Autoimmune diseases, including psoriasis (Ps), rheumatoid arthritis (RA) and ulcerative colitis (UC), pose significant health burdens worldwide. A more refined classification of these diseases is essential for enabling targeted therapeutic strategies. Traditional Chinese Medicine (TCM) is gaining increasing recognition globally, offering potential insights into disease heterogeneity. In this study, we performed comprehensive T cell receptor (TCR) and B cell receptor (BCR) repertoire sequencing in 59 participants, including patients with Ps, RA, UC and healthy controls. Patients were further stratified into Dampness and non-Dampness groups based on standardized TCM diagnostic criteria. Repertoire composition, clonotype richness, diversity metrics, V gene usage and shared CDR3 patterns were analysed. Machine learning approaches (LASSO, GLM and OPLS-DA) were applied to identify diagnostic biomarkers, followed by validation in an independent cohort. Compared with healthy controls, Ps, RA and UC patients exhibited reduced clonotype richness and diminished TCR/BCR diversity, indicating adaptive immune contraction. Dampness ZHENG-specific alterations were observed, including selective IgK and IgL clonotype richness reduction in Ps with dampness, increased TRA/TRB diversity in RA with dampness, and elevated TRG clonotype counts/read proportions in UC with dampness. Stratification by Dampness ZHENG revealed distinct immune repertoire architectures characterized by increased D50 index, reduced proportions of large clones and preferential V gene usage, including TRAV20, TRAV38-2DV8 and TRAV8-3. Unsupervised dimensionality reduction demonstrated significant separation between Dampness and non-Dampness groups across diseases. A three-gene V-segment model achieved an AUC of 0.804 and 74.7% accuracy in an independent validation cohort, supporting its potential utility as an objective biomarker for Dampness ZHENG. Our findings suggest that TCM-based phenotyping may offer a meaningful approach for subgrouping autoimmune diseases, thereby providing a foundation for more syndrome differentiation-based treatment strategies.

BACKGROUND:Atherosclerosis is fundamentally a pathology of unresolved inflammation perpetuated by the collapse of Regulatory T cell (Treg)-mediated tolerance. Emerging evidence indicates that Treg functional integrity is intrinsically dictated by mitochondrial fatty acid oxidation (FAO), a metabolic checkpoint often compromised under systemic metabolic stress. Current lipid-lowering therapies, such as statins, often fall short in correcting this maladaptive immunometabolic defect and may introduce collateral metabolic perturbations. PURPOSE:This study aimed to elucidate the immunometabolic therapeutic mechanism of Dingxin Recipe III (DXR III) in ameliorating atherosclerosis. METHODS:We employed an integrated systems pharmacology strategy-combining serum pharmacochemistry, multi-omics profiling, and extensive high-dimensional flow cytometry-to elucidate the therapeutic mechanism of DXR III, a traditional Chinese herbal formula in an in vivo study. ApoE-/- mice were fed with a high-fat diet for 16 weeks, and treated intragastrically with DXR III (at doses of 6.5 g/kg/day and 13 g/kg/day) or Simvastatin (positive control, 5 mg/kg/day) over the last 12 weeks. RESULTS:DXR III treatment effectively attenuating atherosclerotic progression. Serum pharmacochemistry identified 254 prototypical absorbed constituents, including Tanshinone I (a potential Peroxisome Proliferator-Activated Receptor Gamma agonist), as bioactive candidates. Multi-omics analysis revealed that DXR III modulated the metabolic environment, coinciding with restored FAO flux. This shift was associated with a favorable metabolic niche characterized by increased FAO substrates, which correlated with the rescue of Treg differentiation and phenotypic stability. Specifically, DXR III facilitated the redistribution of Tregs from the spleen to plaque sites and significantly inhibited their trans-differentiation into Th1-like or Th17-like phenotypes. Conversely, Simvastatin treatment, despite lowering lipids, resulted in peripheral Th17 accumulation and failed to alleviate hyperglycemia. In contrast, DXR III maintained Th17 homeostasis-abolishing the pathogenic non-classical Th17 subset-and exerted dual-regulatory effects on both lipid and glucose metabolism. CONCLUSION:DXR III ameliorates atherosclerosis, a process closely associated with the modulation of the FAO metabolic checkpoint to correct the immune imbalance driving plaque progression. By rescuing the Treg differentiation, functional integrity, and phenotypic fidelity while avoiding the immunological trade-offs associated with Th1/Th17, DXR III represents a promising candidate for comprehensive cardiovascular protection.

