PATHOLOGY RESEARCH AND PRACTICE病理学研究与实践
PATHOLOGY RESEARCH AND PRACTICE(英文缩写 PATHOL RES PRACT),ISSN 0344-0338,eISSN 1618-0631,中文译名:病理学研究与实践 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-11-01 至 2026-10-31，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 3.309 | Q2 |
| 2022 | 2.800 | Q2 |
| 2023 | 2.900 | Q2 |
| 2024 | 3.200 | Q2 |
| 2025 | 3.700 | Q1 |
PATHOLOGY RESEARCH AND PRACTICE 最新收录文献
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1. FOXM1-mediated transcriptional activation of CILP2 promotes malignant phenotypes and EMT-associated remodeling in clear cell renal cell carcinoma.
1. FOXM1介导的CILP2转录激活促进透明细胞肾细胞癌的恶性表型及EMT相关重塑PMID:日期:2026-10-02Clear cell renal cell carcinoma (ccRCC) is the most common histological subtype of renal cancer and remains associated with aggressive progression and poor clinical outcomes. Cartilage intermediate layer protein 2 (CILP2), an extracellular matrix-associated secreted protein, has been implicated in tumor-related processes, but its biological role and regulatory mechanism in ccRCC remain unclear. CILP2 expression and its association with clinical outcomes were evaluated using multiple public datasets and further examined in clinical specimens. Gain- and loss-of-function assays were performed in A498 and 786-O cells to assess the effects of CILP2 on proliferation, migration, invasion, and colony formation. Xenograft experiments were conducted to evaluate tumor growth in vivo. The transcriptional regulation of CILP2 by FOXM1 was examined by ChIP-PCR and dual-luciferase reporter assays. Gene set enrichment analysis, RT-qPCR, western blotting, and immunofluorescence were used to investigate downstream pathways. Associations between CILP2 and the immune microenvironment were also analyzed. CILP2 was significantly upregulated in ccRCC and its high expression was associated with advanced clinicopathological features and poor survival. Functionally, CILP2 knockdown suppressed proliferation, migration, invasion, and clonogenicity of ccRCC cells, whereas CILP2 overexpression exerted the opposite effects. In vivo, CILP2 depletion reduced xenograft growth. Mechanistically, FOXM1 directly bound to the CILP2 promoter and positively regulated its transcription. Transcriptomic and experimental analyses indicated that CILP2 promoted an EMT-associated malignant phenotype, accompanied by decreased epithelial markers and increased mesenchymal markers. Exploratory bioinformatic analyses further showed that elevated CILP2 expression was associated with computationally inferred Treg abundance and CAF-related stromal features. These findings support CILP2 as a candidate prognostic marker and a contributor to malignant phenotypes in ccRCC. FOXM1-mediated transcriptional regulation of CILP2 is associated with EMT-related remodeling, whereas the observed immune- and stromal-related associations remain exploratory. The clinical utility and therapeutic targetability of the FOXM1/CILP2 axis require validation in larger prospective cohorts and more physiologically relevant models.
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2. Inflammatory rhabdomyoblastic tumor: Clinicopathologic and genomic features, association with neurofibromatosis type 1, and progression to rhabdomyosarcoma.
PMID:日期:2026-09-26Inflammatory rhabdomyoblastic tumor (IRMT) is a rare myogenic neoplasm with a morphologic spectrum and incompletely defined clinical behavior. It is characterized by a prominent inflammatory infiltrate, skeletal muscle differentiation, and recurrent near-haploidization, with occasional progression to rhabdomyosarcoma. Its relationship with neurofibromatosis type 1 (NF1) remains incompletely understood, despite recurrent NF1 alterations and reports of IRMT arising in patients with NF1. We analyzed five IRMTs: three conventional tumors, one tumor with increased mitotic activity without overt malignant features, and one malignant tumor. Two arose in patients with clinically overt NF1 and Targeted next-generation sequencing identified pathogenic NF1 alterations in four out of five tumors, supporting an association between IRMT and NF1. Whole-genome sequencing demonstrated near-haploid genomes in conventional IRMTs, whereas the malignant tumor showed whole-genome duplication, genome-wide loss of heterozygosity, and homozygous CDKN2A inactivation. When included with other genomically characterized and published conventional IRMTs and malignant progressions, integrated data supports a view in which near-haploidization represents the genomic background of conventional IRMT, with complete CDKN2A inactivation and whole-genome duplication as candidate contributors to malignant progression. Although this small retrospective series cannot establish temporal sequence or causality, our findings provide additional clinicopathologic and molecular support for an association between IRMT and NF1 and further characterize the genomic alterations associated with malignant progression. Complete CDKN2A loss and whole-genome duplication should be regarded as candidate progression-associated findings requiring validation in larger cohorts and longitudinal and functional studies.
