Predictors of Survival Without Intestinal Resection after First-Line Endovascular Revascularization in Patients with Acute Arterial Mesenteric Ischemia.

Background Acute arterial mesenteric ischemia requires emergency treatment and is associated with high mortality rate and poor quality of life. Identifying factors associated with survival without intestinal resection (hereafter, intestinal resection-free [IRF] survival) could help in treatment decision-making after first-line endovascular revascularization. Purpose To identify factors associated with 30-day IRF survival in patients with acute arterial mesenteric ischemia whose first-line treatment was endovascular revascularization. Materials and Methods Patients with acute arterial mesenteric ischemia whose first-line treatment was endovascular revascularization because of a low probability of bowel necrosis were included in this single-center retrospective cohort (May 2014 to August 2022). Patient demographics, laboratory values, clinical characteristics at admission, CT scans, angiograms, and endovascular revascularization-related variables were included. The primary end point was 30-day IRF survival, and secondary end points were 3-month, 1-year, and 3-year overall survival. Factors independently associated with 30-day IRF survival were identified with binary logistic regression. Results A total of 117 patients (median age, 70 years [IQR, 60-77]; 53 female, 64 male) were included. Within 30 days after revascularization, 73 of 117 patients (62%) survived without resection, 28 of 117 (24%) survived after resection, 14 of 117 (12%) died without resection, and two of 117 (2%) underwent resection but died. The 30-day IRF survival was 63% (74 of 117). The 3-month, 1-year, and 3-year mortality rate was 18% (21 of 117), 21% (25 of 117), and 27% (32 of 117), respectively. Independent predictors of 30-day IRF survival were persistent bowel enhancement at initial CT (odds ratio [OR], 0.3; 95% CI: 0.2, 0.8; P = .013) and C-reactive protein (CRP) level less than 100 mg/L (OR, 0.3; 95% CI: 0.1, 0.8; P = .002). The 30-day IRF survival was 86%, 61%, 47%, and 23% in patients with both favorable features, persistent bowel enhancement but CRP level greater than 100 mg/L, no bowel enhancement but CRP level less than 100 mg/L, and both unfavorable features, respectively. Conclusion Independent predictors associated with 30-day IRF survival in patients with acute arterial mesenteric ischemia whose first-line treatment was endovascular revascularization were persistent bowel wall enhancement at initial CT and CRP level less than 100 mg/L. © RSNA, 2024 Supplemental material is available for this article.

Successful rescue TNF-α blocking for Mycobacterium genavense - Related immune reconstitution inflammatory syndrome: A case report.

Immune reconstitution inflammatory syndrome (IRIS) has been reported in immunocompromised patients with disseminated Mycobacterium genavense. Management relies on high-dose corticosteroids. We describe two cases of late-onset corticosteroid-refractory IRIS related to disseminated infection in a HIV-positive patient and a renal transplant patient who had a favorable outcome with a monoclonal TNF-α blocker.

Pancytopenia related to acquired sea-blue histiocytosis during chronic parenteral nutrition.

Bone marrow smear showing histiocytes (black arrow) containing sea blue granules stained with May-Grünwald Giemsa.

Insights into acute mesenteric ischaemia: an up-to-date, evidence-based review from a mesenteric stroke centre unit.

Radiologists play a central role in the diagnostic and prognostic evaluation of patients with acute mesenteric ischaemia (AMI). Unfortunately, more than half of AMI patients undergo imaging with no prior suspicion of AMI, making identifying this disease even more difficult. A confirmed diagnosis of AMI is ideally made with dynamic contrast-enhanced CT but the diagnosis may be made on portal-venous phase images in appropriate clinical settings. AMI is diagnosed on CT based on the identification of vascular impairment and bowel ischaemic injury with no other cause. Moreover, radiologists must evaluate the probability of bowel necrosis, which will influence the treatment options.AMI is usually separated into different entities: arterial, venous, non-occlusive and ischaemic colitis. Arterial AMI can be occlusive or stenotic, the dominant causes being atherothrombosis, embolism and isolated superior mesenteric artery (SMA) dissection. The main finding in the bowel is decreased wall enhancement, and necrosis can be suspected when dilatation >25 mm is identified. Venous AMI is related to superior mesenteric vein (SMV) thrombosis as a result of a thrombophilic state (acquired or inherited), local injury (cancer, inflammation or trauma) or underlying SMV insufficiency. The dominant features in the bowel are hypoattenuating wall thickening with submucosal oedema. Decreased enhancement of the involved bowel suggests necrosis. Non-occlusive mesenteric ischaemia (NOMI) is related to impaired SMA flow following global hypoperfusion associated with low-flow states. There are numerous findings in the bowel characterised by diffuse extension. An absence of bowel enhancement and a thin bowel wall suggest necrosis in NOMI. Finally, ischaemic colitis is a sub-entity of arterial AMI and reflects localised colon ischaemia-reperfusion injury. The main CT finding is a thickened colon wall with fat stranding, which seems to be unrelated to SMA or inferior mesenteric artery lesions. A precise identification and description of vascular lesions, bowel involvement and features associated with transmural necrosis is needed to determine patient treatment and outcome.

