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Supplementary Table S1: patient characteristics including age, sex, tumor type, and treatment

Detailed information about Material and Methods used throughout the manuscript including information about cell lines, antibodies, biochemical assays and in vitro and in vivo assays.

Supplementary Figure 1-7 on irradiation of CAF; effect of irradiated CAF on cancer cells; glutamine metabolism; proteome analysis of CM CAF; effect of recombinant IGF1 on cancer cells; effect of recombinant IGF1 on metabolism of cancer cells; schematic of in vivo set-up and Figure legends or respective figures

Preoperative radiotherapy (RT) is a mainstay in the management of rectal cancer, a tumor characterized by desmoplastic stroma containing cancer-associated fibroblasts (CAF). Although CAFs are abundantly present, the effects of RT to CAF and its impact on cancer cells are unknown. We evaluated the damage responses of CAF to RT and investigated changes in colorectal cancer cell growth, transcriptome, metabolome, and kinome in response to paracrine signals emerging from irradiated CAF. RT to CAF induced DNA damage, p53 activation, cell-cycle arrest, and secretion of paracrine mediators, including insulin-like growth factor-1 (IGF1). Subsequently, RT-activated CAFs promoted survival of colorectal cancer cells, as well as a metabolic switch favoring glutamine consumption through IGF1 receptor (IGF1R) activation. RT followed by IGF1R neutralization in orthotopic colorectal cancer models reduced the number of mice with organ metastases. Activation of the downstream IGF1R mediator mTOR was significantly higher in matched (intrapatient) samples and in unmatched (interpatient) samples from rectal cancer patients after neoadjuvant chemoradiotherapy. Taken together, our data support the notion that paracrine IGF1/IGF1R signaling initiated by RT-activated CAF worsens colorectal cancer progression, establishing a preclinical rationale to target this activation loop to further improve clinical responses and patient survival.Significance: These findings reveal that paracrine IGF1/IGF1R signaling promotes colorectal cancer progression, establishing a preclinical rationale to target this activation loop. Cancer Res; 78(3); 659–70. ©2017 AACR.

Background & Aims: Patients with alcoholic hepatitis and a modified Maddrey's discriminant function (mDF), SCOPUS: ar.j, info:eu-repo/semantics/published

© Author(s) (or their employer(s)) 2022. No commercial re-use. See rights and permissions. Published by BMJ., Objective: Alcohol-related liver disease (ALD) ranges from never-decompensated ALD (ndALD) to the life-threatening decompensated phenotype, known as alcohol-related hepatitis (AH). A multidimensional study of the clinical, histological and molecular features of these subtypes is lacking. Design: Two large cohorts of patients were recruited in an international, observational multicentre study: a retrospective cohort of patients with ndALD (n=110) and a prospective cohort of patients with AH (n=225). Clinical, analytical, immunohistochemistry and hepatic RNA microarray analysis of both disease phenotypes were performed. Results: Age and mean alcohol intake were similar in both groups. AH patients had greater aspartate amino transferase/alanine amino transferase ratio and lower gamma-glutamyl transferase levels than in ndALD patients. Patients with AH demonstrated profound liver failure and increased mortality. One-year mortality was 10% in ndALD and 50% in AH. Histologically, steatosis grade, ballooning and pericellular fibrosis were similar in both groups, while advanced fibrosis, Mallory-Denk bodies, bilirubinostasis, severe neutrophil infiltration and ductular reaction were more frequent among AH patients. Transcriptome analysis revealed a profound gene dysregulation within both phenotypes when compare to controls. While ndALD was characterised by deregulated expression of genes involved in matrisome and immune response, the development of AH resulted in a marked deregulation of genes involved in hepatocyte reprogramming and bile acid metabolism. Conclusions: Despite comparable alcohol intake, AH patients presented with worse liver function compared with ndALD patients. Bilirubinostasis, severe fibrosis and ductular reaction were prominent features of AH. AH patients exhibited a more profound deregulation of gene expression compared with ndALD patients., This work was supported by the National Institute on Alcohol Abuse and Alcoholism (NIAAA 1U01AA021908-01, 1U01AA020821 and P50AA011999) and the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK P30DK120531 and P30DK120515). PSwas supported by Fondo de Investigación Sanitaria Carlos III, cofinanced by Fondo Europeo de Desarrollo Regional (FEDER), Unión Europea, 'Una manera de hacer Europa' PI17/00673; PI20/00765 and Miguel Servet, CPII16/0004. MV-C is a recipient of the Juan Rodés JR19/00015. JA is a recipient of a grant from Agencia Estatal de Salud (PI20/01663).

