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The optimal fecal occult blood test (FOBT) and hemoglobin (Hb) threshold for balancing diagnostic accuracy and endoscopic demand in colorectal cancer (CRC) screening among Chinese outpatients remained unclear. A prospective multicenter trial was conducted from January 2017 to April 2021 across eight tertiary hospitals. Eligible outpatients were enrolled, whose stool samples were analyzed using quantitative fecal immunochemical test (FIT), self-administered qualitative FIT, general qualitative FIT, and gFOBT. All participants underwent colonoscopy. The primary outcome was the sensitivity of FOBTs for CRC detection. A total of 2,930 participants were enrolled, with 2,618 participants meeting inclusion criteria and completing FOBTs and colonoscopies. At the threshold of 5.2&#xa0;&#xb5;g/g, quantitative FIT demonstrated comparable sensitivity for CRC detection (90.1%) to self-administered qualitative FIT (87.1%), general qualitative FIT (91.1%), and gFOBT (82.2%) (all P&#x2009;>&#x2009;0.05). The positive rate of quantitative FIT (12.4%) was significantly lower than that of self-administered qualitative FIT (27.5%), general qualitative FIT (24.2%), and gFOBT (23.0%) (all P&#x2009;<&#x2009;0.05). Quantitative FIT showed superior specificity (93.9%) compared to self-administered qualitative FIT (79.5%), general qualitative FIT (83.6%), and gFOBT (80.7%) (all P&#x2009;<&#x2009;0.05). Furthermore, quantitative FIT at 5.2&#xa0;&#xb5;g/g exhibited higher PPV and LR&#x2009;+&#x2009;for CRC, advanced adenoma (AA) and advanced neoplasia (AN) than other FOBTs. Receiver operating characteristic (ROC) analysis and area under the curve (AUC) revealed excellent accuracy for CRC detection (AUC: 0.951, 95% CI: 0.920-0.981). The quantitative FIT with a threshold of 5.2&#xa0;&#xb5;g/g demonstrated superior performance for early CRC screening in Chinese outpatients.

Blood-based circulating tumour DNA (ctDNA) assays have emerged as a promising tool for minimally invasive colorectal cancer (CRC) screening. However, their diagnostic accuracy in asymptomatic, average-risk populations remains uncertain. This systematic review and meta-analysis aimed to synthesise current evidence on the performance of ctDNA-based blood tests for detecting advanced colorectal neoplasia (ACN), defined as the composite of invasive CRC and advanced precancerous lesions (APL). A comprehensive search of PubMed, EMBASE, and the Cochrane Library was conducted through July 2025. Studies evaluating ctDNA-based blood assays against colonoscopy and histopathology in asymptomatic, average-risk adults were included. Pooled estimates were calculated using a bivariate random-effects model following Cochrane DTA guidance. Three population-based prospective studies were included (n&#x202f;=&#x202f;36,381). For invasive CRC, pooled sensitivity was 0.72 (95% CI 0.49-0.88) and specificity 0.91 (95% CI 0.89-0.92), with an area under the curve (AUC) of 0.92. Sensitivity increased progressively from stage I (0.53) to stage IV (0.89). For APL, pooled sensitivity was 0.13 (95% CI 0.12-0.14) and specificity 0.90 (95% CI 0.88-0.91). When CRC and APL were considered together (ACN), overall sensitivity was 0.16 (95% CI 0.14-0.18) with specificity 0.91 (95% CI 0.89-0.92). ctDNA-based blood testing demonstrates high specificity and clinically relevant accuracy for invasive CRC, but limited detection of precancerous lesions. These findings consolidate current evidence by defining the complementary role of ctDNA in population screening. As a non-invasive, patient-centred approach, ctDNA testing could increase participation and access in CRC prevention, but large-scale studies are needed to confirm its clinical and economic viability.

