CRP, TNFα, IL-1ra, IL-6, IL-8 and IL-10 in blood serum of colorectal cancer patients

Blood serum cytokines: TNFalpha, IL-1ra, IL-6, IL-8, IL-10 as well as CRP were investigated in patients with colorectal cancer, prior treatment and 1, 10 and 42 days after surgery. There was an increase of the levels of CRP, IL-6 and IL-10 in most patients 24 hours after surgery. The levels of IL-1ra were elevated in patients in stage C and in several patients in stage B of the disease and there was a decrease of circulating TNFalpha in stage B patients. On day 10 and 42 after surgery, the levels of cytokines followed various patterns.     

Down-regulation of IL-6, IL-8, TNF-α and IL-1β by glucosamine in HaCaT cells, but not in the presence of TNF-α

There is considerable evidence that glucosamine exerts an inhibitory effect on inflammatory cytokine expression in cells. Glucosamine has been recommended as a promising anti-inflammatory modulator, which has been applied in clinical trials for attenuation of the inflammatory process. However, it is unknown whether glucosamine reduces the expression of TNF-α-induced inflammatory cytokines in HaCaT cells. The anti-inflammatory effects of curcumin in HaCaT cells have been extensively investigated in several studies. Thus, in this study we investigated the expression of IL-6, IL-8, TNF-α and IL-1β in glucosamine-treated HaCaT cells, and the effects of glucosamine were compared to those of curcumin-treated HaCaT cells. Our data showed that the expression of IL-6, IL-8, TNF-α and IL-1β was decreased by glucosamine treatment in the HaCaT cells. In contrast, the expression of IL-6, IL-8, TNF-α and IL-1β was not attenuated by glucosamine treatment in the TNF-α-treated HaCaT cells. Notably, curcumin induced an increased expression of IL-8 and IL-1β in the HaCaT cells, but not that of IL-6 and TNF-α. On the other hand, curcumin attenuated the expression of IL-6 and IL-8 in the TNF-α-treated HaCaT cells. Our data indicated that glucosamine induced the down-regulation of IL-6, IL-8, TNF-α and IL-1β expression in the HaCaT cells. However, the stimulation of TNF-α abolished the inhibitory effects of glucosamine on the expression of inflammatory cytokines in the HaCaT cells. Thus, even though glucosamine induces the down-regulation of inflammatory cytokines in HaCaT cells, the anti-inflammatory role of glucosamine in TNF-α-mediated inflammatory skin diseases should be investigated.     

Intratumoral delivery of encapsulated IL-12, IL-18 and TNF-α in a model of metastatic breast cancer

Intratumoral (i.t.) cytokine release through the use of poly-lactic acid microspheres (PLAM) holds tremendous potential for the immunotherapy of breast cancer as it harnesses the immunologic potential of autologous tumor in a clinically feasible and minimally toxic manner. We examined the potential of combinations of i.t. IL-12, IL-18 and TNF-α PLAM to generate a tumor-specific immune response and improve outcome in a model of metastatic breast cancer. Balb/c mice with established 4T1 mammary carcinomas were treated with a single injection of BSA, IL-12, IL-18 or TNF-α-loaded PLAM alone or in combination after spontaneous metastases occurred. Combined treatment with IL-12 and TNF-α PLAM was superior to all other treatments, including the triple combination of IL-12, IL-18 and TNF-α in ablation of the primary tumor, eradicating distant disease and enhancing survival. Simultaneous delivery of IL-12 and TNF-α was superior to sequential delivery of IL-12 followed by TNF-α, but not TNF-α followed by IL-12. In vivo lymphocyte depletion studies established that the effects of IL-12 alone are mediated primarily by NK cells, while the combination of IL-12 and TNF-α is dependent upon CD8+ T-cells. Only the combination of IL-12 and TNF-α results in an increase in both CD4+ and CD8+ T-cells and a reduction in CD4+CD25+ cells. While there was no change in the dendritic cell population, IL-12 and TNF-α resulted in a dramatic increase in DC maturation and antigen presentation. Neoadjuvant immunotherapy with simultaneous intratumoral delivery of IL-12 and TNF-α PLAM augments DC antigen presentation and increases cytotoxic T-cells without increasing regulatory T-cells, resulting in a T-cell based anti-tumor immune response capable of eradicating disseminated disease. The addition of IL-18 did not improve the efficacy.     

