating that the Caco-2 model would unlikely predict accurate drug absorption for colon cancer sites.

ATP-Binding Cassette Transporters↗

PubMed2002

The colon-selective spasmolytic otilonium bromide inhibits muscarinic M(3) receptor-coupled calcium signals in isolated human colonic crypts.

1. Otilonium bromide (OB) is a smooth muscle relaxant used in the treatment of irritable bowel syndrome. Otilonium bromide has been shown to interfere with the mobilization of calcium in intestinal smooth muscle, but the effects on other intestinal tissues have not been investigated. We identified the muscarinic receptor subtype coupled to calcium signals in colonic crypt derived from the human colonic epithelium and evaluated the inhibitory effects of OB. 2. Calcium signals were monitored by fluorescence imaging of isolated human colonic crypts and Chinese hamster ovary cells stably expressing the cloned human muscarinic M(3) receptor subtype (CHO-M(3)). Colonic crypt receptor expression was investigated by pharmacological and immunohistochemical techniques. 3. The secretagogue acetylcholine (ACh) stimulated calcium mobilization from intracellular calcium stores at the base of human colonic crypts with an EC(50) of 14 micro M. The muscarinic receptor antagonists 4-DAMP, AF-DX 384, pirenzepine and methroctamine inhibited the ACh-induced calcium signal with the following respective IC(50) (pK(b)) values: 0.78 nM (9.1), 69 nM (7.2), 128 nM (7.1), and 2510 nM (5.8). 4. Immunohistochemical analyses of muscarinic receptor expression demonstrated the presence of M(3) receptor subtype expression at the crypt-base. 5. Otilonium bromide inhibited the generation of ACh-induced calcium signals in a dose dependent manner (IC(50)=880 nM). 6. In CHO-M(3) cells, OB inhibited calcium signals induced by ACh, but not ATP. In addition, OB did not inhibit histamine-induced colonic crypt calcium signals. 7. The present studies have demonstrated that OB inhibited M(3) receptor-coupled calcium signals in human colonic crypts and CHO-M(3) cells, but not those induced by stimulation of other endogenous receptor types. We propose that the M(3) receptor-coupled calcium signalling pathway is directly targeted by OB at the level of the colonic epithelium, suggestive of an anti-secretory action in IBS patients suffering with diarrhoea.

Acetylcholine↗

PubMed1986

Expression of type C-related endogenous retroviral sequences in human colon tumors and colon cancer cell lines.

Type C-related human endogenous retroviral sequences have been previously discovered and characterized [Martin, M. A., Bryan, T., Rasheed, S. & Khan, A.S. (1981) Proc. Natl. Acad. Sci. USA 78, 4892-4896]. We investigated the transcriptional pattern of these sequences to determine whether and to what extent their expression is altered in colon tumors and colon cancer cell lines as compared to normal colon mucosa (NCM). Of two long terminal repeat (LTR)-specific transcripts [3.6 and 2.1 kilobases (kb)], the 3.6-kb RNA was particularly abundant in NCM but strikingly decreased in most primary colon cancers tested. In NCM we identified three envelope gene (env)-related transcripts--namely, 3.0, 1.7, and 0.6 kb. Colon tumors appeared to express higher levels of these transcripts, especially the 1.7-kb species. In one case of dysplasia and in one benign tumor, this 1.7-kb transcript was clearly increased. We also examined the pattern of transcription in colon cancer cell lines HCT and Caco2. The LTR-homologous 3.6-kb transcript, very abundant in NCM, was decreased in primary tumors and in HCT cells and virtually absent in Caco2 cells. The latter, however, appeared to produce the transcript when growing exponentially, indicating that Caco2 cultures provide an inducible system susceptible to in vitro manipulation. Both cell lines also contained higher amounts of the 1.7-kb env-related transcript. The decrease of the 3.6-kb RNA in colon tumors versus NCM may be the result of an altered pattern of differentiation, whereas the increase of the 1.7-kb RNA in tumors may represent an early marker of colon neoplasia.

Base Sequence↗

PubMedDate not supplied

The combined effect against colon-26 cells of heat treatment and immunization with heat treated colon-26 tumour cell extract.

Cancer vaccines represent a promising new strategy for immunotherapy against cancer, but their effects are insufficiently understood. The effect of heat treatment against mouse colon adenocarcinoma cell line (colon-26), and combined effects of heat treatment and immunizing host animals with heat treated colon-26 cell extracts were investigated. Heat treatment of colon-26 cells induced heat-shock protein 70 (HSP70), but not other HSP. Immunization of BALB/cJ mice with heat treated colon-26 cell extract, which was enriched in HSP70, elicited antitumour immunity against subcutaneously injected colon-26 cells. Furthermore, combination therapy of heat treatment and immunization with heat treated colon-26 cell extract significantly reduced tumour volumes compared with heat treatment alone. Similar immunization enhanced the cytotoxic activity of mouse splenic lymphocytes against untreated and heat treated colon-26 cells in an in vitro assay, as well as against heat treated allogenic mouse lymphoma cell line (YAC-1). These findings suggest possible usefulness of heat treated cancer cell extract as a cancer vaccine, especially if given in combination with hyperthermia.

Adenocarcinoma↗

PubMed2000

Usefulness of preoperative colonic lavage using transanal ileus tube for obstructing carcinoma of left colon: device to perform one-stage operation safely.

Surgical treatments for patients with obstructing carcinoma of the left colon still remain controversial, and many devices to perform a one-stage operation for such cases have been reported. The aim of the current study was to demonstrate the usefulness of preoperative colonic lavage using a transanal ileus tube to perform a one-stage operation for patients with obstructing carcinoma of the left colon. Five patients with intestinal obstruction due to advanced carcinoma of the left colon were investigated. An ileus tube was transanally inserted and placed in the colon proximal to the tumor under the guidance of a colonoscope and guidewire. Preoperative colonic lavage was done with oral administration of an irrigating solution over several days. By using a transanal ileus tube, preoperative colonic lavage can be done, which enables us to safely perform a one-stage operation for patients with obstructing carcinoma of the left colon with no increase in complications or anastomotic leakage.

Aged↗