Reliable blood-based biomarkers for distinguishing invasive cervical cancer (ICC) from cervical intraepithelial neoplasia (CIN) remain limited. Placenta-specific protein 1 (PLAC1), a protein normally restricted to placental tissue, has been implicated in tumorigenesis. This prospective observational study enrolled 213 women who underwent colposcopy and biopsy at our hospital between January 2022 and February 2025. Participants were classified as CIN or ICC based on histopathology. Peripheral venous blood samples were collected before any cervical lesion-related treatment, and serum PLAC1 levels were measured using enzyme-linked immunosorbent assay. A total of 122 patients with CIN and 91 patients with ICC were included. HPV16/18 positivity was notably higher in ICC than in CIN. Serum PLAC1 levels were significantly higher in patients with CIN2-3 than in those with CIN1 and were further elevated in patients with ICC. SCC-Ag levels were also significantly higher in ICC than in CIN, whereas CEA and CA125 showed no meaningful differences between groups. Among patients with ICC, serum PLAC1 levels also increased across microinvasive, locally invasive, and advanced-stage subgroups. ROC curve analysis showed that PLAC1 had diagnostic value for distinguishing ICC from CIN, with an AUC of 0.815, a sensitivity of 73.6%, and a specificity of 70.5%. Multivariable analysis further showed that serum PLAC1 remained independently associated with ICC after adjustment for clinical variables. These findings indicate that serum PLAC1 is elevated in ICC and has potential value as a blood-based biomarker for differentiating malignant cervical disease from precancerous lesions, although further validation in larger cohorts is needed. The online version contains supplementary material available at 10.1007/s10616-026-00938-4.

Hereditary leiomyomatosis and renal cell carcinoma is a rare genetic disorder characterized by a predisposition to the development of multiple cutaneous and uterinne leiomyomas with a potential for malignant transformation and a risk of renal carcinoma. A 39-year-old woman suffered from this disease underwent hysterectomy due to uterus myomatosus. Histologically, some tumors showed typical appearance of fumarate hydratase-deficient leiomyomas. There were foci of adenomyosis in the myometrium. As an incidental finding, multiple thin-walled blood vessels filled with conglomerates of endometrial stroma and glandular epithelium were found in the myometrium and leiomyoma. At the first look, this feature suggested an intravascular cancer propagation. However, this endometrial tissue showed bland appearance with no atypia or mitoses and revealed low proliferative activity. Even after extensive sampling of the uterus, no malignant neoplasia was revealed. The finding was reported as intravascular form of adenomyosis. A propagation of adenomyosis within the uterine blood vessels is a rare histological finding causing diagnostic difficulties as it resembles intravascular spreading of malignant neoplasm. Although this is not a tumor entity, it represents an important differential diagnosis in the oncopathological practice. The pathologist's knowledge about this phenomenon is crucial to avoid confusion with vascular dissemination of malignancy.

Hypercalcemia is a common clinical manifestation of Multiple Endocrine Neoplasia 2A (MEN 2A) through primary hyperparathyroidism.The objective of this report is to describe a rare and unique case of sarcoidosis-related hypercalcemia in a patient with a history of MEN2A. A 59-year-old female with past medical history of MEN2A, REarranged during Transfection mutation C609Y, diagnosed in 2007 status post-total thyroidectomy presented to the hospital with an acute abdominal pain aggravated with eating. Review of systems was significant for a 40 lbs. weight loss, fatigue, dry mouth, and polydipsia. Computed tomography (CT) abdomen showed liver and spleen nodules and a few mildly enlarged retroperitoneal lymph nodes. CT chest noted enlarged left axillary lymph nodes but otherwise no enlarged mediastinal lymph nodes. Blood work showed a calcium level of 13.6 [8.5-10.3 mg/dl], intact parathyroid hormone: 6.3 [10-65 pg/mL], 25-OH vitamin D level: 21.5 [18-50 ng/mL], 1,25-vitamin D: 51 [18-64 pg/mL]. Liver biopsy showed noncaseating granuloma. Positron emission tomography-computed tomography showed hypodense splenic nodules, heterogenous liver, diffuse pancreatic atrophy, and lack of abnormal neck/lung adenopathy. The patient was then referred to rheumatology for evaluation for sarcoidosis. Angiotensin-converting enzyme level was 124. Patient was managed acutely with calcitonin and was started on prednisone and hydroxychloroquine. Calcium level normalized. The co-occurrence of both MEN 2A and sarcoidosis is rare, adding an unexpected layer of complexity to the diagnosis. The rarity of sarcoidosis co-occurring with MEN 2A highlights the importance of considering a broad differential diagnosis, even in patients with known genetic syndromes, to ensure accurate management.