Oesophageal involvement is a very rare presentation of Crohn’s disease. It can occur as an isolated mass causing dysphagia and can be mistaken for malignancy. Here, we report a case of a 75-year-old woman presenting with dysphagia and weight loss. Gastroscopy showed an ulcerating mass, and her barium swallow showed a bird beak appearance at the level of the gastro-oesophageal junction (GEJ). Repetitive biopsies were inconclusive. Fluorodeoxyglucose-positron emission tomography showed high glucose uptake (standardised uptake value: 10.2) at the level of the GEJ. Endoscopic ultrasound classified the lesion as uT3N1. Step-by-step surgical exploration revealed an oesophageal mass. A frozen section examination showed an absence of malignancy and the presence of inflammatory tissue. A partial oesophagogastrostomy was performed, and reconstruction was achieved by a Merendino procedure. Definitive histopathological examination revealed isolated oesophageal Crohn’s disease.

Background and aims Endoscopic ultrasound fine-needle aspiration/biopsy (EUS-FNA/FNB) is highly accurate, but discrepancies between cytological and surgical diagnoses are still observed. We aimed to determine its accuracy and monitor quality indicators in our facilities. Patients and methods We performed a retrospective review of all cases of pancreatic solid lesions evaluated by EUS-FNA/FNB, between July 2015 and June 2018, in two centers. Cytological and surgical findings were categorized into five groups: benign, malignant, suspect of malignancy, undetermined and insufficient for diagnosis. Final diagnosis was based on surgical diagnosis and, in patients who did not undergo surgery, on clinical outcome after 6 months follow-up. Results Altogether, 142 patients were included. FNA was the preferred tissue acquisition method (88%), with a predilection for the FNA 22G needle (57%). Cytology was insufficient for diagnosis in 2 cases, therefore a full diagnostic sample was available in 98.6% of the patients (>90%, ESGE target). Fifty-five (38.7%) patients underwent surgery. In term of cancer diagnosis, comparison with final surgical pathology (n=55) revealed 89% true positives, 5.5% true negatives, 3.6% false positives and 1.8% false negatives. When combining surgical diagnosis and clinical outcomes together, EUS-guided sampling sensitivity was 97.4% (92.5-99.5), specificity was 92.3% (74.9-99.1), positive predictive value was 98.2% (93.6- 99.5), negative predictive value was 88.9% (72.3-96.1) and accuracy was 96.4% (91.9-98.8). Post-procedural acute pancreatitis was reported in 2 patients (1.4%). Conclusions These results reveal a performance for diagnostic tissue sampling well above the ESGE proposed target standard. Also, the uncommon high specificity illustrates the determining role of the pathologist's final interpretation and diagnosis.

Resume Introduction D’apres les series europeenne et americaine, jusqu’a 20 % des cancers colorectaux sont caracterises par une instabilite microsatellitaire. Les cancers colorectaux MMR deficients sont principalement retrouves dans le colon droit. Bien qu’on observe une augmentation du nombre de cancers colorectaux dans les pays en voie de developpement, notamment en Afrique de l’Ouest, les donnees sur l’epidemiologie et la biologie du cancer colorectal de cette region sont rares. Materiels et methodes Nous avions pour but d’etudier l’incidence du deficit MMR en Cote d’Ivoire et de comparer les donnees avec un centre tertiaire belge. Les immunohistochimies dirigees contre les proteines MLH1, MSH2, MSH6 et PMS2 ont ete realisees sur des echantillons de tissus inclus en paraffine provenant de 83 cancers colorectaux (46 % d’hommes) operes a Abidjan et de 343 cancers colorectaux (53 % d’hommes) operes a Bruxelles. Resultats Les cancers colorectaux survenaient a un plus jeune âge en Cote d’Ivoire compare a la Belgique (âge median : 53 versus 66). Le deficit MMR a ete detecte dans 11,7 % des cas belges et dans 13,3 % des cas ivoiriens. Cependant, les cancers colorectaux MMR deficients bruxellois etaient principalement retrouves chez des femmes (24/40, c’est-a-dire, 60 %), contrairement aux Ivoiriens (3/11) (27 %). De plus, la localisation predominante des cancers colorectaux MMR deficients etait differente entre les deux series : a Bruxelles, a droite (24/40, c’est-a-dire, 60 %), tandis qu’a Abidjan c’etait a gauche (10/11, c’est-a-dire, 91 %). A Bruxelles, on observait dans la plupart des cas (67,5 %), une perte d’expression de MLH1 et PMS2. A Abidjan il s’agissait plutot d’une perte d’expression de MSH2 et MSH6 (54,5 %). Conclusions Notre etude revele des differences dans la presentation du cancer colorectal MMR deficient entre deux regions geographiques, suggerant des differences dans l’epidemiologie et la biologie du cancer colorectal des Africains natifs.