Unexpected upper gastrointestinal polyps in patients with short bowel syndrome treated with teduglutide: need for close monitoring.

BACKGROUND: Teduglutide is a GLP-2 analog indicated for the treatment of short bowel syndrome (SBS) since 2015. Its efficacy in reducing parenteral nutrition (PN) has been shown in patients with SBS. OBJECTIVES: Because teduglutide is a trophic factor, the aim of this study was to assess risk of developing polypoid intestinal lesions during treatment. METHODS: A retrospective study was conducted in 35 patients with SBS treated with teduglutide for ≥1 y in a home PN expert center. All patients underwent ≥1 follow-up intestinal endoscopy during treatment. RESULTS: In the 35 patients, the small bowel length was 74 cm (IQR: 25-100), and 23 patients (66%) had a colon in continuity. Upper and lower gastrointestinal endoscopy was performed after a mean treatment duration of 23 mo (IQR: 13-27), and polypoid lesions were found in 10 patients (6 with a colon in continuity, 4 with an end jejunostomy) and no lesion in 25 patients. In 8 out of the 10 patients, the lesion was found in the small bowel. Five of these lesions presented an aspect of hyperplastic polyp without dysplasia, and 3 of a traditional adenoma with low-grade dysplasia. CONCLUSIONS: Our study highlights the importance of performing follow-up upper and lower gastrointestinal endoscopy in SBS patients treated with teduglutide and the potential need to make changes to the recommendations with respect to treatment initiation and follow-up.

Mismatch Repair Deficiency and Lynch Syndrome Among Adult Patients With Glioma.

PURPOSE: The Lynch syndrome (LS)-glioma association is poorly documented. As for mismatch repair deficiency (MMRd) in glioma, a hallmark of LS-associated tumors, there are only limited data available. We determined MMRd and LS prevalence in a large series of unselected gliomas, and explored the associated characteristics. Both have major implications in terms of treatment, screening, and prevention. METHODS: Somatic next-generation sequencing was performed on 1,225 treatment-naive adult gliomas referred between 2017 and June 2022. For gliomas with ≥1 MMR pathogenic variant (PV), MMR immunohistochemistry (IHC) was done. Gliomas with ≥1 PV and protein expression loss were considered MMRd. Eligible patients had germline testing. To further explore MMRd specifically in glioblastomas, isocitrate dehydrogenase (IDH)-wild type (wt), we performed IHC, and complementary sequencing when indicated, in a series of tumors diagnosed over the 2007-2021 period. RESULTS: Nine gliomas were MMRd (9/1,225; 0.73%). Age at glioma diagnosis was <50 years for all but one case. Eight were glioblastomas, IDH-wt, and one was an astrocytoma, IDH-mutant. ATRX (n = 5) and TP53 (n = 8) PV were common. There was no TERT promoter PV or EGFR amplification. LS prevalence was 5/1,225 (0.41%). One 77-year-old patient was a known LS case. Four cases had a novel LS diagnosis, with germline PV in MSH2 (n = 3) and MLH1 (n = 1). One additional patient had PMS2-associated constitutional mismatch repair deficiency. Germline testing was negative in three MSH6-deficient tumors. In the second series of glioblastomas, IDH-wt, MMRd prevalence was 12.5% in the <40-year age group, 2.6% in the 40-49 year age group, and 1.6% the ≥50 year age group. CONCLUSION: Screening for MMRd and LS should be systematic in glioblastomas, IDH-wt, diagnosed under age 50 years.

