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Inflammatory bowel disease-associated serrated lesions with dysplasia are frequently associated with advanced neoplasia: supporting a unified classification approach
No full textAIMS: Inflammatory bowel disease (IBD)-associated serrated lesions are categorized into three distinct subtypes: traditional serrated adenoma (TSA)-like lesion, sessile serrated lesion (SSL)-like lesion, and serrated lesion, not otherwise specified (NOS). Although the risk of neoplastic progression of serrated lesions without dysplasia has not been shown to exceed that of sporadic cases, the clinicopathologic features of the three serrated subtypes with dysplasia remain poorly understood in the context of IBD.; METHODS AND RESULTS: We analysed 87 serrated lesions with dysplasia (collectively referred to as serrated dysplasia) identified endoscopically in 58 IBD patients, including 51 (59%) TSA-like dysplasia, 24 (28%) SSL-like dysplasia, and 12 (14%) serrated dysplasia NOS. Inclusion criteria required all three serrated subtypes to show morphologic evidence of dysplasia and to be located within areas of colitis. We also compared the clinicopathologic features of serrated dysplasia with those of 239 conventional (adenomatous) dysplastic lesions from 149 IBD patients. The cohort included 39 (67%) men and 19 (33%) women, with a mean age of 54years and a mean IBD duration of 20years. Most patients had ulcerative colitis (n=41; 71%) and pancolitis (n=48; 83%). The majority of serrated lesions with dysplasia had a polypoid or visible endoscopic appearance (n=73; 84%), with a mean size of 1.4cm, and were found in the left colon (n=66; 76%). Most lesions (n=73; 84%) demonstrated low-grade dysplasia at the time of biopsy diagnosis, whereas high-grade dysplasia (HGD) was identified in the remaining 14 (16%) lesions. SSL-like dysplasia was more frequently associated with ulcerative colitis (94%) compared to TSA-like dysplasia (67%) and serrated dysplasia NOS (56%) (P=0.042). Although only seven (12%) patients had a concurrent history of primary sclerosing cholangitis, it was exclusively identified in the TSA-like dysplasia group (19% versus 0% in both the SSL-like dysplasia group and the serrated dysplasia NOS group; P=0.017). Serrated dysplasia NOS more commonly demonstrated HGD at the time of biopsy diagnosis (42%) compared to TSA-like dysplasia (12%) and SSL-like dysplasia (13%) (P=0.022). Serrated dysplasia NOS was also more frequently associated with synchronous and/or metachronous nonconventional dysplasia (60%) compared to TSA-like dysplasia (16%) and SSL-like dysplasia (9%) (P=0.037). Serrated dysplasia, regardless of subtype, was associated with high rates of advanced neoplasia (HGD or colorectal cancer) at the previous biopsy site or in the same colonic segment during follow-up. Within a mean follow-up time of 13months, advanced neoplasia was detected in 50% of the TSA-like dysplasia group, 67% of the SSL-like dysplasia group, and 100% of the serrated dysplasia NOS group (P=0.622). Moreover, at least one-third of patients in each group (58% in the TSA-like dysplasia group, 44% in the SSL-like dysplasia group, and 33% in the serrated dysplasia NOS group; P=0.332) developed synchronous/metachronous dysplasia, with at least 50% of these lesions progressing to advanced neoplasia within a mean follow-up time of 11months (P=1.000). The serrated dysplasia group showed nearly six times the incidence of advanced neoplasia upon follow-up (59%) compared to the conventional dysplasia group (10%) (P<0.001).; CONCLUSION: TSA-like dysplasia, SSL-like dysplasia, and serrated dysplasia NOS show distinct clinicopathologic features. However, all three serrated subtypes were associated with high rates of advanced neoplasia (50%-100%) during follow-up, suggesting that these lesions could potentially be combined into one diagnostic category, such as serrated dysplasia. © 2025 John Wiley & Sons Ltd
Insight into the structural changes upon ultrasonic fragmentation and dispersion of carbon nanomaterials of different dimensions and bulk moduli
Get PDFIntroducing MLOps to Facilitate the Development of Machine Learning Models in Agronomy: A Case Study
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Role of the putative sit1 gene in normal germination of spores and virulence of the Mucor lusitanicus