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3. Polyploid giant cancer cells: Survival, progeny formation, and therapeutic targeting.
3. 多倍体巨癌细胞：生存、子代形成及治疗靶向PMID:日期:2026-09-26Polyploid giant cancer cells (PGCCs) are enlarged tumor cells with markedly increased genomic content that can arise or become enriched after therapeutic or microenvironmental stress. Some survive for prolonged periods and generate smaller daughter cells, but progeny formation does not invariably lead to sustained growth or inherited drug resistance. This review examines PGCC biology through three distinct outcomes: survival, progeny formation, and sustained progeny expansion. We integrate experimental and human evidence on these outcomes while distinguishing PGCC-specific findings from work on whole-genome doubling and related polyploid states. Apoptosis regulation, autophagy-lysosomal activity, and mitochondrial and redox adaptation support survival in defined models. Progeny formation involves nuclear reorganization, extracellular signaling, lipid metabolism, and membrane separation. The resulting progeny vary in proliferative capacity, genomic organization, and phenotypic plasticity, while giant cells and their progeny can influence stromal and immune responses. Human studies associate PGCC-related phenotypes with adverse pathology or outcomes, but their contribution to recurrent tumor lineages remains unresolved. Preclinical interventions act at different stages, from giant-cell establishment and survival to progeny release, progeny growth, and tumor-supportive signaling. Their effects therefore depend on treatment context and timing, and cannot be inferred from short-term changes in PGCC abundance alone. Linking these stage-specific responses to sustained tumor control is central to evaluating PGCC-directed therapy.
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4. Autosomal recessive Alport syndrome associated with two heterozygous COL4A4 variants.
PMID:日期:2026-09-19该文献暂无摘要。
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5. Bu Shen Huo Xue Formula ameliorates chronic kidney disease and suppresses NLRP3 inflammasome-mediated pyroptosis and renal fibrosis.
5. 补肾活血方改善慢性肾病并抑制NLRP3炎症小体介导的细胞焦亡和肾纤维化PMID:日期:2026-09-19Bu Shen Huo Xue Formula (BSHX) is used in traditional Chinese medicine for chronic kidney disease (CKD), but its pharmacological mechanisms remain unclear. This study investigated whether effects of BSHX against CKD are associated with modulation of NLRP3 inflammasome-mediated pyroptosis and the inflammation-fibrosis axis. BSHX constituents were characterized by UPLC-MS/MS. Network pharmacology and molecular docking were used to predict potential targets. CKD was induced in mice by unilateral nephrectomy with contralateral ischemia-reperfusion injury. Mice received low- or high-dose BSHX or losartan potassium. Renal function, histopathology, fibrosis, inflammatory responses, and pyroptosis-related markers were assessed by serum biochemistry, staining, Western blotting, qPCR, and immunohistochemistry. Safety was evaluated in healthy mice. UPLC-MS/MS identified multiple BSHX constituents, and bioinformatic analyses suggested involvement of NLRP3-related inflammatory and fibrotic pathways. In CKD mice, BSHX dose-dependently reduced serum creatinine and blood urea nitrogen, attenuated renal injury and interstitial fibrosis, and decreased renal NLRP3, caspase-1, GSDMD, IL-1β, and IL-18 expression. BSHX also suppressed FN, α-SMA, MMP-9, IL-6, TNF-α, and MCP-1. In healthy mice receiving BSHX alone, no significant abnormalities were observed in the evaluated serum biochemical indices of renal or hepatic function. BSHX ameliorated renal dysfunction and injury in CKD mice and was associated with suppression of NLRP3 inflammasome-mediated pyroptosis, inflammation, and fibrosis. Under the present experimental conditions, BSHX did not induce detectable abnormalities in the evaluated serum indices of hepatic or renal function.
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6. DDR2 deficiency attenuates doxorubicin-induced cardiotoxicity by reducing cardiac dysfunction and oxidative stress in mice.
PMID:日期:2026-09-17Doxorubicin (DOX) is a highly effective anthracycline chemotherapeutic drug. However, the clinical application is limited due to its dose-dependent cardiotoxicity. Discoidin domain receptor 2 (DDR2), the main collagen-binding receptor tyrosine kinase is a major player of various degrees of fibrosis or tissue restructuring in pathological conditions and unknown its role for DOX-induced heart injuries. We investigated the impacts of DDR2 deficiency from acute DOX cardiotoxicity in vivo, by utilizing DDR2-knockout (DDR2) and wild-type (Wt) mice. Genetic deletion of DDR2 significantly reduced DOX-induced cardiac dysfunction. Furthermore, we observed a substantial reduction in reactive oxygen species generation within the vasculature of DDR2 + DOX mice, along with decreased mRNA expression of Hmox1 and Nfe2l2 in cardiac tissue. Additionally, DDR2 deficiency suppressed the DOX-induced Inflammatory cytokines. Finally, DDR2 attenuated DOX-induced cardiac fibrosis. The work demonstrates that DDR2 plays a pivotal role in the pathogenesis of DOX-mediated cardiotoxicity.