[Eosinophilic inflammation of the digestive tract]. / Inflammation à éosinophiles du tube digestif.

Eosinophilic inflammation of the digestive tract is an inflammatory disease characterized by extensive infiltration of eosinophils into the gastrointestinal tract. It can be either a primary disorder of the digestive tract or be secondary to another cause of tissue eosinophilia. Primary disorders include eosinophilic esophagitis (OE) and eosinophilic gastroenteritis (GEEo). These are 2 rare pathologies considered to be diseases related to a Th2-mediated food allergy. The role of the pathologist is twofold: (1) he must make the diagnosis of tissue esosinophilia and propose the various causes, knowing that a secondary cause is the most frequently observed; (2) identify the abnormal number of polymorphonuclear eosinophils, which implies knowing the normal distribution of eosinophils in the different digestive segments. To carry the diagnosis of EO, the threshold of polymorphonuclear eosinophils must be ≥ 15/fields × 400. There is no predefined threshold concerning the other segments of the digestive tract to carry the diagnosis of GEEO. In addition, to make the diagnosis of primary digestive tissue eosinophilia, the patient must be symptomatic with histological evidence of eosinophilia and have ruled out all secondary causes. The main differential diagnosis of OE is gastroesophageal reflux disease. The differential diagnoses of GEEo are multiple, including primarily drugs and parasitic infections.

Insights into the expanding intestinal phenotypic spectrum of SOCS1 haploinsufficiency and therapeutic options.

PURPOSE: Hyper activation of the JAK-STAT signaling underlies the pathophysiology of many human immune-mediated diseases. Herein, the study of 2 adult patients with SOCS1 haploinsufficiency illustrates the severe and pleomorphic consequences of its impaired regulation in the intestinal tract. METHODS: Two unrelated adult patients presented with gastrointestinal manifestations, one with Crohn's disease-like ileo-colic inflammation refractory to anti-TNF and the other with lymphocytic leiomyositis causing severe chronic intestinal pseudo-occlusion. Next-generation sequencing was used to identify the underlying monogenic defect. One patient received anti-IL-12/IL-23 treatment while the other received the JAK1 inhibitor, ruxolitinib. Peripheral blood, intestinal tissues, and serum samples were analyzed before-and-after JAK1 inhibitor therapy using mass cytometry, histology, transcriptomic, and Olink assay. RESULTS: Novel germline loss-of-function variants in SOCS1 were identified in both patients. The patient with Crohn-like disease achieved clinical remission with anti-IL-12/IL-23 treatment. In the second patient with lymphocytic leiomyositis, ruxolitinib induced rapid resolution of the obstructive symptoms, significant decrease of the CD8+ T lymphocyte muscular infiltrate, and normalization of serum and intestinal cytokines. Decreased frequencies of circulating Treg cells, MAIT cells, and NK cells, with altered CD56bright:CD16lo:CD16hi NK subtype ratios were not modified by ruxolitinib. CONCLUSION: SOCS1 haploinsufficiency can result in a broad spectrum of intestinal manifestations and need to be considered as differential diagnosis in cases of severe treatment-refractory enteropathies, including the rare condition of lymphocytic leiomyositis. This provides the rationale for genetic screening and considering JAK inhibitors in such cases.

Crohn-like Disease Affecting Small Bowel Due to Monogenic SLCO2A1 Mutations: First Cases of Chronic Enteropathy Associated with SLCO2A1 Gene [CEAS] in France.

INTRODUCTION: Multiple chronic ulcers of small intestine are mainly ascribed to Crohn's disease. Among possible differential diagnoses are chronic ulcers of small bowel caused by abnormal activation of the prostaglandin pathway either in the archetypal but uncommon non-steroidal anti-inflammatory drug [NSAID]-induced enteropathy, or in rare monogenic disorders due to PLA2G4A and SLCO2A1 mutations. SLCO2A1 variants are responsible for CEAS [chronic enteropathy associated with SLCO2A1], a syndrome which was exclusively reported in patients of Asian origin. Herein, we report the case of two French female siblings, P1 and P2, with CEAS. CASE REPORT: P1 underwent iterative bowel resections [removing 1 m of small bowel in total] for recurrent strictures and perforations. Her sister P2 had a tight duodenal stricture which required partial duodenectomy. Next-generation sequencing was performed on P1's DNA and identified two compound heterozygous variants in exon 12 in SLCO2A1, which were also present in P2. CONCLUSION: CEAS can be detected within the European population and raises the question of its incidence and recognition outside Asia. Presence of intractable recurrent ulcerations of the small intestine, mimicking Crohn's disease with concentric strictures, should motivate a genetic search for SLCO2A1 mutations, particularly in the context of family history or consanguinity.