Get PDFMucormycosis is a life-threatening infection caused by certain members of the fungal order Mucorales, with increased incidence in recent years. Individuals with untreated diabetes mellitus, and patients treated with deferoxamine are particularly susceptible to this infection. Elevated free iron concentrations in serum contribute to the development of mucormycosis. Pathogenic fungi have evolved multiple mechanisms to acquire and utilize free iron or extract it from the various iron-binding molecules within the host. The utilization of hydroxamate siderophores as xenosiderophores may contribute to the development of mucormycosis. The genome of Mucor lusitanicus encodes one Sit1 siderophore transporter. In this study, the role of the sit1 gene was characterized by generating knockout mutants using CRISPR-Cas9. Relative transcript level of the sit1 gene significantly increased in the presence of deferoxamine- and deferasirox-iron complexes. Lack of sit1 resulted in altered germination of spores and growth ability, and decreased virulence. Furthermore, absence of the gene caused elevated transcript levels of a ferric reductase (FRE), a low-affinity iron permease (FET4) and a copper dependent iron oxidase (FET3). Our result suggests that expressions of the genes involved in iron uptake affect each other. The lack of Sit1 resulted in an increased transcript level of the FRE3 gene, which may be able to reduce iron from the siderophore-iron complex. The reduced and liberated iron may be then taken up by activated FET4a. This study highlights the significance of understanding the iron acquisition mechanisms of pathogenic fungi to develop effective treatments for fungal infections
Transcriptomic Predictors of Survival for Palbociclib + Endocrine Therapy Versus Capecitabine in Aromatase Inhibitor-Resistant Breast Cancer From the GEICAM/2013-02 PEARL Trial
Get PDFPURPOSE: For hormone receptor-positive/human epidermal growth factor receptor 2-negative (HR+/HER2-) metastatic breast cancer (MBC), first-line cyclin-dependent kinase 4/6 inhibitors (CDK4/6i) + endocrine therapy (ET) is the standard of care. They are also used after progression on first-line aromatase inhibitors (AIs), but some patients may respond better to chemotherapy-based options. We examined tumor features associated with survival from GEICAM/2013-02 PEARL, a phase III trial of palbociclib + ET versus capecitabine in AI-resistant HR+/HER2- MBC.; METHODS: For 158 and 155 patients from each arm, 878 previously published gene expression signatures were derived using RNA sequencing on pretreatment tumor specimens, both primary and metastatic. Multivariable Cox models for progression-free survival (PFS) and overall survival (OS) were constructed with 16 preselected signatures related to proliferation, loss of retinoblastoma, and immune infiltration, and via Elastic Net using all signatures.; RESULTS: Significant PFS difference by PAM50 intrinsic subtype was observed with palbociclib + ET. Comparing treatment arms, luminal A subtype trended toward longer PFS with palbociclib + ET, and luminal B and nonluminal subtypes had significantly longer PFS with capecitabine. Three B-cell (B-lymphocyte)-associated signatures correlated with shorter OS with palbociclib + ET. The immune-activated Immune1 TCGA breast cancer signature had significant treatment arm interaction for OS. Elastic Net iteratively selected B-cell-associated signatures independently associated with shorter OS with palbociclib + ET.; CONCLUSION: PAM50 intrinsic subtype predicted PFS differences between palbociclib + ET and capecitabine. Lower B-cell-associated gene expression predicted longer OS with palbociclib + ET versus capecitabine. These features may help identify HR+/HER2- tumors resistant to further ET-based treatment with CDK4/6i
Phenanthrene Monomers and Dimers from Juncus tenuis with Antiproliferative Activity and Synergistic Effect with Doxorubicin Against Human Colon Cancer Cell Lines
Get PDFContinuing our search for bioactive compounds in species from the Juncaceae family, we investigated Juncus tenuis. The structures of five previously undescribed phenanthrenes—tenuins A–E (1–5)—and 14 known phenanthrenes (6–19), along with other components, were isolated and characterized using nuclear magnetic resonance and high-resolution mass spectrometry measurements. The antiproliferative activity of all of the isolated phenanthrenes was evaluated against the human colorectal adenocarcinoma cell lines COLO 205 (doxorubicin-sensitive) and COLO 320 (doxorubicin-resistant), as well as a non-tumorigenic human fibroblast cell line (CCD-19Lu), using the MTT viability assay. Diphenanthrenes 4, 5, and 19 showed the most potent antiproliferative effects, with IC50 values ranging from 7.60 to 17.32 μM; however, these compounds lacked selectivity toward cancer cells. To explore potential chemosensitizing properties, the synergistic effects of the phenanthrenes with the anticancer drug doxorubicin were also examined in the COLO 320 cells. Notably, compound 2 exhibited very strong synergism (CI = 0.021), indicating a highly potent interaction. These findings highlight J. tenuis as a valuable source of phenanthrenes and demonstrate the synergistic anticancer potential of natural phenanthrenes with doxorubicin, offering promising prospects for overcoming multidrug resistance in colorectal cancer therapy