BACKGROUND:The prevalence of metabolic syndrome has shown a progressive rise, while contemporary pharmacological treatments are often associated with significant adverse effects. Huanglian Wendan Decoction (HLWD), a traditional formulation in Traditional Chinese Medicine utilized for the management of metabolic syndrome, has an underlying mechanism that remains not yet well understood. PURPOSE:This research aims to thoroughly explore how HLWD alleviates metabolic syndrome through a comprehensive multi-omics approach, including liquid mass spectrometry, network pharmacology, gut microbiota, metabolomics, and liver proteomics. METHODS:The constituents of HLWD were analyzed utilizing UPLC-MS. A metabolic syndrome mouse model was developed through the administration of a high-fat diet (HFD) along with streptozocin. Our research assessed the effects of HLWD on various metabolic parameters, including insulin sensitivity, body weight, hyperglycemia, hyperlipidemia, and hepatic fat accumulation. The mechanisms of HLWD on metabolic syndrome were investigated through a multi-omics approach, encompassing network pharmacology, 16S rRNA gene sequencing of gut microbiota, serum metabolomics, and liver tissue proteomics. RESULT:123 constituents were characterized in HLWD. HLWD demonstrated a marked enhancement in insulin sensitivity, as well as reductions in obesity, hyperglycemia, hyperlipidemia, inflammatory responses, and hepatic steatosis in mice with metabolic syndrome. 16S rRNA analysis indicated that HLWD effectively reduced the prevalence of microbial communities that facilitate lipid accumulation and inflammatory responses. Serum metabolomics studies revealed that, following HLWD treatment, numerous metabolites related to lipid metabolism exhibited significant improvements. Results from proteomics, immunohistochemistry, and multicolor immunofluorescence confirmed that HLWD effectively inhibited the M1 polarization of macrophages while promoting M2 polarization. CONCLUSION:This study offers a comprehensive and detailed exploration of the potential molecular mechanisms by which HLWD may mitigate metabolic syndrome, and firstly reveals that HLWD ameliorates metabolic syndrome through reprogramming hepatic macrophage polarization in mice, thereby positioning it as a promising new therapeutic option.

Colorectal cancer (CRC) is one of the most common malignant tumours and is the second leading cause of cancer-related mortality worldwide. Despite the availability of preventative, diagnostic and treatment methods including endoscopic treatment, surgical intervention, radiotherapy, biologics, salvage therapy and immunotherapy, the mortality rate associated with CRC remains alarming. Consequently, there is a pressing need to search for medicines for the treatment of CRC. Phytomedicines have been shown to suppress the proliferation and metastasis of CRC through various mechanisms, including immune regulation, modulation of gut microbiota, targeting of stem cells, macrophage polarisation, glycolysis, ferroptosis induction, modulation of extracellular vesicles, activation of mitochondria-induced apoptosis, inflammation reduction, oxidative stress management and intervention of autophagy. Furthermore, numerous studies have reported the anti-cancer and anti-metastatic effects of various phytomedicines, including curcumin, resveratrol, berberine, shikonin, dihydroartemisinin, fucoidan, luteolin, andrographolide, piperine, kaempferol, emodin, cannabidiol, tanshinone IIA and evodiamine. In this review, we sort out the effects and mechanisms of phytomedicines on CRC and outline the major phytomedicines commonly used in CRC treatment. We hope that these phytomedicines may serve as promising drugs or important lead compounds for the management of CRC.

Psoriasis is a common inflammatory skin disease with characterization of epidermal hyperplasia and sustained skin inflammation. Long noncoding RNAs (lncRNAs), which contain more than 200 nucleotide-long transcripts, are emerging as the crux of epigenetic regulators in multiple biological processes and diseases. However, how lncRNAs contribute to the etiology of psoriasis remains to be elucidated. For the first time, this study revealed that SNHG15, which was elevated in cytokines-stimulated keratinocytes and psoriasis lesions, promoted keratinocytes hyperproliferation. Mechanistically, SNHG15 fueled epithelial pathology through activation of STAT3/Cyclin D1 axis. Intriguingly, activation of STAT3 enhanced SNHG15 transcription to form a positive feed-back modulatory loop and consequently augmented the skin lesions in psoriasis. Furthermore, knock down the expression of SNHG15 can counteract the IMQ-induced keratinocytes hyperproliferation in vivo. Taken together, our findings uncover that SNHG15 facilitates epidermal hyperplasia via STAT3/Cyclin D1 axis, which might provide a novel therapeutic avenue for psoriasis treatment.