TNF-α and IL-10 promoter polymorphisms, HPV infection, and cervical cancer risk

Although the implication of genetic factors in cervical cancer development remains to be elucidated, accumulative epidemiological evidence suggests that polymorphisms of cytokine genes may be involved in the etiology of cervical carcinoma. Tumor necrosis factor alpha (TNF-??) and interleukin-10 (IL-10) are two multifunctional cytokines implicated in inflammation, immunity, and cellular organization, and were proposed to play important roles in cancer biology. In order to determine whether IL-10 -1082 (G/A) and TNF-?? -238 (G/A) and -308 (G/A) polymorphisms are associated with susceptibility to cervical cancer, a case?Ccontrol study of 122 cancer patients and 176 healthy controls was conducted. Cervical samples were genotyped for both TNF-?? polymorphisms by PCR-RFLP assay. SNP-1082 from IL-10 gene was genotyped using pyrosequencing technology. The association between cervical cancer risk and the studied SNPs was evaluated by logistic regression. Under univariate analysis, none of these polymorphisms appeared associated with susceptibility of cervical cancer development or HPV infection. However, individuals carrying heterozygous genotype for TNF-?? -238 polymorphism seem to be at lower risk for cervical cancer development, with borderline significance (OR?=?0.42, P?=?0.069), as well as those carrying heterozygous genotypes for IL-10 and TNF-?? -238 (OR?=?0.40, P?=?0.08). In conclusion, these results suggest a potential effect of TNF-?? -238 G/A in the reduction of cervical cancer risk in Argentine women, but not TNF-?? -308 or IL-10. Larger studies are needed to fully understand the genetic predisposition for the development of cervical cancer.     

Reduced Expression of IL-1β and IL-18 Proinflammatory Interleukins Increases the Risk of Developing Cervical Cancer

Background: The objective of this study was to analyze the gene expression profile of the proinflammatoryinterleukins, (IL-1β and IL-18) in patients with premalignant lesions and cervical cancer. Methods: Total IL-1β andIL-18 mRNA was quantified by qPCR to obtain the expression data in cervical tissues. A total of 74 cervical biopsieswere obtained from women undergoing a colposcopy. The samples were divided into: normal (19), low level lesions(LSIL) or NIC I (17), high level lesions (HSIL) or CIN II and CIN III (29) and cancer (9). The normal cervical tissuesamples were included as controls. The OR and 95% CI were calculated for the determination of the risk of progressionbetween each type of lesion and cancer using logistic regression. Results: The results showed that an increase in therisk of progression of pre-neoplastic lesions to cancer was between 2.5 and 2.08 times higher in women with lowerIL-1β and IL-18 expression, respectively. Conclusions: This study provided evidence that IL-1β and IL-18 are potentialbiomarkers that can be explored in further studies for monitoring the evolution of pre-neoplastic lesions and avoidingovertreatment or undertreatment of the patients.     

Serum Levels of IL-lβ, IL-6, TNF-α, sTNF-RI and CRP in Patients with oral cavity cancer

Pro-inflammatory cytokines, such as interleukin-lβ (IL-lβ), interleukin-6 (IL-6) and tumor necrosis factor- (TNF-α) play an essential role in the regulation of immune response to, and may have prognostic significance in, cancer. The aim of this study was to examine the relationship between the serum levels of IL-lβ, IL-6 and TNF-α as well as the concentrations of soluble TNF receptor I (sTNF-RI) and C-reactive protein (CRP) in patients with squamous cell carcinoma of oral cavity. Results obtained were confronted with squamous cell carcinoma antigen (SCO concentrations. IL-lβ IL-6 and TNF-α serum levels as well as sTNF-RI and CRP concentrations were higher in patients than in controls. The increased serum levels appeared to be related to the clinical stage of disease. There was a correlation between IL-lβ and sTNF-RI. IL-6 and IL-lβ correlated with CRP levels. The mean concentrations of SCC were also elevated. IL-6 and sTNF-RI seemed to be the most sensitive parameters in early stages and may be used as additional markers in oral cancer     

Overall Survival and Clinicopathological Characteristics of Patients with Breast Cancer in Relation to the Expression Pattern of HER-2, IL-6, TNF-α and TGF-β1

