Histology and histopathology最新文献

{"title":"Collagen fiber arrangement in the normal bladder lamina propria and their potential impact on the pathological substaging of bladder cancer stage T1.","authors":"Ofer N Gofrit, Vladimir Yutkin, Mordechai Duvdevani, Guy Hidas, Tzahi Neuman","doi":"10.14670/HH-18-817","DOIUrl":"https://doi.org/10.14670/HH-18-817","url":null,"abstract":"<p><p>The lamina propria (LP) of the urinary bladder lies between the urothelial mucosa and the muscularis propria. This complex stratum is composed of extracellular matrix, several cell types, and collagen types I and III fibers. LP invasion by urothelial carcinoma (progression from stage Ta to T1) is a determinant of bladder cancer advancement. We attempted to characterize collagen fiber arrangement in the LP. This could enrich our understanding of this important layer and potentially provide clues for sub-staging of the T1 bladder cancer. A total of 24 Masson trichrome-stained images of normal bladder, including 12,530 collagen fibers were quantitatively analyzed using the Dragonfly software. The LP was divided according to fiber orientation into superficial LP (SLP, 15% of the thickness) and the deep LP (DLP, 85% of the thickness). Collagen fiber geometry analysis demonstrated that the SLP fibers are more parallel to the urothelium with an average angle of 26⁰±23⁰ compared to 40⁰±26⁰ in the DLP (p=3.4X10^-144), more packed (average distance to the closest fiber of 0.61±0.67 compared to 0.66±0.77, p=0.0001), and their aspect ratio is considerably longer (average of 1.93±0.12 compared to 0.20±0.11, p=2.84x10^-8). No difference was found in fiber perimeter or Feret diameter. Thus, we conclude that bladder collagen fibers are arranged in two distinct layers: a dense-ordered SLP and a loose disorder DLP. This indicates that the physical barrier to cancer cell invasion probably lies in the SLP, immediately underneath the urothelium. Once this barrier is breached, the looser and disorganized DLP poses no remarkable obstacle. Thus, we believe that histology-based subdivisions of stage T1 are expected to fail in providing clinically meaningful prognostic information.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18817"},"PeriodicalIF":2.5,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142464134","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ameliorative effects of HGF-overexpressed exosomes derived from ADMSCs on oxidative stress in hepatic fibrosis.","authors":"Hanyu Zhou, Yanyan Wu, Junchao Xue, Liushenyan Yu","doi":"10.14670/HH-18-816","DOIUrl":"https://doi.org/10.14670/HH-18-816","url":null,"abstract":"<p><strong>Background: </strong>Hepatic fibrosis, ultimately causing hepatic sclerosis, remains significant health concerns. Adipose-derived mesenchymal stem cell (ADMSC)-derived exosomes (Exo) exhibit amelioration of liver injury. Hepatocyte growth factor (HGF) regulates hepatocyte growthn. However, its involvement during hepatic fibrosis remains unclear.</p><p><strong>Methods: </strong>Isolation of ADMSCs and Exo, transfection of HGF overexpression, and activation of hepatic stellate cells (HSCs) by Angiotensin II (AngII) were conducted. Cells were randomized into HSC, AngII-HSC, ADMSCs-Exo, ADMSCs<supblank</sup>-Exo, and ADMSCs<sup>HGF</sup-Exo, DPI, LY294002, and SB203580 groups. MTT for cell viability, cell migration, and flow cytometry for ROS were performed. BALB/c mice were treated with CCL4 for hepatic fibrosis models. The mice were randomized into Control, PBS, ADMSCs-Exo, ADMSCs^blank-Exo, and ADMSCs^HGF-Exo groups (n=6). HE, Sirius red, and Oil Red O staining, liver function indicators, and ELISA for oxidative stress were performed. ROS generation-related and PI3K/Akt/P38MAPK-related factors were detected by immunofluorescence, immunohistochemistry, and western blot.</p><p><strong>Results: </strong>After identification of ADMSC-Exo and transfection, AngII increased cell viability, migration, Collagen I (CoLI), α-smooth muscle actin (α-SMA), ROS, NADPH oxidase 4 (NOX4), PI3K, p-Akt, p-P38MAPK, ras-related C3 botulinum toxin substrate 1 (RAC1), p47^phox, and p22^phox expression. However, ADMSCs^HGF-Exo, DPI, LY294002, and SB203580 reversed the above effects. Moreover, ADMSCs^HGF-Exo inhibited pathological damage, fibrosis, lipid accumulation, ALT, AST, TBIL, CoLI, α-SMA, NOX4, MDA, PI3K, p-Akt, and p-P38MAPK expression, and increased ALB, SOD, GPx, CAT, GSH, Mn-SOD, Na⁺-K⁺-ATPase, and Ca²⁺-Mg²⁺-ATPase levels in hepatic fibrosis mice.