Myelodysplastic neoplasia (MDS) comprises heterogeneous clonal hematologic disorders characterized by peripheral cytopenia, bone marrow dysplasia, and a risk of leukemic transformation. A hypoplastic variant (MDS-h) shares features with aplastic anemia and responds to immunosuppressive therapy (IST). We report three low-risk MDS-h cases treated with IST and monitored over 9-17&#x2009;years using serial cytogenetic and molecular analyses. All patients achieved transfusion independence after IST, and two experienced durable, long-term remissions. One patient developed late clonal evolution culminating in secondary acute myeloid leukemia. Molecular follow-up revealed diverse mutational dynamics, including stable and fluctuating clones and delayed mutational emergence, detectable in peripheral blood. These findings suggest that in MDS-h, disease activity is largely driven by immune dysregulation rather than early molecular changes, and that repeated IST can yield sustained remissions. However, accumulating mutations may eventually predict malignant transformation, underscoring the importance of long-term molecular monitoring.

Xeroderma pigmentosum (XP) is a rare autosomal recessive congenital syndrome characterized by defective nucleotide excision repair (NER), leading to extreme photosensitivity and a strong predisposition to skin cancer. One of the 8 complementation groups, XP complementation group C (XP-C), is defective specifically in the global genome component of NER and presents not only with increased skin cancer but also with hematologic cancers. Using error-corrected single-molecule sequencing, we show a uniquely high spontaneous somatic mutational load in peripheral blood mononuclear cells (PBMCs) of patients with XP-C but not in those of patients from other XP complementation groups (XP-A, XP-D, and XP-F). The hypermutability observed in XP-C was markedly lower in fibroblasts than in PBMCs. The XP-C mutational profile was characterized by elevated single-nucleotide variants (SNVs) associated with mutational signatures SBS5, SBS8, and SBS32, as well as an enrichment of single-nucleotide cytosine deletions, with SNV profiles closely mirroring those found in XP-C leukemias. These findings indicate that a cancer-like mutation burden is already present in normal lymphocytes before malignant transformation, revealing distinct molecular subtypes within XP defined by spontaneous mutational load in normal blood cells.

Outside organised colorectal cancer (CRC) screening programmes, faecal occult blood testing helps general practitioners decide whether to refer symptomatic patients for a colonoscopy. In France, practices vary widely, have not been evaluated, and are based on several qualitative and quantitative faecal immunochemical tests (FITs) with very different performance characteristics that clinicians do not appreciate. In the United Kingdom, this practice is generally based on two recommended automated quantitative FITs and usually follows very specific recommendations. Quantitative FITs have been extensively evaluated and have demonstrated their superiority, both in organised CRC screening programmes and in the investigation of symptomatic patients, albeit with different decision thresholds. In a symptomatic patient, the threshold of 10&#xa0;&#x3bc;g haemoglobin/gram of faeces (&#x3bc;g/g) from the English guidelines is not applicable in France. We suggest a threshold of 2&#xa0;&#x3bc;g/g, offering a sensitivity of 94.7&#xa0;% for the diagnosis of CRC, which must be confirmed by further studies in the French symptomatic population. The advantages of quantitative faecal immunochemical tests (FIT) are such that they will gradually replace qualitative FITs: self-collection, a single sample, at most two, lower cost, control of the pre-analytical phase, automation, a significant reduction in equivocal and uninterpretable results, control of the positivity threshold, information on the degree of urgency of colonoscopy, better analytical and clinical performance, and better cost-effectiveness ratio. It is urgent that the French National Authority for Health (HAS) draw up recommendations and a framework for use in symptomatic patients and update the nomenclature of medical biology procedures.

Objective. Multiple endocrine neoplasia type 1 (MEN1) is a very rare genetic disorder characterized by an autosomal dominant inheritance. We aim through this case series to delineate the wide spectrum of its clinical features. Methods. In the present study, we report the clinical and genetic findings of four siblings affected by this disorder. DNA was extracted from patients' blood leukocytes using a phenol-chloroform method and assessed for purity with a NanoDrop spectrophotometer. Ten exons of the MEN1 gene were amplified by PCR, verified by gel electrophoresis, and sequenced using Big Dye Terminator chemistry followed by capillary electrophoresis. The sequences were than analyzed with CHROMAS and compared to reference sequences. As for the variant, interpretation and pathogenicity were assessed using Ensembl, ClinVar, dbSNP, gnomAD, Alamut Visual, and VARSOME. Results. We highlight the wide range of phenotypes encompassing primary hyperparathyroidism, macroprolactinoma, lipomas, papillary thyroid carcinoma, ectopic thyroid, multinodular goiter, and bilateral adrenal nodules observed in this family contrasting with the same pathogenic frameshift mutation. We also pinpoint to a second mutation detected in two of the siblings while discussing its pathogenicity. Finally, we provide an overview of the clinical manifestations of MEN1 and its genetic background. Conclusion. This research sets the stage to further investigate the molecular mechanisms underlying the novel nonsense mutation. Additionally, it incites other research to explore the frequency of this mutation in other populations and finally to conduct functional studies.