The present study was conducted to investigate the prognostic significance of co-expression patterna of HER-2,IL-6, TNF-a and TGF-β1 in breast cancer, by correlating the number of markers with positive expression withclinicopathological characteristics indicative of tumor progression and overall survival. One hundred thirtyconsecutive patients with primary breast cancer were prospectively included and evaluated. Serum concentrationsof the above markers were measured by ELISA. Median split was used to subdivide patients with marker positiveor negative expression. The presence of ≥3 positive markers was independently associated with extended lymphnode (>3) involvement (aOR, 11.94, p=0.001) and lymphovascular invasion (aOR, 12.04, p=0.018), increasingthe prognostic significance of each marker considered separately. Additional prognostic information regardingsurvival was also provided; as the number of positive markers increased, a gradually reduction of survival timewas observed. In addition, patients with 4 positive markers had significantly shorter survival (25 vs 39 months,p=0.006) and a more than 4 fold increased risk of death (aHR, 4.35, p=0.003) compared to patients with 3 positivemarkers. Our findings suggest that the coexpression pattern of these four markers could be used clinically as auseful marker for tumor extension and outcome of breast cancer.     

Exploration of Multigene, Mulfistep and Multipathway Models of Nasopharyngeal and Colorectal Carcinogenesis

OBJECTIVE To construct tree models for nasopharyngeal carcinoma (NPC) and colorectal carcinoma (CC) and explore the oncogeneic process of NPC and CC .METHODS Based on the software that Desper et al. developed, tree models were constructed for CC from the comparative genomic hybridization (CGH) data of 118 CC patients and for NPC from the CGH data of 140 southern Chinese patients, respectively. RESULTS Tree models for CC suggested that loss of 18q and gain of 20q were important early events in colorectal carcinogenesis. As changes in -18q occurred prior to those in -17p, a cause-effect relationship might exist between them. Tree models for NPC suggested that loss of 3p was an important early event in nasopharyngeal carcinogenesis, and deletion of 11q, 14q, 16q and 9p were also nonrandom genetic events in carcinogenesis, suggesting that there might be tumor-associated genes existing on these chromosome arms. The tree model also indicated the existence of oncogenes on the short arm of chromosome 12.CONCLUSION Constructing tree models based on the CGH data to demonstrate the initiation and progression of NPC might help elucidate its multigene, multistep and multipathway development. It may provide valuable clues to explore the mechanism of tumorigenesis.     

Dietary intake of vegetables, folate, and antioxidants and the risk of Barrett’s esophagus

Purpose

Diet is a potentially modifiable risk factor for Barrett’s esophagus (BE). We investigated the associations between intakes of fruits and vegetables and risk of BE.

Methods

We identified study subjects from 1,859 participants who underwent the endoscopy in a single VA Medical Center in the US between 2008 and 2011. Dietary intake in the previous year was elicited using a self-administered Block food frequency questionnaire (FFQ). Logistic regression model was used to estimate odds ratio (OR) and its 95 % confidence interval (CI) for BE.

Results

A total of 151 cases with definite BE and 777 controls completed the FFQ. When highest tertile of intake was compared with the lowest, the OR (95 % CI) was 0.46 (0.26–0.81) for dark green vegetables, 0.52 (0.30–0.90) for legumes, 0.50 (0.28–0.90) for total fiber, 0.45 (0.25–0.81) for isoflavones, 0.52 (0.30–0.67) for total folate, and 0.45 (0.26–0.79) for lutein, adjusting for multiple confounding factors including use of aspirin or proton pump inhibitor, gastro-esophageal reflux symptoms, and physical activity. The association for dark green vegetables was attenuated after adjustment for lutein, total fiber, and total folate (OR = 0.82; 95 % CI 0.30–2.22).

Conclusion

Higher intake of dark green vegetables was associated with a decreased risk of BE in a veteran population. Such an inverse association may be partially mediated by lutein, fiber, and folate. The novel findings on the association between intake of lutein, total folate, or isoflavones and risk of BE need further confirmation.     