</p><p><strong>Conclusion: </strong>ADMSCs^HGF-Exo attenuated hepatic fibrosis by inhibiting oxidative stress through activating the PI3K/Akt/P38MAPK pathway, providing valuable insights for potential treatment of liver fibrosis.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18816"},"PeriodicalIF":2.5,"publicationDate":"2024-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142464133","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Progress on three-dimensional visualizing skin architecture with multiple immunofluorescence staining and tissue-clearing approaches.","authors":"Yuqing Wang, Wanzhu Bai, Xiaoyu Wang","doi":"10.14670/HH-18-815","DOIUrl":"https://doi.org/10.14670/HH-18-815","url":null,"abstract":"<p><p>The skin forms the external covering of the body and is its largest organ, comprising many different cell types. Although the diversity of these cells has been widely studied with various histological methods, our understanding of skin architecture is mainly established on thin tissue sections, which restricted the information available to two dimensions. The development of innovative techniques to induce optical transparency (\"clearing\") in biological tissues has enabled researchers to visualize the three-dimensional reconstruction of intact organs and thick tissue sections at a cellular resolution. With the aid of tissue-clearing treatment, the labeled cutaneous nerve fibers and blood vessels can be followed for a longer distance on the thicker skin section or the whole mount skin under a fluorescence microscopy or a confocal microscopy. It is beneficial for demonstrating the morphological characteristics of nerve fibers and blood vessels themselves, as well as their spatial interconnection. In this review, we provide a brief summary of the literature on the use of tissue optical clearing methods and describe our experience of multiple fluorescent staining and tissue clearing approaches on thicker skin sections and whole-mount skin in our laboratory. Given the existing conventional methods, we expected to provide a more effective approach to comprehensively study skin architecture.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18815"},"PeriodicalIF":2.5,"publicationDate":"2024-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142400197","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Melatonin protects against sarcopenia in middle-aged mice.","authors":"Fei Fang, Ping Yu, Xiaoying Sun, Zhixing Shen, Fan Zhang, Jianwei Sun","doi":"10.14670/HH-18-814","DOIUrl":"https://doi.org/10.14670/HH-18-814","url":null,"abstract":"<p><strong>Background: </strong>Sarcopenia is a common age-related disease. Melatonin (MEL) is an age-related endocrine hormone, which displays a crucial role in resisting oxidative stress during aging. Importantly, the antioxidant properties of MEL can be mediated by mitochondria.</p><p><strong>Objective: </strong>Therefore, we wondered whether MEL could mitigate oxidative stress caused by mitochondria in sarcopenia.</p><p><strong>Methods: </strong>The middle-aged mice were administered 5 mg/kg/d and 10 mg/kg/d of MEL for 2 months. Young mice were used as the control group.</p><p><strong>Results: </strong>After treatment with MEL, the grip strength of the fore/hind limbs, running time, and distance were elevated, and the weights of the gastrocnemius (GA), tibialis anterior (TA), extensor digitorum longus (EDL), and soleus (SOL) were enhanced in middle-aged mice. Additionally, MEL was observed to alleviate histological damage and increase the cross-sectional area of muscle fibers in GA tissues of middle-aged mice. Furthermore, following MEL treatment, there was an increase in the percentage and size of normal mitochondria as well as mtDNA copy number but a reduction in the levels of malondialdehyde (MDA), protein carbonyl, and reactive oxygen species (ROS) in the GA tissues of middle-aged mice. At the molecular level, MEL repressed the levels of ATROGIN-1, muscle RING-finger protein-1 (MURF-1), and the ratio of p-P38/P38, but elevated the expression of cytochrome c oxidase subunit 4 (COX4), cystatin C (CYTC), nuclear respiratory factor 1 (NRF-1), mitochondrial transcription factor A (TFAM), and peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) in the GA tissues of middle-aged mice. Importantly, 10 mg/kg MEL was more efficacious in the treatment of sarcopenia than 5 mg/kg MEL.