Hepatic venous pressure gradient in sinusoidal obstruction syndrome: diagnostic value and link with histological lesions.

Background & Aims: Liver sinusoidal obstruction syndrome (SOS) is a well-established complication of myeloablative conditioning regimens used in hematopoietic stem cell transplantation. Hepatic venous pressure gradient (HVPG) >10 mmHg was described as an accurate diagnostic tool for SOS in the 1990s. However, epidemiology and presentation of SOS have dramatically changed. Moreover, elementary histological lesions influencing HVPG are unknown. Methods: We retrospectively analyzed the charts of all patients who underwent transjugular liver biopsy with HVPG measurement for a clinical suspicion of SOS at our center. Two expert pathologists unaware of the presence or absence of SOS reviewed all liver samples and graded elementary histological lesions according to a semi-quantitative scoring defined a priori. Results: Out of the 77 included patients, the 30 patients with SOS had higher HVPG than the 47 patients without SOS (median 14 mmHg [IQR 10-18], vs. 6 mmHg [3-9], respectively p <0.001). HVPG >10 mmHg had a specificity of 78% and a positive predictive value of 66% for the diagnosis of SOS. However, almost 40% of the patients with SOS had an HVPG ≤10 mmHg. HVPG correlated with sinusoidal congestion (r = 0.57; p = 0.001) and hepatocyte necrosis (r = 0.42; p = 0.02), but not with other lesions. Conclusion: Even though HVPG is higher in patients with SOS, low HVPG values do not rule out SOS. Thus, HVPG cannot be used alone, and should be combined with transjugular liver biopsy, for the diagnosis of SOS. Lay summary: Hepatic venous pressure gradient >10 mmHg has been described as an accurate tool for the diagnosis of liver sinusoidal obstruction syndrome after hematopoietic stem cell transplantation. This study shows that the sensitivity and specificity of hepatic venous pressure gradient measurement for sinusoidal obstruction syndrome are insufficient, so that liver pressure measurement should be combined with a liver biopsy in this setting.

A Preclinical Validation of Iron Oxide Nanoparticles for Treatment of Perianal Fistulizing Crohn's Disease.

Fistulizing anoperineal lesions are severe complications of Crohn's disease (CD) that affect quality of life with a long-term risk of anal sphincter destruction, incontinence, permanent stoma, and anal cancer. Despite several surgical procedures, they relapse in about two-thirds of patients, mandating innovative treatments. Ultrasmall particles of iron oxide (USPIO) have been described to achieve in vivo rapid healing of deep wounds in the skin and liver of rats thanks to their nanobridging capability that could be adapted to fistula treatment. Our main purpose was to highlight preclinical data with USPIO for the treatment of perianal fistulizing CD. Twenty male Sprague Dawley rats with severe 2,4,6-trinitrobenzenesulfonic acid solution (TNBS)-induced proctitis were operated to generate two perianal fistulas per rat. At day 35, two inflammatory fistulas were obtained per rat and perineal magnetic resonance imaging (MRI) was performed. After a baseline MRI, a fistula tract was randomly drawn and topically treated either with saline or with USPIO for 1 min (n = 17 for each). The rats underwent a perineal MRI on postoperative days (POD) 1, 4, and 7 and were sacrificed for pathological examination. The primary outcome was the filling or closure of the fistula tract, including the external or internal openings. USPIO treatment allowed the closure and/or filling of all the treated fistulas from its application until POD 7 in comparison with the control fistulas (23%). The treatment with USPIO was safe, permanently closed the fistula along its entire length, including internal and external orifices, and paved new avenues for the treatment of perianal fistulizing Crohn's disease.

Magnetic Resonance Enterography and Histology in Patients With Fibrostenotic Crohn's Disease: A Multicenter Study.