Mucinous cystadenocarcinoma (MCA) of the breast is a rare, invasive carcinoma that resembles pancreatobiliary or ovarian MCA in terms of histological appearance. Most cases of MCA of the breast are negative for the estrogen receptor, progesterone receptor and ERBB2 (HER2). To the best of our knowledge, only five reports of HER2-positive MCA cases have been reported in the English language, and no reports focusing on the molecular characteristics of HER2-positive MCAs have been published. In the present study, a rare case of a 64-year-old woman with HER2-positive MCA who underwent long-term follow-up without recurrence or distant metastasis is reported. In addition, a detailed analysis of the genomic characteristics of the tumor is provided.

Psoriasis, a common chronic inflammatory skin disease affecting approximately 2-3% of the global population, frequently co-occurs with depression. This highly prevalent comorbidity significantly impairs patients' quality of life. Despite the substantial physical and mental health burden imposed by psoriatic depression, the underlying pathophysiological mechanisms connecting psoriasis and depression remain poorly understood. In this review, we explored several pathological processes that may contribute to psoriasis-associated depression, including immune cells dysregulations, hormones imbalances, hypothalamic-pituitary-adrenal (HPA) axis dysfunctions, neuropeptides expression abnormalities, and gut dysbiosis. The primary purpose of this review was to present a comprehensive overview of the pathogenic mechanisms linking psoriasis and depression. These insights may guide trans-disciplinary interventions aimed at both skin and mood symptoms.

ETHNOPHARMACOLOGICAL RELEVANCE:Xiaoji Decoction (XJD), a traditional Chinese herbal formula, has been used for decades to effectively treat non-small cell lung cancer (NSCLC), improving patients' quality of life and prolonging overall survival. Nevertheless, the molecular mechanisms responsible for the effectiveness of XJD on NSCLC remain largely unexplored. AIM OF THE STUDY:This study aims to investigate the therapeutic effects of XJD in NSCLC and to elucidate the molecular mechanisms involved. MATERIALS AND METHODS:In vitro experiments were conducted by treating A549 cells with XJD at concentrations of 0, 6.25, 12.5, 25, and 50 mg/mL, and H1975 cells with XJD at concentrations of 0, 10, 20, 30, and 40 mg/mL. Ruxolitinib was used at a concentration of 10 μM. MTT assays were used to evaluate cell viability, and EdU assays were employed to measure cell proliferation. Apoptosis and cell cycle progression were analyzed by flow cytometry in vitro. The JAK1, p-STAT3, STAT3, PD-L1, BAX, Bcl-2, Cleaved Caspase-9, and Cleaved Caspase-3 were examined through Western blot analysis. In vivo experiments involved allocating mice into six groups (n = 5), including a saline control group, XJD treatment group (13.4 g/kg/day by gavage), αPD-L1 group (200 mg/mouse), Ruxolitinib group (10 mg/kg/day by gavage), XJD + Ruxolitinib group, and XJD + αPD-L1 group. Animal weight and tumor size were recorded daily for two weeks, and on day 18, the animals were sacrificed for tumor and spleen analysis. The number of macrophages present in the abdominal cavity, fresh tumors, and spleen was also measured. RESULTS:XJD effectively inhibited cell growth, triggered apoptosis, and induced cell cycle arrest in NSCLC cells. XJD was shown to downregulate JAK1 expression, inhibit the phosphorylation of STAT3, and reduce PD-L1 protein levels. It also decreased Bcl-2 expression while increasing the levels of BAX, Cleaved Caspase-9, and Cleaved Caspase-3, promoting cell apoptosis. Furthermore, inhibiting STAT3 phosphorylation alongside XJD treatment further amplified cell growth inhibition, induced stronger apoptosis, and more effectively arrested the cell cycle. Additionally, XJD enhanced the anti-cancer efficacy of αPD-L1, with tumor growth inhibition linked to reduced M2 macrophage infiltration and increased M1 macrophage presence. Mechanistically, combination therapies incorporating XJD with either Ruxolitinib or αPD-L1 exhibited dual therapeutic effects: 1) promotion of tumor apoptosis through enhanced caspase activation, and 2) effective suppression of the oncogenic JAK1/STAT3 signalling axis and its downstream PD-L1 expression. CONCLUSIONS:Our results indicate that XJD suppresses NSCLC cell growth, induces cell cycle arrest, and promotes apoptosis by inhibiting the JAK1/STAT3/PD-L1 signaling pathway. XJD has been shown to enhance the anti-cancer efficacy of αPD-L1 and exerts its anti-tumor effects by modulating macrophage polarization.