Background and study aims Endoscopic full-thickness resection (EFTR) is used to achieve R0 resection in difficult situations and as a way to overcome the limitations of endoscopic submucosal dissection. Multiple techniques have been described but adequate tools are still under evaluation. In this study, we evaluated the safety and feasibility of non-exposed endoscopic full-thickness resection using a novel endoscopic suturing device. Materials and methods Full-thickness resections of gastric predetermined lesions were performed on five pigs using the Endomina platform. After creating virtual lesion > 20 mm, sutures were placed around it using this triangulation platform. After tightening the knots, the bulging lesion, internalized into the gastric lumen, was cut with a needle knife. Results R0 resections of large lesions (42 to 60 mm) were achieved in all cases. One perforation occurred and prompted us to improve the procedure by shortening the sutures for more maneuverability and reinforcing the suture line before section. Procedure duration dropped by 50 % between the first case and the fourth case. Histological analysis confirmed successful full-thickness resection of all resected specimens. Conclusion EFTR using this triangulation platform seems feasible for lesions > 20 mm. Additional possible improvements were identified to simplify the procedure before moving to human trials.

Objectives To evaluate the efficacy and safety of a 10-day quadruple therapy containing colloidal bismuth sub-citrate (CBS), esomeprazole (ESO), amoxicillin (AMO), and metronidazole (MET) for Helicobacter pylori (H. pylori) eradication in children. Methods Monocentric, open-label, prospective, single-arm clinical trial in children aged 6-17 years with H. pylori infection. The study was carried out on consecutive patients with upper gastrointestinal symptoms and H. pylori infection confirmed by histology and culture of gastric biopsies. The outcome was evaluated using a 13 C-urea breath test 8-10 weeks post-therapy. Adverse events and compliance were evaluated by daily journal and pill counting. Results A total of 36 children fulfilling the inclusion criteria were enrolled. Eight (22.2%) of them had a prior H. pylori eradication treatment. Thirteen (36.1%) patients were infected by a strain resistant to MET and 8 (22.2%) by a strain resistant to both MET and Clarithromycin (CLA). In the intention-to-treat population (ITT), eradication was achieved in 35/36 patients (95%CI: 85%-99%). Twenty-three children reported at least one adverse event (63.8%), mostly mild (nausea, vomiting, abdominal pain, diarrhea, dark stool, metallic taste, headache, and rash). The compliance rate was high, with 30 (83.3%) patients taking >90% of the treatment. Conclusion 10-day quadruple therapy containing CBS, ESO, AMO, and MET for H. pylori eradication in children is a safe and very effective solution, especially for previously treated patients and those infected with double resistant strains.

The liver ischemia-reperfusion (IR) injury that occurs consequently to hepatic resection performed in patients with metastases can lead to tumor relapse for not fully understood reasons. We assessed the effects of liver IR on tumor growth and the innate immune response in a mouse model of colorectal (CR) liver metastasis. Mice subjected to liver ischemia 2 days after intrasplenic injection of CR carcinoma cells displayed a higher metastatic load in the liver, correlating with Kupffer cells (KC) death through the activation of receptor-interating protein 3 kinase (RIPK3) and caspase-1 and a recruitment of monocytes. Interestingly, the immunoregulatory mediators, tumor necrosis factor-α (TNF-α) and heme oxygenase-1 (HO-1) were strongly upregulated in recruited monocytes and were also expressed in the surviving KC following IR. Using TNFflox/flox LysMcre/wt mice, we showed that TNF deficiency in macrophages and monocytes favors tumor progression after IR. The antitumor effect of myeloid cell-derived TNF involved direct tumor cell apoptosis and a reduced expression of immunosuppressive molecules such as transforming growth factor-β, interleukin (IL)-10, inducible nitric oxyde synthase (iNOS), IL-33 and HO-1. Conversely, a monocyte/macrophage-specific deficiency in HO-1 (HO-1flox/flox LysMcre/wt ) or the blockade of HO-1 function led to the control of tumor progression post-liver IR. Importantly, host cell RIPK3 deficiency maintains the KC number upon IR, inhibits the IR-induced innate cell recruitment, increases the TNF level, decreases the HO-1 level and suppresses the tumor outgrowth. In conclusion, tumor recurrence in host undergoing liver IR is associated with the death of antitumoral KC and the recruitment of monocytes endowed with immunosuppressive properties. In both of which HO-1 inhibition would reinforce their antitumoral activity., info:eu-repo/semantics/published