Acacia ferruginea Inhibits Tumor Progression by RegulatingInflammatory Mediators-(TNF-a,iNOS, COX-2, IL-1ß, IL-6, IFN-γ, IL-2, GM-CSF) and Pro-Angiogenic Growth Factor-VEGF

The aim of the present investigation was to evaluate the effect of A ferruginea extract on Dalton’s lymphomaascites (DLA) induced tumours in BALB/c mice. Experimental animals received A ferruginea extract (10 mg/kg.b.wt) intraperitoneally for 14 consecutive days after DLA tumor challenge. Treatment with extract significantlyincreased the life span, total white blood cell (WBC) count and haemoglobin (Hb) content and decreased the level ofserum aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), gamma glutamyltransferase (γ-GT) and nitric oxide (NO) in DLA bearing ascites tumor models. In addition, administration ofextract significantly decreased the tumour volume and body weight in a DLA bearing solid tumor model. Thelevels of pro-inflammatory cytokines such as tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β),interleukin-6 (IL-6) and granulocyte monocyte-colony stimulating factor (GM-CSF), as well as pro-angiogenicgrowth factors such as vascular endothelial growth factor (VEGF) and inducible nitric oxide synthase (iNOS)were elevated in solid tumour controls, but significantly reduced by A ferruginea administration. On the otherhand, the extract stimulated the production of interleukin-2 (IL-2) and interferon-gamma (IFN-γ) in animals withDLA induced solid tumours. Increase in CD4+ T-cell population suggested strong immunostimulant activity forthis extract. GC/MS and LC/MS analysis showed quinone, quinoline, imidazolidine, pyrrolidine, cyclopentenone,thiazole, pyrazole, catechin and coumarin derivatives as major compounds present in the A ferruginea methanolicextract. Thus, the outcome of the present study suggests that A ferruginea extract has immunomodulatory andtumor inhibitory activities and has the potential to be developed as a natural anticancer agent.     

Effect of Intraoperative Glucose Fluctuation and Postoperative IL-6, TNF-α, CRP Levels on the Short-term Prognosis of Patients with Intracranial Supratentorial Neoplasms

Objective: To investigate the effect of intraoperative glucose fluctuation and postoperative interlukin-6 (IL-6),tumor necrosis factor-α (TNF-α), C-reactive protein (CRP) levels on the short-term prognosis of patients withintracranial supratentorial neoplasms. Materials and Methods: Eighty-six patients undergoing intracranialexcision were selected in The Second Hospital of Jilin University. According to the condition of glucose fluctuation,the patients were divided into group A (glucose fluctuation <2.2 mmol/L, n=57) and group B (glucose fluctuation≥2.2 mmol/L, n=29). Glucose was assessed by drawing 2 mL blood from internal jugular vein in two groupsin the following time points, namely fasting blood glucose 1 d before operation (T0), 5 min after anesthesiainduction (T1), intraoperative peak glucose (T2), intraoperative lowest glucose (T3), 5 min after closing the skull(T4), immediately after returning to intensive care unit (ICU) (T5) and 2 h after returning to ICU (T6). 1 d beforeoperation and 1, 3 and 6 d after operation, serum IL-6 and TNF-α levels were detected with enzyme-linkedimmunosorbent assay (ELISA), and CRP level with immunoturbidimetry. Additionally, postoperative adversereactions were monitored. Results: There was no statistical significance between two groups regarding theoperation time, anesthesia time, amount of intraoperative bleeding and blood transfusion (P>0.05). The glucoselevels in both groups at T1~T6 went up conspicuously compared with that at T0 (P<0.01), and those in group Bat T2, T4, T5 and T6 were significantly higher than in group A (P<0.01). Serum IL-6, TNF-α and CRP levels inboth groups 1, 3 and 6 d after operation increased markedly compared with 1 d before operation (P<0.01), butthe increased range in group A was notably lower than in group B (P<0.05 or P<0.01). Postoperative incidencesof hypoglycemia, hyperglycemia and myocardial ischemia in group A were significantly lower than in group B(P<0.05), and respiratory support time obviously shorter than in group B (P<0.01). Conclusions: The glucosefluctuation of patients undergoing intracranial excision is related to postoperative IL-6, TNF-α and CRP levelsand those with small range of glucose fluctuation have better prognosis.     

Serum levels of IL-6 and IL-1β can predict the efficacy of gemcitabine in patients with advanced pancreatic cancer

Background:

With this study, we sought to characterise the impact of pro-inflammatory cytokines on the outcomes of gemcitabine monotherapy (GEM) in patients with pancreatic cancer (PC).