Metabolic syndrome encompasses a cluster of predictive metabolic risk factors, including obesity, insulin resistance, dyslipidemia, hyperglycemia and hypertension. It is strongly associated with the development of type 2 diabetes and cardiovascular disease. Given the increasing morbidity and mortality associated with metabolic syndrome, along with the limited availability of drug treatments, it is high time to investigate the pathogenesis of this condition and explore potential pharmacotherapies. Macrophages, well-known innate immune cells, play an essential role in maintaining tissue immune homeostasis and multiple physiological processes, including glucose and lipid metabolism, oxidative stress and inflammation. Emerging evidence indicates that the effects of macrophages in metabolic syndrome are linked to macrophage-mediated metaflammation. Phytochemicals derived from natural plants have been shown to exert therapeutic effects on metabolic syndrome by modulating macrophage function. In this review, we sort out the role of macrophage-mediated metaflammation in the pathogenesis of metabolic syndrome and summarise potential phytochemicals that target macrophages for the treatment of this condition.

Emerging evidence suggests that gut microbiota and its metabolites significantly influence the effectiveness of EGFR-TKIs (e.g., gefitinib, erlotinib) in lung cancer treatment. Plant polysaccharides can interact with gut microbiota, leading to changes in the host-microbe metabolome that may affect drug metabolism and therapeutic outcomes. Our previous research demonstrated the efficacy of basil polysaccharide (BPS) in treating various cancers by regulating hypoxic microenvironment and inhibiting epithelial-mesenchymal transition process. However, the potential impact of BPS on gut microbiota has not been thoroughly explored. In this study, we employed an immunodeficient gefitinib-resistant xenograft mouse model to explore whether BPS enhances the antitumor effects of gefitinib. A multi-omics approach, including 16S rDNA amplicon sequencing and LC-MS, was used to elucidate these synergistic effects. Our findings indicate that BPS can enhance tumor responsiveness to gefitinib by modulating the gut microbiota and its metabolites through multiple metabolic pathways. These changes in gut microbiota and metabolites could potentially affect cancer related signaling pathway and lung resistance-related protein, which are pivotal in determining the efficacy of EGFR-TKIs in cancer treatment.

Metabolic syndrome is a prevalent non-communicable disease characterized by central obesity, insulin resistance, hypertension, hyperglycemia, and hyperlipidemia. Epidemiological statistics indicate that one-third of the world's population is affected by metabolic syndrome. Unfortunately, owing to complicated pathogenesis and limited pharmacological options, the growing prevalence of metabolic syndrome threatens human health worldwide. Autophagy is an intracellular degradation mechanism that involves the degradation of unfolded or aggregated proteins and damaged cellular organelles, thereby maintaining metabolic homeostasis. Increasing evidence indicates that dysfunctional autophagy is closely associated with the development of metabolic syndrome, making it an attractive therapeutic target. Furthermore, a growing number of plant-derived polysaccharides have been shown to regulate autophagy, thereby alleviating metabolic syndrome, such as Astragalus polysaccharides, Laminaria japonica polysaccharides, Ganoderma lucidum polysaccharides and Lycium barbarum polysaccharides. In this review, we summarize recent advances in the discovery of autophagy modulators of plant polysaccharides for the treatment of metabolic syndrome, with the aim of providing precursor compounds for the development of new therapeutic agents. Additionally, we look forward to seeing more diseases being treated with plant polysaccharides by regulating autophagy, as well as the discovery of more intricate mechanisms that govern autophagy.