INTRODUCTION: Magnetic resonance enterography (MRE) is useful for detecting bowel strictures, whereas a number of imaging biomarkers may reflect severity of fibrosis burden in Crohn's disease (CD). This study aimed to verify the association of MRE metrics with histologic fibrosis independent of inflammation. METHODS: This prospective European multicenter study performed MRE imaging on 60 patients with CD with bowel strictures before surgical resection. Locations of 61 histological samples were annotated on MRE examinations, followed by central readings using the Chiorean score and measurement of delayed gain of enhancement (DGE), magnetization transfer ratio, T2-weighted MRI sequences (T2R), apparent diffusion coefficient (ADC), and the magnetic resonance index of activity (MaRIA). Correlations of histology and MRE metrics were assessed. Least Absolute Shrinkage and Selection Operator and receiver operator characteristic (ROC) curve analyses were used to select composite MRE scores predictive of histology and to estimate their predictive value. RESULTS: ADC and MaRIA correlated with fibrosis (R = -0.71, P < 0.0001, and 0.59, P < 0.001) and more moderately with inflammation (R = -0.35, P < 0.01, and R = 0.53, P < 0.001). Lower or no correlations of fibrosis or inflammation were found with DGE, magnetization transfer ratio, or T2R. Least Absolute Shrinkage and Selection Operator and ROC identified a composite score of MaRIA, ADC, and DGE as a very good predictor of histologic fibrosis (ROC area under the curve = 0.910). MaRIA alone was the best predictor of histologic inflammation with excellent performance in identifying active histologic inflammation (ROC area under the curve = 0.966). DISCUSSION: MRE-based scores for histologic fibrosis and inflammation may assist in the characterization of CD stenosis and enable development of fibrosis-targeted therapies and clinical treatment of stenotic patients.

Identification of Gene Expression Profiles Associated with an Increased Risk of Post-Operative Recurrence in Crohn's Disease.

BACKGROUND AND AIMS: Ileocolonic resection is frequently needed in the course of Crohn's disease [CD] treatment and post-operative recurrence is extremely common. Our main objective was to analyse gene expression in the mucosa of CD patients at the time of surgery and at post-operative endoscopy, in order to identify predictors and mechanisms of early endoscopic recurrence. METHODS: We conducted transcriptome analyses on ileal mucosa samples collected from inflamed sections of the surgical specimens [n = 200], from ileal resection margins [n = 149] and in the neo-terminal ileum 6 months after surgery [n = 122]; these were compared with non-inflammatory bowel disease controls [n = 25]. The primary endpoint was post-operative endoscopic recurrence at 6 months. We applied regression models to identify gene signatures predicting endoscopic recurrence. RESULTS: Chronic inflammation was associated with strong expression of inflammatory genes [IL-6, IL-8, IL-1B] and decreased expression of genes involved in metabolic processes, but with a high inter-individual heterogeneity. Gene signatures associated with early endoscopic recurrence were mainly characterized by upregulation of TNFα, IFNγ, IL23A and IL17A. Pathway analyses showed that upregulation of mitochondrial dysfunction within the inflamed sections and JAK/STAT at the ileal margin were predictive of post-operative recurrence. A combined model integrating these top pathway signatures improved the prediction of endoscopic recurrence [area under the curve of 0.79]. STAT3 phosphorylation at the surgical ileal margin was associated with severe recurrence at 6 months. CONCLUSION: We identified several biological pathways in surgical ileal mucosa specimens associated with an increased risk of disease recurrence. Integration of the JAK/STAT and mitochondrial dysfunction pathways in the clinical model improved the prediction of post-operative recurrence.

Colonic involvement in acute mesenteric ischemia: prevalence, risk factors, and outcomes.