Colorectal cancer (CRC) remains one of the most important causes of cancer-related mortality worldwide, underscoring the need to better understand systemic inflammatory pathways across the colorectal neoplasia spectrum. In this exploratory case-control study, we characterized plasma levels of key inflammatory mediators in healthy individuals and patients with colorectal polyps or CRC. Healthy controls (n = 10), patients with colorectal polyps (CP, n = 16), early-onset CRC (EO-CRC, n = 11), and late-onset CRC (LO-CRC, n = 51) were prospectively enrolled. Plasma levels of sTNF-R, total TNF-&#x3b1;, PDGF-AA, IL-17A, and IL-1&#x3b2; were measured by ELISA. Group comparisons used Kruskal-Wallis tests with epsilon-squared effect sizes. PDGF-AA showed the strongest differences between controls and all neoplastic groups (&#x3b5;2 &#x2265; 0.15), and these comparisons remained significant after Benjamini-Hochberg false discovery rate correction. IL-17A levels were slightly higher in EO-CRC than in LO-CRC; however, this difference did not remain significant after adjustment for multiple testing. TNF-&#x3b1; and IL-1&#x3b2; showed no significant differences across groups. Overall, this study primarily provides descriptive and hypothesis-generating evidence of differential inflammatory patterns across colorectal neoplasia, with PDGF-AA emerging as the most robust signal in this exploratory dataset. These findings do not support immediate diagnostic application and require validation in larger, prospectively recruited cohorts.

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T-cell lymphoblastic lymphoma (T-LBL) and T-cell acute lymphoblastic leukemia (T-ALL) originate from thymic T-cell precursors, with ongoing debate on whether they are variants of the same disease or distinct entities. For 211 patients, including pediatric and adult T-ALL and T-LBL cases, targeted next-generation sequencing and SNP-arrays were performed, and single-nucleotide variants, indels and copy-number variants (CNVs) were analyzed. We aimed to assess genetic differences between T-ALL and T-LBL across age. Generally, mutational landscape analysis identified mutated PHF6 being associated with higher, NOTCH1 with lower age at diagnosis for both T-LBL and T-ALL. Association of CNVs with higher age was evident for T-ALL, but not T-LBL. Analysis of clonal evolution revealed that CNVs - especially deletions and LOH in chromosome 9 (LOH_in_9p) - were observed as first mutational event in both pediatric T-ALL and T-LBL. The sequence of genetic events, starting with LOH_in_9p followed by mutations in NOTCH1, was significantly more frequent in pediatric T-ALL and T-LBL. Detailed evaluation of the patients' individual clonal evolution indicated that the proportion of malignant cells without NOTCHMT determines the risk of relapse (hazard ratio 1.032, p&#x2009;=&#x2009;4.65*10-5). In T-ALL, aside from MRD, validated molecular markers for risk-group stratification remain limited. Our data suggest that molecular metrics analogous to those in T-LBL may help refining risk stratification in T-ALL as well.