Circulating tumor cells (CTCs) and tumor-derived extracellular vesicles (tEVs) are two crucial methodologies of liquid biopsy. Given their distinct size differences and release dynamics, CTCs and tEVs potentially offer synergistic capabilities in the non-invasive detection of differentiated thyroid cancer (DTC), a typically indolent tumor. We present the Combined DTC CTC/tEV Assay, integrating dual liquid biopsy processes: i) DTC CTC enrichment by Click Chips, followed by analysis of seven DTC-specific genes, and ii) DTC tEV enrichment by Click Beads, succeeded by mRNA cargo quantification in DTC tEVs. This method utilizes click chemistry, leveraging a pair of biorthogonal , highly reactive functional motifs (tetrazine, Tz , trans-cyclooctene, TCO), to over- come the challenges encountered in the conventional immunoaffinity-based enrichment of CTCs and t EVs. The Combined DTC CTC/tEV t EV Assay synergistically combines the diagnostic precision of CTCs with the sensitivity of t EVs, demonstrating superior diagnostic accuracy in DTC detection and boasting an AUROC of 0.99. This out- performs the individual diagnostic performance of using either DTC CTC or DTC t EV alone. This integration enables full utilization of a patient's blood sample, and marks a significant evolution in the development of nanomaterial-based liquid biopsy technologies to address challenging unmet clinical needs in cancer care.

BACKGROUND:Excessive growth of keratinocytes is the critical event in the etiology of psoriasis. However, the underlying molecular mechanism of psoriatic keratinocyte hyperproliferation is still unclear. OBJECTIVE:This study aimed to figure out the potential contributory role of S-phase kinase-associated protein 2 (SKP2) in promoting the hyperproliferation of keratinocytes in psoriasis. METHODS:We analyzed microarray data (GSE41662) to investigate the gene expression of SKP2 in psoriatic lesion skins compared with their adjacent non-lesional skin. Then, we further confirmed the mRNA and protein expression of SKP2 in human psoriatic skin tissues, imiquimod (IMQ)-induced psoriatic mice back skins and tumor necrosis factor α (TNF-α), interleukin (IL)-17A and IL-6-stimulated keratinocytes by using real-time quantitative polymerase chain reaction and western blot (WB). Furthermore, we explored the potential pathogenic role and its underlying cellular mechanism of SKP2 in promoting keratinocytes hyperproliferation through 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, cell cycle detection, 5-ethynyl-2'-deoxyuridine staining and WB. Finally, we determined whether inhibition of SKP2 can effectively alleviate the keratinocytes hyperproliferation in vivo. RESULTS:We identified that SKP2 is aberrantly upregulated in the psoriatic lesion skin and cytokines-stimulated keratinocytes. Moreover, upregulated SKP2 augments cytokines-induced keratinocytes hyperproliferation. Mechanistically, enhanced SKP2 increased the S phase ratio through inhibiting Cyclin-Dependent Kinase Inhibitor p27 (P27 Kip1) expression. Correspondingly, suppression of SKP2 with SMIP004 can significantly ease the epidermis hyperplasia in vivo. CONCLUSION:Our results suggest that elevated SKP2 can empower keratinocytes proliferation and psoriasis-like epidermis hyperplasia via downregulation of P27 Kip1. Therefore, targeting SKP2-P27 Kip1 axis might be a promising therapeutic strategy for the treatment of psoriasis in future.

Background Infectious diseases are a serious threat to human especially since the COVID-19 outbreak has proved the importance and urgency of their diagnosis and treatment again. Metagenomic next-generation sequencing (mNGS) has been widely used and recognized in clinical and carried out localized testing in hospitals. Increasing the training of mNGS detection technicians can enhance their professional quality and more effectively realize the application value of the hospital platform. Methods Based on the initial theoretical understanding and practice of the mNGS platform for localization construction, we have designed a training program to enhance the ability of technicians to detect pathogens by utilizing mNGS, and hence to conduct training practices nationwide. Results Until August 30, 2022, the page views of online classes have reached 51,500 times and 6 of offline small-scale training courses have been conducted. A total of 67 trainees from 67 hospitals have participated in the training with a qualified rate of 100%. After the training course, the localization platform of 1 participating hospital has been put into use, 2 have added the mNGS localization platform for admission, among which 3 have expressed strong intention of localization. Conclusions This study focuses on the training procedures and practical experience of the project which is the first systematic standardized program of mNGS in the world. It solves the training difficulties in the current industry, and effectively promotes the localization construction and application of mNGS in hospitals. It has great development potential in the future and is worth further promotion.