OBJECTIVES: This study aimed to investigate the prevalence, risk factors, and outcomes of colonic involvement in patients with acute mesenteric ischemia (AMI). METHODS: CT scans from a prospective cohort of 114 AMI patients treated in an intestinal stroke center between 2009 and 2018 were blindly reviewed by two radiologists. Colon involvement was defined on CT scan by the presence of at least one of the following CT colonic features: wall thickening, pneumatosis, decreased wall enhancement, dilatation, or perforation. In addition, the clinical, biological, and radiological characteristics of patients with and without colonic involvement were compared to identify risk factors for colonic involvement on CT and its impact on morbidity and mortality. RESULTS: Colonic involvement was identified in 32/114 (28%) patients with AMI, the right colon being more frequently involved (n = 29/32, 91%). Wall thickening (n = 27/32) was the most common CT finding. Occlusion of the inferior mesenteric artery was the only statistically significant risk factor for colonic involvement (35% vs. 15%, p = 0.02). Patients with colonic involvement on CT vs. those without had more frequently transmural colonic necrosis (13% vs. 0%, p = 0.006), short bowel syndrome (16% vs. 4%, p = 0.04), need for long-term parenteral support (19% vs. 5%, p = 0.03), and death during follow-up (22% vs. 10%, p = 0.03). DISCUSSION: In patients with AMI, colonic involvement is associated with increased morbidity and mortality and should be carefully searched for during initial CT scan assessment. KEY POINTS: • In a prospective cohort of acute mesenteric ischemia patients from an intestinal stroke center, 28% had an associated colonic involvement on CT. • Colonic involvement on CT most commonly affected the right colon, and the occlusion of the inferior mesenteric artery was the only risk factor. • Colonic involvement on CT was associated with increased morbidity and mortality and should be carefully searched for during initial CT scan assessment.

A novel SMARCA2-CREM fusion: expanding the molecular spectrum of intracranial mesenchymal tumors beyond the FET genes.

A novel histomolecular tumor of the central nervous system, the "intracranial mesenchymal tumor (IMT), FET-CREB fusion-positive" has recently been identified in the literature and will be added to the 2021 World Health Organization Classification of Tumors of the Central Nervous System. However, our latest study using DNA-methylation analyses has revealed that intracranial FET-CREB fused tumors do not represent a single molecular tumor entity. Among them, the main subgroup presented classical features of angiomatoid fibrous histiocytoma, having ultrastructural features of arachnoidal cells, for. Another tumor type with clear cell component and histopathological signs of aggressivity clustered in close vicinity with clear cell sarcoma of soft tissue. Herein, we report one case of IMT with a novel SMARCA2-CREM fusion which has until now never been described in soft tissue or the central nervous system. We compare its clinical, histopathological, immunophenotypic, genetic and epigenetic features with those previously described in IMT, FET-CREB fusion-positive. Interestingly, the current case did not cluster with IMT, FET-CREB fusion-positive but rather presented histopathological (clear cell morphology with signs of malignancy), clinical (with a dismal course with several recurrences, metastases and finally the patient's death), genetic (fusion implicating the CREM gene), and epigenetic (DNA-methylation profiling) similarities with our previously reported clear cell sarcoma-like tumor of the central nervous system. Our results added data suggesting that different clinical and histomolecular tumor subtypes or grades seem to be included within the terminology "IMT, FET-CREB fusion-positive", and that further series of cases are needed to better characterize them.

Smooth muscular layer: A new helpful criterion to reclassify tumor deposits into metastatic lymph nodes in patients with colo-rectal adenocarcinoma.

CONTEXT: The origin of tumor deposit in colorectal cancer is still unknown, and currently there is no single morphological feature to distinguish a metastatic lymph node from a tumor deposit. Histologically, the normal lymph node capsule and trabeculae contain a smooth muscular layer, which when present in extramural deposits would strongly suggest their lymph node origin. OBJECTIVE: We analyze the value of the smooth muscular layer criterion in reclassifying tumor deposit into metastatic lymph node. DESIGN: A total of 458 colo-rectal carcinomas surgical specimens treated or not by neoadjuvant (radio)chemotherapy were retrospectively included. Harvested tumor deposits were analyzed by Hematoxylin and Eosin and elastin staining on 10 consecutive serial sections and by α- smooth muscle actin immunostaining. RESULTS: A total of 129 tumor deposits were identified. 77 (60%) tumor deposits were reclassified into metastatic lymph node, of which 63 (49%) presented a smooth muscular layer on the initial Hematein Eosin staining and/or after serial tissue sections, confirmed by positive α-smooth muscle actin immunostaining in 43 out of 45 cases (90%). Fourteen (18%) additional tumor deposits were reclassified into metastatic lymph node by the appearance of lymphoid tissue after serial sections. CONCLUSIONS: The presence of a smooth muscular layer in a presumable tumor deposit is helpful in pointing out its lymph node origin in patients with colo-rectal carcinomas. This criterion could improve the inter-observer agreement of tumor deposit identification, allowing accurate nodal staging and better assessment of patient's prognosis.