Patients with polycythaemia vera are at a higher risk for thrombotic events, which may occur at any time before diagnosis, at diagnosis or later during the disease. Besides an increased haematocrit, thrombocytosis may be an early marker of polycythaemia vera. Our study aimed to analyse the frequency of thromboembolic events and the presence of thrombocytosis/erythrocytosis preceding the diagnosis of polycythaemia vera. This monocentric, retrospective study included patients diagnosed with polycythaemia vera, aged 18 years or over, seen at our institution between January 2008 and December 2018. Baseline demographics, polycythaemia vera diagnosis information, comorbidities, presence and type of thromboembolic events, and blood counts before thromboembolic events and polycythaemia vera diagnosis were analysed. A total of 79 eligible patients were included. There was a slight male predominance (57%) with a median age at polycythaemia vera diagnosis of 69 years. Fifty-two patients (66%) had a thromboembolic event (24 before or concomitant with polycythaemia vera diagnosis, 11 after polycythaemia vera diagnosis and 17 both before and after polycythaemia vera diagnosis). Overall, 40 patients experienced arterial thrombotic events and 31 experienced venous thrombotic events. For the 41 patients with thromboembolic events before or concomitant to the polycythaemia vera diagnosis, the median platelet count at the time of the thromboembolic event was 365&#xd7;109/l before and 479&#xd7;109/l at polycythaemia vera diagnosis; the median leukocyte count was 11.2&#xd7;109/l and 11.5&#xd7;109/l, respectively; haemoglobin (haematocrit) level was 168 g/l (50%) and 179 g/l (53%), respectively. We had access to 90 blood counts performed before polycythaemia vera diagnosis in 17 patients with a thromboembolic event prior or concomitant with the polycythaemia vera diagnosis. For these patients, the median time from the first blood count showing platelets >350&#xd7;109/l or >450&#xd7;109/l to the diagnosis of polycythaemia vera was 36 months and 24 months, respectively. Four patients had a thromboembolic event prior to polycythaemia vera diagnosis with a normal platelet count. In these four patients, the median delay between the thromboembolic event and the polycythaemia vera diagnosis was 32 months. For the remaining 13 patients, the median time from the first blood count with platelets >350&#xd7;109/l or >450&#xd7;109/l and the thromboembolic event was 46 months and 10 months, respectively. The median time from the earliest available blood count showing Hb >16.5&#x2009;g/dl (Hct >49%) for men or Hb&#x2009;>16.0&#x2009;g/dl (Hct >48%) for women to the diagnosis of polycythaemia vera was 25 months and 24 months, respectively, and to the thromboembolic event was 12 months and 13 months, respectively. Our study shows that both thrombocytosis and/or erythrocytosis are frequently present months and even years before the diagnosis of polycythaemia vera. In addition, the occurrence of a thrombotic event may be the earliest indicator of polycythaemia vera, particularly with thrombocytosis >350&#xd7;109/l. The presence of thrombocytosis and/or erythrocytosis, even moderate, in the absence of a secondary cause, should evoke suspicion of a myeloproliferative neoplasia, including polycythaemia vera.

The reliance on LI-RADS 5 imaging criteria for the non-invasive diagnosis of hepatocellular carcinoma (HCC) can be precarious in the setting of advanced liver fibrosis, where benign inflammatory mimics may exhibit deceptive vascular kinetics. Hepatic xanthogranulomatous inflammation (XGI) represents a rare but significant diagnostic pitfall, as it can strictly simulate the arterial phase hyperenhancement and subsequent washout characteristic of malignancy. This diagnostic ambiguity is exacerbated in diabetic patients by"diabetic immunoparesis"which masks localized infection through a deceptive absence of systemic leukocytosis. This study highlights a novel diagnostic signature, termed "WBC-HBP Dissociation"utilizing Heparin-Binding Protein (HBP) to unveil occult neutrophil activation otherwise obscured by normocytosis. A 50-year-old male with chronic hepatitis B and biopsy-confirmed advanced fibrosis (LSM: 11.6 kPa) presented with a solitary, hypervascular liver mass. Despite uncontrolled Type 2 Diabetes (HbA1c: 12.00%) and a broad panel of negative tumor markers (AFP, PIVKA-II, CEA, CA19-9), both CEUS and MRI yielded a definitive LI-RADS 5 classification with suspected local invasion. Notably, while the white blood cell (WBC) count remained within the normal range (5.83&#xd7; 10^9/L), a marked elevation in HBP (16.7ng/mL; Ref: <11.4ng/mL) suggested a localized inflammatory response. Guided by the radiological mandate for malignancy, the patient underwent an anatomical hepatectomy. Postoperative histopathology revealed XGI characterized by dense infiltration of lipid-laden foamy histiocytes, with immunohistochemistry (CD68+, SMA+, ALK-, IgG4-) effectively excluding neoplasia and IgG4-related disease. XGI can authentically mimic the hemodynamic signature of HCC, a challenge compounded by the "relative washout" effect of background fibrosis. The "WBC-HBP Dissociation" identified here serves as a critical serological red flag for occult inflammation in patients with metabolic comorbidities. Integrating HBP assessment into the diagnostic algorithm for LI-RADS 5 masses-especially when tumor markers are negative-may justify advanced metabolic imaging or biopsy, potentially sparing high-risk patients from unnecessary and morbid major hepatic resections. Diagnosing Hepatocellular Carcinoma usually relies on specific patterns seen on CT or MRI scans. Yet, this method has a flaw. In patients with liver fibrosis, benign inflammatory lumps can mimic the exact appearance of a tumor. Such mimicry creates a dangerous trap, often leading to unnecessary major surgeries. The risk is even higher for diabetic patients. Diabetes causes &#x201c;diabetic immunoparesis&#x201d; a condition where the immune system reacts slowly. Consequently, standard blood tests may show normal white blood cell counts despite an active, hidden infection. We report a case where a diabetic patient&#x2019;s liver mass mimicked cancer on all imaging modalities. His normal blood counts initially masked the infection. However, we detected a sharp rise in Heparin-Binding Protein (HBP). Unlike routine markers, HBP is released early and remains elevated even in diabetic patients. We term this mismatch &#x201c;WBC-HBP Dissociation&#x201d;.It was the critical clue identifying the mass as Xanthogranulomatous Inflammation, not cancer. Testing for HBP offers a safety net, helping surgeons avoid operating on inflammatory mimics.