Methods:

Treatment-naive patients with advanced PC and no obvious infections were eligible for enrolment. All of the patients were scheduled to undergo systemic chemotherapy. Serum pro-inflammatory cytokines were measured using an electro-chemiluminescence assay method before chemotherapy. High cytokine levels were defined as values greater than the median. Clinical data were collected prospectively.

Results:

Sixty patients who received GEM were included in the analysis. High IL-6 and IL-1β levels were poor prognostic factors for overall survival in a multivariate analysis (P=0.011 and P=0.048, respectively). Patients with both a high IL-6 level and a high IL-1β level exhibited shortened overall and progression-free survival, a reduction in the tumour control rate, and a high dose intensity of GEM compared with patients with low levels of both IL-6 and IL-1β.

Conclusion:

The serum levels of IL-6 and IL-1β predict the efficacy of GEM in patients with advanced PC.     

Alterations of the CD4+, CD8+ T Cell Subsets, Interleukins-1β, IL-10, IL-17, Tumor Necrosis Factor-α and Soluble Intercellular Adhesion Molecule-1 in Rheumatoid Arthritis and Osteoarthritis: Preliminary Observations

Rheumatoid arthritis is a multisystem disease with underlying immune mechanisms. Osteoarthritis is a debilitating, progressive disease of diarthrodial joints associated with the aging process. Although much is known about the pathogenesis of rheumatoid arthritis and osteoarthritis, our understanding of some immunologic changes remains incomplete. This study tries to examine the numeric changes in the T cell subsets and the alterations in the levels of some cytokines and adhesion molecules in these lesions. To accomplish this goal, peripheral blood and synovial fluid samples were obtained from 24 patients with rheumatoid arthritis, 15 patients with osteoarthritis and six healthy controls. The counts of CD4 (+) and CD8 (+) T lymphocytes were examined using flow cytometry. The levels of some cytokines (TNF-alpha, IL1-beta, IL-10, and IL-17) and a soluble intercellular adhesion molecule-1 (sICAM-1) were measured in the sera and synovial fluids using enzyme linked immunosorbant assay. We found some variations in the counts of T cell subsets, the levels of cytokines and sICAM-1 adhesion molecule between the healthy controls and the patients with arthritis. High levels of IL-1beta, IL-10, IL-17 and TNF-alpha (in the serum and synovial fluid) were observed in arthritis compared to the healthy controls. In rheumatoid arthritis, a high serum level of sICAM-1 was found compared to its level in the synovial fluid. A high CD4(+)/CD8(+) T cell ratio was found in the blood of the patients with rheumatoid arthritis. In rheumatoid arthritis, the cytokine levels correlated positively with some clinicopathologic features. To conclude, the development of rheumatoid arthritis and osteoarthritis is associated with alteration of the levels of some cytokines. The assessment of these immunologic changes may have potential prognostic roles.     

Combined treatment of IL-1α and TNF-α potentiates the antitumour effect of hyperthermia

Vasoactive cytokines, such as IL-1α and TNF-α, modulate the homeostatic state at the endothelial surface and cause various types of pathological damage in vascular systems. We investigated the potential therapeutic effects of IL-1α and TNF-α in combination with hyperthermia on SCK tumours grown in the legs of A/J mice. We first determined the effect of cytokines on tumour blood perfusion with the ⁸⁶Rb uptake method. When the host mice were given an i.p. injection of 25 μg/kg IL-1α or 50 μg/kg TNF-α, the tumour blood perfusion markedly declined to 46 and 82% of control, respectively. The combination of IL-1α and TNF-α reduced the ⁸⁶Rb uptake to 41% of control. Hyperthermia at 42·5°C for 1 h reduced the tumour blood flow to 71% of control. The tumour blood perfusion decreased further to 20% of control when the tumours were heated for 1 h at 42.5°C starting 4h after the injection of both IL-1α and TNF-α. The changes in clonogenic cell numbers in SCK tumours, as determined by the in vivo-in vitro assay, following various treatments was also investigated. At 4h after an i.p. injection of 25 μg/kg IL-1α or 50 μg/kg TNF-α, the clonogenicity of SCK tumours significantly decreased to 29 or 37% of control, respectively. Heating at 42.5°C for 1h caused a decline in the clonogenic cell number to 30% of control. When both IL-1α and TNF-α were given and tumours were heated 4h later at 42·5°C for 1h, the clonogenic cell number markedly declined to 0.4% of control. The time needed for control tumours to reach 4x their initial volume was about 3 days, and treatment with IL-1α or hyperthermia alone induced a tumour delay growth by about 1 day. The combined injection of IL-1α and TNF-α followed by a heating at 42·5°C for 1h delayed the tumour growth by 6 days. The results in this study suggest that prior impairment of blood circulation by the combined treatment of IL-1α and TNF-α potentiates hyperthermic damage in tumours.     