Undifferentiated carcinoma of the pancreas is an aggressive but rare tumor for which several other terms have been used to describe its histological appearance. In addition, as osteoclast-like giant cells may accompany undifferentiated carcinoma of the pancreas, the WHO Classification distinguishes undifferentiated carcinoma with osteoclast-like giant cells (UC-OGC) from plain undifferentiated carcinoma since there are a few histopathological and clinical differences. UC-OGC was initially thought to be associated with worse prognosis compared to invasive ductal pancreatic adenocarcinoma, since it is often unresectable at diagnosis and tends to recur rapidly even if completely resected. When true UC-OGGs are carefully dissected out from other anaplastic carcinomas, it becomes, however, clear that UC-OGCs do have more indolent behavior, especially the pure UC-OGCs. This mini-review summarizes the current knowledge on UC-OGC., SCOPUS: re.j, info:eu-repo/semantics/published

Background: Esophageal immature squamous metaplasia is poorly reported in the literature. This entity can, however, be misinterpreted as high grade dysplasia or invasive squamous cell carcinoma and hence represent a potential pitfall. Case presentation: Histopathological examination of a superficial esoophageal lesion removed by endoscopic submucosal dissection revealed a squamous cell carcinoma associated with immature squamous cell metaplasia arising from esophageal glands. Immunohistochemical stainings allowed to distinguish malignant from metaplastic cells.Conclusions: Immunohistochemistry for Ber-EP4 is helpful in making the distinction between esophageal squamous cell carcinoma and immature squamous metaplasia. This can avoid overstaging and overtreatment, especially in early esophageal cancer.

Intestinal/enteric heterotopia of the vulva is an extremely rare disease with only 3 cases described in the literature. We report here an unusual case of this disease occurring in a 26-year-old patient in a context of Crohn’s disease. To the best of our knowledge, such type of association has not been previously described. The potential origins of these lesions including metaplastic transformation, dysontogenetic changes, or epithelial colonic displacement/implantation are discussed.

Targeting immune checkpoint molecules has become a major new strategy in the treatment of several cancers. Indoleamine 2,3-dioxygenase (IDO)-inhibitors are a potential next-generation immunotherapy, currently investigated in multiple phase I-III trials. IDO is an intracellular immunosuppressive enzyme and its expression/ activity has been associated with worse prognosis in several cancers. The aim of this study was to investigate the expression pattern of IDO in colorectal cancer (CRC). In a cohort of 94 CRC patients, primary tumors (PTs) with corresponding tumor-draining lymph nodes (TDLNs, n = 93) and extranodal/distant metastases (n = 27) were retrospectively analyzed by immunohistochemical staining for IDO, CD8 and Foxp3. 45 MSS and 37 MSI-H tumors were selected to compare IDO expression, as these tumors are considered to have different immunogenicity. A highly consistent expression pattern of IDO was observed in the PT, TDLNs and metastases, indicating that immune resistance may be determined very early in the disease course. IDO was expressed both by tumoral cells and host endothelial cells and these expressions were highly correlated (p < 0.001). IDO expression was observed more frequently in the MSI-H subset compared with the MSS subset (43% vs 22% for tumoral expression (p = 0.042) and 38% vs 16% for endothelial expression (p = 0.021)). Endothelial IDO expression was demonstrated to be a negative prognostic marker for recurrence free survival independent of disease stage and DNA mismatch repair (MMR) status (HR 20.67, 95% CI: 3.05-139.94; p = 0.002). These findings indicate that endothelial IDO expression in primary CRC, in addition to the MMR profile, may be helpful in disease stratification., SCOPUS: ar.j, info:eu-repo/semantics/published