This study aimed to evaluate the operative safety, efficiency, and oncologic outcomes of a standardized misoprostol-assisted surgical evacuation protocol for molar pregnancies. We conducted a single-center retrospective cohort study of 118 patients with histologically confirmed hydatidiform moles. All patients received 400 &#x3bc;g of vaginal misoprostol for cervical ripening 3-4 hours before undergoing ultrasound-guided suction curettage. The primary outcomes included operative metrics (need for mechanical dilation, blood loss, operative time) and the incidence of post-molar gestational trophoblastic neoplasia (GTN). Beta-human chorionic gonadotropin (&#x3b2;-hCG) normalization and reproductive outcomes were also analyzed. The protocol demonstrated high operative efficiency. Cannula passage was achieved without mechanical dilators in 94.9% of patients, with a mean operative time of 15.2 minutes. No major complications (uterine perforation, cervical laceration, or trophoblastic embolism) occurred. Blood transfusion was required in 4.2% of cases. The overall post-molar GTN incidence was 13.6%, which is consistent with established literature; the rate for complete moles was 20.3%, with no cases following partial moles. Among patients desiring future pregnancy, the live birth rate was 81.5%. The use of misoprostol for cervical ripening before surgical evacuation of molar pregnancy is safe and effective. It facilitates a controlled procedure with favorable operative outcomes and does not appear to increase the risk of GTN.

Primary sclerosing cholangitis-associated UC (PSC-UC) carries excess colorectal neoplasia despite often mild-appearing endoscopy, implicating persistent microscopic inflammation and microbiota-bile acid (BA) dysfunction. To test whether PSC-UC neoplasia is driven by transferable microbiota-mediated inflammation linked to secondary BA loss. Surveillance colonoscopies (2012-2022) from PSC-UC (n=251) and UC-only (n=8839) were compared for segmental endoscopic/histological activity and dysplasia. We generated multidrug resistance protein 2 (MDR2)-/- &#xd7; interleukin (IL)-10-/- double-knockout (DKO) mice and used germ-free (GF) derivation, faecal microbiota transplantation (FMT), antibiotic conditioning and cohousing with shotgun metagenomics and liquid chromatography-tandem mass spectrometry BA profiling. PSC-UC showed greater inflammatory activity and a right-shifted dysplasia burden versus UC-only. Under specific-pathogen-free conditions, DKO mice developed early right-predominant colitis and multifocal dysplasia progressing with age. DKO communities were depleted of 7&#x3b1;-dehydroxylation capacity with near absence of deoxycholic and lithocholic acids and no enrichment of canonical bacterial genotoxins. GF DKO mice were protected, whereas live DKO donor FMT reinstated severe colitis and dysplasia; sterile-filtered stool supernatant was inactive. IL-10-/- donor FMT or cohousing attenuated colitis and increased recipient secondary BA, whereas wild-type/MDR2-/- donor transfers were non-colitogenic. In GF DKO mice, direct deoxycholic acid repletion caused hepatotoxicity. PSC-UC neoplasia associates with transmissible microbiota-dependent inflammation and secondary BA deficiency. Controlled restoration of BA-transforming microbial functions, rather than indiscriminate secondary BA replacement, is a rational translational direction.