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7. Quercetin protects brain microvascular endothelial cells against hypoxia/reoxygenation-induced injury and ferroptosis by targeting the TCF3/ALOX15 axis: Implications for cerebral small vessel disease.
7. 槲皮素通过靶向TCF3/ALOX15轴保护脑微血管内皮细胞免受缺氧/复氧诱导的损伤和铁死亡：对脑小血管病的意义PMID:日期:2026-09-15Cerebral small vessel disease (CSVD) is a leading cause of vascular cognitive impairment and stroke. Quercetin is a natural flavonoid with neuroprotective effects in various cerebrovascular disorders. However, its specific molecular targets and mechanisms in CSVD remain elusive. Bioinformatic analysis identified arachidonate 15-lipoxygenase (ALOX15) as a potential ferroptosis-related target of quercetin in CSVD. The human cerebral microvascular endothelial cells (HCMEC/D3) subjected to hypoxia/reoxygenation (H/R) treatment were used for in vitro experiments. Cell viability, apoptosis, and angiogenesis were measured via 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), flow cytometry, and tube formation assay, respectively. Ferroptosis markers, including Fe²⁺, superoxide dismutase (SOD), malondialdehyde (MDA), and lipid peroxidation were detected by commercial kits or flow cytometry. The expression of ALOX15, transcription factor 3 (TCF3), acyl-CoA synthetase long-chain family member 4 (ACSL4), and glutathione peroxidase 4 (GPX4) was assessed using western blot. Online prediction, dual-luciferase reporter assay, and chromatin immunoprecipitation (ChIP) were performed to validate the TCF3-ALOX15 transcriptional regulation. A bilateral common carotid artery occlusion (BCAO) rat model of CSVD was established for in vivo validation. Quercetin improved H/R-induced HCMEC/D3 cell viability, promoted angiogenesis, and reduced apoptosis. Quercetin also attenuated ferroptosis, characterized by decreased Fe²⁺ accumulation, MDA and lipid peroxidation levels, and restoration of SOD activity and GPX4 expression while suppressing ACSL4 (all P < 0.05). TCF3 was identified as a transcriptional activator of ALOX15. TCF3 knockdown mimicked quercetin's protective effects, which were reversed by ALOX15 overexpression. Conversely, TCF3 overexpression counteracted quercetin-mediated protection. In BCAO rats, quercetin treatment ameliorated hippocampal neuronal damage, reduced brain edema, improved spatial learning and memory, and suppressed expression of TCF3/ALOX15 and ferroptosis markers (all P < 0.05). Quercetin protected against H/R-induced endothelial injury and ferroptosis in CSVD by targeting the TCF3/ALOX15 transcriptional axis, providing mechanistic insights into quercetin's cerebrovascular protective effects.
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8. Impact of ursodeoxycholic acid on histologic and immunophenotypic features in primary biliary cholangitis.
8. 熊去氧胆酸对原发性胆汁性胆管炎组织学和免疫表型特征的影响PMID:日期:2026-09-15Primary biliary cholangitis (PBC) is an immune-mediated cholangiopathy for which ursodeoxycholic acid (UDCA) improves biochemical outcomes and survival, but its effects on tissue phenotype remain uncertain. We examined whether morphology and marker expression change with UDCA status or primarily reflect disease severity. We studied 109 specimens (biopsies and explants) from 67 patients with PBC: 9 same-episode PRE-POST pairs for the primary paired analysis and all 109 specimens for secondary cross-sectional analysis. Semiquantitative scores were analyzed using exact Wilcoxon signed-rank tests and proportional-odds ordinal regression with patient-clustered robust standard errors and Benjamini-Hochberg correction. Among 9 paired patients, no feature differed PRE-POST (all q = 1.00), including CK7 (P = .125), CK19 (P = .25), and fibrosis (P = .656). However, 80%-power minimum detectable differences were 0.89 (S100) and 1.19 (CD1a) units on a 0-3 scale, limiting inference. In fibrosis-adjusted cross-sectional models, UDCA status was not associated with any marker (all q ≥ .95), whereas fibrosis was associated with CK7 (OR 1.37, 95% CI 1.11-1.69; q = .007), CK19 (OR 1.79, 1.45-2.22; q < .001), and CD1a⁺ density (OR 1.31, 1.09-1.57; q = .007); CP grade was exploratory (OR 1.21; q = .021). After explant adjustment, CK7 and CK19 associations persisted, whereas CD1a⁺ and CP grade did not; S100⁺ was not significant in either model. Fibrosis stage, not UDCA status, was the principal correlate of biliary epithelial marker expression. No within-patient change was detected, although changes below one-third of the scoring scale could not be excluded. CK7 and CK19 primarily reflect disease stage rather than treatment effect.