Psoriasis (Ps) is one of the most common chronic inflammatory skin disorders with its pathogenesis correlated with dysregulated innate and adaptive system. Even though biological agents have advanced the treatment of psoriasis, however, there are huge limitations, like high adverse reactions and relapse rate. Therefore, it is of great interest in searching clinical resolutions with better safety and efficacy. In the current study, we utilized the adipose-derived mesenchymal stem cell (AD-MSCs) to treat moderate/severe cases of psoriasis in a single-arm clinical study. This AD-MSC treatment has proven to be clinically safe and effective. Interestingly, a trend of adaptome improvement, including increased diversity, elevated uCDR3s and decreased large clone after AD-MSC treatment in a short (2 weeks) and long (12 weeks) terms. In conclusion, allogenic AD-MSC treatment has shown a good safety and efficacy in treating Ps and can effectively improve the compromised adaptive immune system of Ps patients.

Psoriasis is a chronic inflammatory skin disorder characterized by abnormal keratinocytes proliferation and multiple immune cells infiltration in the dermis and epidermis. Although most psoriasis-related researches have been concentrated on the interleukin-23 (IL-23)/interleukin-17 (IL-17) axis, new data suggest that keratinocytes also play a pivotal role in psoriasis. Previously, we found that punicalagin (PUN), a bioactive ellagitannin extracted from Pericarpium Granati (the pericarpium of Punica granatum L.), exerts a therapeutic effect on psoriasis. However, the underlying mechanism, especially its potential modulatory effect on keratinocytes, remains obscure. Our study aims to reveal the potential regulatory effect and its underlying cellular mechanism of PUN on the hyperproliferation of keratinocytes. We used tumor necrosis factor α (TNF-α), IL-17A and interleukin-6 (IL-6) to induce abnormal proliferation of HaCaT cells (Human Keratinocytes Cells) in vitro. Then, we evaluated the effects of PUN through MTT assay, EdU staining and cell cycle detection. Finally, we explored the underlying cellular mechanisms of PUN via RNA-sequencing, WB in vitro and in vivo. Here, we found that PUN can directly and dose-dependently decrease TNF-α, IL-17A and IL-6-induced abnormal proliferation of HaCaT cells in vitro. Mechanically, PUN suppresses the hyperproliferation of keratinocytes through repressing S-phase kinase-associated protein 2 (SKP2) expression in vitro and in vivo. Moreover, overexpression of SKP2 can partly abolish PUN-mediated inhibition of aberrantly proliferative keratinocytes. These results illustrate that PUN can reduce the severity of psoriasis through directly repressing SKP2-mediated abnormal proliferation of keratinocytes, which gives new insight into the therapeutic mechanism of PUN on psoriasis. Moreover, these findings imply that PUN might be a promising drug candidate for the treatment of psoriasis.

Background: Psoriasis is an immune-mediated inflammatory skin disease. Psoriasis severity evaluation is important for clinicians in the assessment of disease severity and subsequent clinical decision making. However, no objective biomarker is available for accurately evaluating disease severity in psoriasis. Objective: To define and compare biomarkers of disease severity and progression in psoriatic skin. Methods: We performed proteome profiling to study the proteins circulating in the serum from patients with psoriasis, psoriatic arthritis and ankylosing spondylitis, and transcriptome sequencing to investigate the gene expression in skin from the same cohort. We then used machine learning approaches to evaluate different biomarker candidates across several independent cohorts. In order to reveal the cell-type specificity of different biomarkers, we also analyzed a single-cell dataset of skin samples. In-situ staining was applied for the validation of biomarker expression. Results: We identified that the peptidase inhibitor 3 (PI3) was significantly correlated with the corresponding local skin gene expression, and was associated with disease severity. We applied machine learning methods to confirm that PI3 was an effective psoriasis classifier, Finally, we validated PI3 as psoriasis biomarker using in-situ staining and public datasets. Single-cell data and in-situ staining indicated that PI3 was specifically highly expressed in keratinocytes from psoriatic lesions. Conclusion: Our results suggest that PI3 may be a psoriasis-specific biomarker for disease severity and hyper-keratinization. (c) 2023 The Authors. Published by Elsevier B.V. on behalf of Japanese Society for Investigative Dermatology. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

结直肠癌是世界范围内发病率和死亡率都位居前列的恶性肿瘤[1],其发病率在我国所有恶性肿瘤中排第3位,死亡率第5位[2],严重威胁着人们的生命健康.结直肠癌发生的途径常有两种,分别是染色体不稳定(chromosomal instability,CN)途径和微卫星不稳定(microsataellite instability,MSI)途径[3].