The Hugo&#x2122; RAS platform (Medtronic&#xae;), featuring an open-console design and modular configuration, represents a novel alternative to established robotic systems. Limited large-scale series of colorectal procedures using this platform have been published. This study aimed to evaluate the feasibility, safety, and learning curve of implementing the Hugo&#x2122; RAS platform for colorectal surgery in a center without prior robotic experience. We retrospectively analyzed 100 consecutive adult patients (median age 68&#xa0;years; 51% male) undergoing elective colorectal resection using Hugo&#x2122; RAS between April 2023 and December 2024. Surgical indications included malignancy (78%), benign neoplasia, and inflammatory disease. Primary outcomes included operative time, blood loss, conversion rate, oncologic adequacy, complications (Clavien-Dindo classification), and length of stay. Learning curves were assessed via CUSUM analysis. Median operative time was 180&#xa0;min (IQR 147.5-240.0), with blood loss of 50&#xa0;mL (IQR 50-100). No conversions occurred. R0 resection was achieved in 93% of applicable cases, with median lymph node harvest of 20. Overall morbidity was 28%, including 5% major complications (Clavien-Dindo&#x2009;&#x2265;&#x2009;IIIb) and zero grade&#xa0;IV/V events. Median stay was 6&#xa0;days. Male patients had significantly higher complication rates (39.2% vs 16.3%, p&#x2009;=&#x2009;0.011). Comparing first versus last 50 cases, complications decreased from 34% to 22% (p&#x2009;=&#x2009;0.181), while major complications remained stable. CUSUM analysis revealed stabilization after approximately 50 cases. The Hugo&#x2122; RAS platform enabled safe and effective colorectal surgery with zero conversions and oncologic outcomes meeting established benchmarks. The learning curve stabilized at 50 cases with progressive reduction in minor complications. These results support Hugo&#x2122; RAS as a valuable addition to minimally invasive colorectal surgery.

Recently, stool- and blood-based cancer screening kits have been approved in clinical practice as convenient and noninvasive methods for colon cancer screening. One such test in long-standing practice has included the fecal immunochemical test (FIT), wherein home-based testing has rendered it a convenient initial assay to complement screening colonoscopy, despite limitations in diagnostic performance. In a recent original study published in the journal by Nguyen and colleagues, the feasibility and performance of combining FIT with circulating tumor cell (CTC) enumeration for predicting colorectal neoplasia and the risk of developing colorectal cancer were described. In this commentary, we highlight the potential of this combination as a novel colorectal cancer screening technique. The introduction of CTC as a potential colorectal cancer screening assay is timely, given the emergence of liquid biopsies that hold promise in their ability to detect a multitude of cancer-specific signals, from the detection of minimal residual disease to the detection of molecular alterations for precision therapies in oncology. We place the importance of their results in the context of the evolving landscape of stool- and blood-based colorectal cancer screening tests involving multitarget fecal DNA and cell-free DNA assays. See related article by Nguyen et al., Cancer Epidemiol Biomarkers Prev 2026;35:79-87.

A 60-year-old woman presented with polyarthritis in the aftermath of an upper respiratory tract infection. Further investigation revealed infective mitral valve endocarditis necessitating acute surgical valve replacement due to Streptococcus dysgalactiae, as evidenced by positive blood and intraoperative cultures, with disseminated infection and septic emboli in kidneys, multiple joints, and brain. Subsequent colonoscopy revealed a hitherto undetected rectal adenocarcinoma. The co-occurrence of S. dysgalactiae endocarditis and colorectal malignancy in this patient, who was within the age range of elevated baseline risk, may represent coincidental coexistence rather than a causal relationship. This case adds to the sparse literature linking S. dysgalactiae infection with colorectal neoplasia and suggests that colonoscopy may be considered on an individualized, risk-adapted basis in selected patients with S. dysgalactiae endocarditis-an approach distinct from the evidence-based colonoscopy recommendations applicable to Streptococcus gallolyticus endocarditis.