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9. FGF19 as a site-specific candidate biomarker in colorectal neuroendocrine carcinomas.
PMID:日期:2026-09-13Gastrointestinal neuroendocrine carcinomas (GI-NECs) are aggressive tumors with marked site-specific heterogeneity, yet molecular markers for colorectal origin are lacking. This study characterized genomic and protein expression profiles to identify origin-specific biomarkers. Nineteen GI-NECs (7 esophageal, 6 gastric, 6 colorectal) were analyzed by targeted next-generation sequencing (NGS) of 425 genes and immunohistochemistry (IHC). Genetic variations across primary sites were compared, and associations between FGF19 expression, clinicopathological features, microsatellite (MS) status, and tumor mutational burden (TMB) were assessed. FGF19 transcriptional expression was further examined in The Cancer Genome Atlas (TCGA) colorectal cohort using the UALCAN platform. A total of 163 genomic alterations were identified. FGF19 was the only gene showing site-specific alterations, being exclusively mutated or amplified in colorectal NECs (50%, 95% CI: 11.8-88.2%) with significantly elevated protein expression (83.3%, 95% CI: 35.9-99.6%) compared with other sites. A microsatellite instability-high (MSI-H) subgroup (10.5%, 95% CI: 1.3-33.1%) exhibited markedly higher TMB. TCGA data confirmed upregulated FGF19 in colorectal tumors but showed no survival association, consistent with the prognostic neutrality in our cohort. FGF19 may act as a site-specific candidate biomarker for colorectal NECs, with 83.3% protein positivity and exclusive site-specific alterations in 50% of cases. Detection of MSI-H suggests that mismatch repair (MMR) testing may be considered in selected patients with suggestive clinical or family histories to inform immunotherapy decisions.
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10. Clinicopathological characteristics of giant cell tumor of bone and identification of a novel H3F3A p.V36_K37insL mutation.
10. 骨巨细胞瘤的临床病理特征及一种新型H3F3A p.V36_K37insL突变的鉴定PMID:日期:2026-09-11Osteoclast-rich bone lesions present overlapping clinical and radiological features, while their biological behaviors and treatment protocols differ greatly, posing challenges for differential diagnosis. H3.3G34W immunohistochemistry serves as the primary biomarker for giant cell tumor of bone (GCTB), yet this marker is not expressed in all GCTB cases. Denosumab, the first-line targeted drug, induces profound tumour remodelling that raises diagnostic difficulties for post-treatment specimens. A total of 45 osteoclast-rich bone lesions collected between 2020 and 2024 at the First Affiliated Hospital of Zhejiang University School of Medicine were retrospectively screened, with 16 cases harbouring H3F3A mutations enrolled for analysis. All hematoxylin and eosin (HE) staining and immunohistochemical (IHC) slides underwent independent review by two senior pathologists, and full imaging datasets were re-assessed by two radiologists. Sanger sequencing was performed on formalin-fixed paraffin-embedded(FFPE) specimens to identify H3F3A gene variants. Clinicopathological and radiological profiles of mutant GCTB were summarised, and histological as well as molecular changes before and after denosumab intervention were compared. Among the 45 screened lesions, 16 harboured H3F3A mutations, including 14 canonical p.G34W variants, one p.G34L variant and one previously unreported p.V36_K37insL insertion variant undetectable by routine H3.3G34W immunohistochemistry. Typical osteolytic, eccentric and expansile imaging manifestations were observed in most GCTB cases. Conventional untreated lesions exhibited characteristic evenly distributed mononuclear stromal cells and osteoclast-like giant cells. Marked depletion of giant cells, spindle cell proliferation, woven bone formation and weakened IHC staining were common histological alterations after denosumab therapy, accompanied by reduced mutant allele abundance in partial post-treatment specimens. Two patients developed local tumour recurrence during follow-up. Comprehensive integration of clinical, radiological, histological and molecular evidence is essential for accurate differential diagnosis of osteoclast-rich bone lesions after denosumab treatment. The newly identified H3F3A p.V36_K37insL variant may represent a potential rare variant for morphologically‑typical GCTB, and serve as an auxiliary molecular clue for H3.3‑G34W‑immunonegative cases. Further multicenter and functional studies are required to clarify the biological characteristics of this novel variant.