Clinicopathological significance of chemotactic factor IL-8, MCP-1 and MIP-1α expressions in gallbladder carcinoma

Objective:Gal bladder carcinoma was one of the malignant tumors in the digestive system, characterized by high recurrence and invasion. Recent research indicates that chemotactic factors such as IL-8, ...     

Role of cytokines (TNF-α, IL-1β and KC) in the pathogenesis of CPT-11-induced intestinal mucositis in mice: effect of pentoxifylline and thalidomide

Introduction Irinotecan (CPT-11) is an inhibitor of DNA topoisomerase I and is clinically effective against several cancers. A major toxic effect of CPT-11 is delayed diarrhea; however, the exact mechanism by which the drug induces diarrhea has not been established. Purpose Elucidate the mechanisms of induction of delayed diarrhea and determine the effects of the cytokine production inhibitor pentoxifylline (PTX) and thalidomide (TLD) in the experimental model of intestinal mucositis, induced by CPT-11. Materials and methods Intestinal mucositis was induced in male Swiss mice by intraperitoneal administration of CPT-11 (75 mg/kg) daily for 4 days. Animals received subcutaneous PTX (1.7, 5 and 15 mg/kg) or TLD (15, 30, 60 mg/kg) or 0.5 ml of saline daily for 5 and 7 days, starting 1 day before the first CPT-11 injection. The incidence of delayed diarrhea was monitored by scores and the animals were sacrificed on the 5th and 7th experimental day for histological analysis, immunohistochemistry for TNF-α and assay of myeloperoxidase (MPO) activity, tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and KC ELISA. Results CPT-11 caused significant diarrhea, histopathological alterations (inflammatory cell infiltration, loss of crypt architecture and villus shortening) and increased intestinal tissue MPO activity, TNF-α, IL-1β and KC level and TNF-α immuno-staining. PTX inhibited delayed diarrhea of mice submitted to intestinal mucositis and reduced histopathological damage, intestinal MPO activity, tissue level of TNF-α, IL-1β and KC and TNF-α immuno-staining. TLD significantly reduced the lesions induced by CPT-11 in intestinal mucosa, decreased MPO activity, TNF-α tissue level and TNF-α immuno-staining, but did not reduce the severity of diarrhea. Conclusion These results suggest an important role of TNF-α, IL-1β and KC in the pathogenesis of intestinal mucositis induced by CPT-11.     

High expression of IL-13 receptor α2 in colorectal cancer is associated with invasion, liver metastasis, and poor prognosis

Autocrine secretion of cytokines by metastatic colorectal cancer cells and their role during invasion and liver homing has been poorly characterized. In this study, we used cytokine arrays to analyze the secretomes of poorly and highly metastatic colorectal cancer cells. Compared with poorly metastatic cancer cells, highly metastatic cells expressed increased levels of the immunosuppressive cytokines interleukin (IL)-4 and IL-13 in addition to increased surface expression of the high affinity IL-13 receptor IL-13Rα2, suggesting that IL-13Rα2 mediates IL-13 effects in colorectal cancer cells. Silencing of IL-13Rα2 in highly metastatic cells led to a decrease in adhesion capacity in vitro and a reduction in liver homing and increased survival in vivo, revealing a role for this receptor in cell adhesion, migration, invasion, and metastatic colonization. In support of this, IL-13 signaling activated the oncogenic signaling molecules phosphoinositide 3-kinase, AKT, and SRC in highly metastatic cells. Clinically, high expression of IL-13Rα2 was associated with later stages of disease progression and poor outcome in patients with colorectal cancer. Our findings therefore support a critical role for IL-13Rα2 expression in colon cancer invasion and metastasis.