International guidelines made RAS (KRAS and NRAS) status a prerequisite for the use of anti-EGFR agents for metastatic colorectal cancer (CRC) patients. Daily, new data emerges on the theranostic and prognostic role of molecular biomarkers; this is a strong incentive for a validated, sensitive, and broadly available molecular screening test. Next-generation sequencing (NGS) has begun to supplant other technologies for genomic profiling. We report here our 2 years of clinical practice using NGS results to guide therapeutic decisions. The Ion Torrent AmpliSeq colon/lung cancer panel, which allows mutation detection in 22 cancer-related genes, was prospectively used in clinical practice (BELAC ISO 15189 accredited method). The DNA of 741 formalin-fixed paraffinembedded CRC tissues, including primary tumors and metastasis, was obtained from 14 different Belgian institutions and subjected to targeted NGS. Of the tumors tested, 98% (727) were successfully sequenced and 89% (650) harbored at least one mutation. KRAS, BRAF and NRAS mutations were found in 335 (46%), 78 (11%) and 32 (4%) samples, respectively. These mutation frequencies were consistent with those reported in public databases. Moreover, mutations and amplifications in potentially actionable genes were identified in 464 samples (64%), including mutations in PIK3CA (14%), ERBB2 (0.4%), AKT1 (0.6%), and MAP2K1 (0.1%), as well as amplifications of ERBB2 (0.3%) and EGFR (0.3%). The median turnaround time between reception of the sample in the laboratory and report release was 8 calendar days. Overall, the AmpliSeq colon/lung cancer panel was successfully applied in daily practice and provided reliable clinically relevant information for CRC patients., SCOPUS: ar.j, info:eu-repo/semantics/published

A 63-years-old man presented with a condylomatous hemicirconferential exophytic lesion of the anal canal. He had a history of anal squamous cell carcinoma, cT2N0M0, treated by radiochemotherapy and some recurrent condylomata treated by electrocoagulation. Given this background as well as the morbidity of an abdominoperineal amputation, a mucosectomy was performed. Histopathological examination demonstrated a squamous mucosa with papillary architecture, lined by a population of immature cells (Fig. 1). There was only little maturation. P16 immunohistochemistry remained negative. Ki-67 immunohistochemistry was positive essentially in the lower half of the epithelium, with some rare positive cells in the upper layers (Fig. 2). A diagnosis of papillary immature metaplasia of the anal canal was made.

Preoperative radiotherapy (RT) is a mainstay in the management of rectal cancer, a tumor characterized by desmoplastic stroma containing cancer-associated fibroblasts (CAF). Although CAFs are abundantly present, the effects of RT to CAF and its impact on cancer cells are unknown. We evaluated the damage responses of CAF to RT and investigated changes in colorectal cancer cell growth, transcriptome, metabolome, and kinome in response to paracrine signals emerging from irradiated CAF. RT to CAF induced DNA damage, p53 activation, cell-cycle arrest, and secretion of paracrine mediators, including insulin-like growth factor-1 (IGF1). Subsequently, RT-activated CAFs promoted survival of colorectal cancer cells, as well as a metabolic switch favoring glutamine consumption through IGF1 receptor (IGF1R) activation. RT followed by IGF1R neutralization in orthotopic colorectal cancer models reduced the number of mice with organ metastases. Activation of the downstream IGF1R mediator mTOR was significantly higher in matched (intrapatient) samples and in unmatched (interpatient) samples from rectal cancer patients after neoadjuvant chemoradiotherapy. Taken together, our data support the notion that paracrine IGF1/IGF1R signaling initiated by RT-activated CAF worsens colorectal cancer progression, establishing a preclinical rationale to target this activation loop to further improve clinical responses and patient survival. Significance: These findings reveal that paracrine IGF1/IGF1R signaling promotes colorectal cancer progression, establishing a preclinical rationale to target this activation loop. Cancer Res; 78(3); 659–70. ©2017 AACR.