</p><p><strong>Conclusion: </strong>MEL attenuates sarcopenia in middle-aged mice, and the mechanism may relate to mitochondria-induced oxidative stress and the PGC-1α/TFAM pathway.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18814"},"PeriodicalIF":2.5,"publicationDate":"2024-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142390197","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanism of KMT2D-mediated epigenetic modification in IL-1β-induced nucleus pulposus cell degeneration.","authors":"Hongjiang Liu, Haiquan Liu, Zuyu Meng, Wensheng Zhang","doi":"10.14670/HH-18-813","DOIUrl":"https://doi.org/10.14670/HH-18-813","url":null,"abstract":"<p><strong>Background: </strong>Intervertebral disc (IVD) degeneration (IVDD) is characterized by structural destruction accompanied by accelerated signs of aging. This study aimed to investigate the mechanism of lysine methyltransferase 2D (KMT2D) in the proliferation, apoptosis, and inflammation of nucleus pulposus cells (NPCs) in IVDD.</p><p><strong>Methods: </strong>Mouse-derived NPCs were cultured and induced with interleukin-1 beta (IL-1β) to establish cell models. KMT2D expression was detected by western blot and reverse transcription-quantitative polymerase chain reaction (RT-qPCR). KMT2D expression was interfered with, and the contents of IL-18, IL-6, and tumor necrosis factor (TNF) were detected by enzyme-linked immunosorbent assay. Cell proliferation, apoptosis, and the expression of miR-133a-5p and 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 2 (PFKFB2) were measured. The enrichment of KMT2D and Histone 3 Lysine 4 monomethylation/dimethylation (H3K4me1/2) on the miR-133a-5p promoter was analyzed by chromatin immunoprecipitation and qPCR. The binding of miR-133a-5p and PFKFB2 was analyzed by a dual-luciferase assay.</p><p><strong>Results: </strong>IL-1β treatment promoted KMT2D expression in NPCs. KMT2D knockdown reduced inflammation and apoptosis and promoted the proliferation of IL-1β-induced NPCs. Mechanistically, KMT2D upregulated miR-133a-5p expression by increasing the level of H3K4me2 at the miR-133a-5p promoter, thereby promoting the binding between miR-133a-5p and PFKFB2 and downregulating the transcription of PFKFB2. miR-133a-5p overexpression or PFKFB2 knockdown alleviated the protective effect of KMT2D knockdown on IL-1β-induced NPCs.</p><p><strong>Conclusion: </strong>KMT2D promoted miR-133a-5p expression through H3K4me2 methylation, thereby promoting the binding of miR-133a-5p to PFKFB2, reducing the mRNA level of PFKFB2, promoting inflammation and apoptosis of IL-1β-induced NPCs, and inhibiting NPC proliferation.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18813"},"PeriodicalIF":2.5,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142390196","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ABRACL upregulated by transcription factor CBX4 promotes proliferation and migration and inhibits the apoptosis of gastric cancer cells.","authors":"Kai Guo, Xiao Gao","doi":"10.14670/HH-18-812","DOIUrl":"10.14670/HH-18-812","url":null,"abstract":"<p><strong>Background: </strong>Gastric cancer (GC) is a predominant health concern in many countries. Actin-binding Rho activating C-terminal-like (ABRACL) belongs to a new family of low molecular weight proteins and has been implicated in cancers. This study was implemented to elucidate the role and mechanism of ABRACL in GC.</p><p><strong>Methods: </strong>mRNA and protein expression of ABRACL and CBX4 in human gastric epithelium cell line GES-1 and GC cell lines were assessed with RT-qPCR and western blot. The transfection efficacy of sh-ABRACL, oe-CBX4, and sh-CBX4 was examined with RT-qPCR and western blot. AGS cell proliferation, migration, and invasion were evaluated using CCK-8, colony formation assay, wound healing, and Transwell assays, respectively. With western blot analysis, flow cytometry, and caspase-3 assay kits, the expressions of MMP2 and MMP9, cell apoptosis, and caspase-3 activity were estimated. Western blot was adopted to estimate the contents of apoptosis-related proteins. Luciferase reporter and chromatin immunoprecipitation (ChIP) were applied to verify the interaction between ABRACL and CBX4.