SCOPUS: ar.j, info:eu-repo/semantics/published

Introduction Although endoscopic submucosal dissection (ESD) of gastrointestinal (GI) neuroendocrine tumor (NETs) is an increasingly performed minimally invasive technique allowing complete en-bloc resection of mucosal and submucosal lesions, efficacy and safety outcome is limited. The aim of this study is to review two European centers experience of endoscopic treatment of superficial GI NET by ESD. Methods Clinical and technical data of patients treated by ESD from two tertiary European centers were prospectively collected from October 2014 to February 2019. Complete resection (R0) was defined as clear lateral and vertical margins. Results Twenty-four ESDs of NET were performed in 22 patients (females 59%), mean age of 54.8 years. Fifteen NETs (66%) were removed from the stomach, 6 from the rectum (25%), 1 from the esophagus (4%) and 1 from the duodenum (4%). 87.5% of gastric NETs were associated with atrophic gastritis (86.6% of which of autoimmune etiology) and 56% with previous history of multiples NETs. En-bloc resection was achieved in all patients (100%). R0 resection rate was 75% (91.6% clear lateral and 79% clear vertical margins). Lymphovascular infiltration was seen in one case (4%). Median ESD duration time was 77 min (20–240). Two cases presented small perforations, treated conservatively by antibiotics and clip closure. The median specimen size was of 25 mm (12–50). Pathological examination showed 58.3% grade 1, 37.5% grade 2 and 4% grade 3 NETs. Sixteen lesions were characterized as pT1 (72.7%). Three patients were candidates for additional treatment: one had endoscopic mucosal resection for additional known lesions, one underwent surgery with oncological lymph node resection (finally pT2N1) and one refused systemic therapy. At the end of a median follow-up of 18 months, two cases of recurrence were identified: one was managed endoscopically, the second refused treatment. Conclusions Our series of ESD for selected GI NETs showed favorable results in term of efficacy and safety. However, further studies are needed to determine the role of ESD compared to other resection modalities.

In patients with rectal prolapse is the prevalence of colorectal cancer increased, suggesting that a colorectal tumor may induce rectal prolapse. Establishment of tumor xenografts in immunodeficient mice after orthotopic inoculations of human colorectal cancer cells into the caecal wall is a widely used approach for the study of human colorectal cancer progression and preclinical evaluation of therapeutics. Remarkably, 70% of young mice carrying a COLO320DM caecal tumor showed symptoms of intussusception of the large bowel associated with intestinal lumen obstruction and rectal prolapse. The quantity of the COLO320DM bioluminescent signal of the first three weeks post-inoculation predicts prolapse in young mice. Rectal prolapse was not observed in adult mice carrying a COLO320DM caecal tumor or young mice carrying a HT29 caecal tumor. In contrast to HT29 tumors, which showed local invasion and metastasis, COLO320DM tumors demonstrated a non-invasive tumor with pushing borders without presence of metastasis. In conclusion, rectal prolapse can be linked to a non-invasive, space-occupying COLO320DM tumor in the gastrointestinal tract of young immunodeficient mice. These data reveal a model that can clarify the association of patients showing rectal prolapse with colorectal cancer., SCOPUS: ar.j, info:eu-repo/semantics/published

Tumour Budding (TB) is recognized as an adverse prognostic factor in colorectal cancer (CRC). TB is the detachment of isolated cancer cells or small clusters of such cells mainly at the invasion front. One question that arises is of the role of the tumour stroma regarding the permissiveness of the formation and progression of TB. In this review, we will examine potential factors affecting TB, in particular we will analyse the potential effect of inflammation, hypoxia, extracellular matrix and Cancer-Associated Fibroblasts (CAFs).

According to European and American series, up to 20% of colorectal cancers are characterised by instability at microsatellites sites. MMR deficient colorectal cancers are predominantly found in the right colon. Although an increasing rate of colorectal cancer has been observed in many low-income countries including in West-Africa, data on epidemiology and biology of colorectal cancer in native Africans from this region are scarce.We aimed to study the incidence of MMR deficiency in Côte d'Ivoire and to compare the data with those from a tertiary center in Belgium. Immunohistochemistry for MLH1, MSH2, MSH6 and PMS2 was performed on paraffin-embedded tissue samples from 83 colorectal cancers (46% males) operated in Abidjan and from 343 colorectal cancers (53% males) from Brussels.Colorectal cancer was occuring at a younger age in Côte d'Ivoire compared to Belgium (median age: 53 versus 66). MMR deficiency was detected in 11,7% of Belgian cases and in 13,3% of Ivorian cases. Whereas MMR deficient cancers in Brussels were mainly found in women (24/40 i.e. 60%), in Abidjan only 3/11 (27%) were female. Moreover, the predominant location of MMR deficient tumours was different between both series: in Brussels, mainly located in the right colon (24/40 i.e. 60%) whereas in Abidjan predominantly (10/11 i.e. 91%) in the left colon. In Brussels we observed in the majority of cases (67,5%) loss of expression of MLH1 and PMS2, in Abidjan loss of expression of MSH2 and MSH6 (54,5%).Our pilot study reveals differences in presentation of MMR deficient colorectal cancer between the two geographic regions suggesting differences in epidemiology and biology of colorectal cancer in native Africans.