</p><p><strong>Results: </strong>The expression of ABRACL and CBX4 was increased in GC tissues and cells. After interfering with ABRACL, the proliferation, migration, and invasion of GC cells were inhibited while apoptosis was promoted. We also discovered that CBX4 could bind to ABRACL and transcriptionally regulate ABRACL expression in AGS cells. Rescue experiments revealed that CBX4 overexpression partially reversed the regulatory effects of ABRACL silencing on the proliferation, migration, invasion, and apoptosis of GC cells.</p><p><strong>Conclusion: </strong>Collectively, ABRACL transcriptionally upregulated by CBX4 promoted the malignant progression of GC.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18812"},"PeriodicalIF":2.5,"publicationDate":"2024-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142390181","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Morphologic and molecular diagnostic criteria of malignancies in biliary strictures.","authors":"Elisa Albertini, Lucia Miranda, Thais Maloberti, Dario de Biase, Francesco Vasuri","doi":"10.14670/HH-18-811","DOIUrl":"https://doi.org/10.14670/HH-18-811","url":null,"abstract":"<p><p>The differential diagnosis of benign and malignant biliary strictures is not always feasible and still represents a major diagnostic challenge, mainly due to the scarcity of the tissue retrieved for proper cytological or histopathological diagnosis. The present review focuses on morphological criteria in the diagnosis of biliary strictures, in the course of primary sclerosing cholangitis and other pathologies, starting from the limits of the cytological and histological evaluation, as well as the ancillary methodologies currently available in Pathology laboratories The current guidelines suggest fluorescence in situ hybridization for the analysis of chromosomes 3, 7, and 17 polysomies and deletion of the 9p21 locus; however, other more promising techniques are on the horizon for both patient care and research purposes, such as Next-Generation Sequencing, able to analyze multiple genes simultaneously in a cost-effective fashion. Lastly, the most recent approaches proposed in the literature for the differential diagnosis of biliary stricture are described, such as circulating tumor DNA, miRNAs, and DNA methylation, among others.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18811"},"PeriodicalIF":2.5,"publicationDate":"2024-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142390198","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CRISPR-mediated WNK4 point mutation aggravates tumor progression and weakens chemotherapy sensitivity in gastric cancer.","authors":"Xiaojun Ying, Zhen Ying, Xiaobing Gao, Yong Wang, Xinting Lv","doi":"10.14670/HH-18-810","DOIUrl":"https://doi.org/10.14670/HH-18-810","url":null,"abstract":"<p><strong>Objective: </strong>Gastric cancer (GC) is the fifth most common malignancy, the molecular targets of which have been increasingly explored in recent years. As a serine/threonine protein kinase, the role of WNK lysine deficient protein kinase 4 (WNK4) in GC was clarified in this study.</p><p><strong>Methods: </strong>Human GC lines AGS and MKN45 were stably transfected with a WNK4 mutant constructed by the CRISPR/Cas9 method and treated with cis-dichlorodiammine platinum (CDDP, 2 μg/mL) and 5-fluorouracil (5-FU, 5 μg/mL) for 48h. Tumor-bearing mice were established with 5×10⁶ mutant-type AGS cells, and injected with 40 mg/kg WP1066, the inhibitor of signal transducer and activator of transcription 3 (STAT3), for 21 days. Cell malignant potential and tumor growth were assessed. STAT3 activation was identified by western blot and immunohistochemistry. The interaction between WNK4 and STAT3 was determined using co-immunoprecipitation and immunofluorescence co-localization.</p><p><strong>Results: </strong>WNK4 mutation promoted proliferation and invasion, and upregulated the p-STAT3/STAT3 value in GC cells with/without 5-FU and CDDP treatments, while inhibiting apoptosis of GC cells without drug treatment. In tumor-bearing mice, WNK4 mutation accelerated tumor growth, increased levels of p-STAT3, STAT3, and p-STAT3/STAT3, and strengthened the co-immunoprecipitation and co-localizing with STAT3; however, these effects were reversed by WP1066 treatment.</p><p><strong>Conclusion: </strong>Through activating STAT3, WNK4 mutation impacts both the natural and drug-treated growth of GC cells or tumors, suggesting a new avenue for preclinical research.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18810"},"PeriodicalIF":2.5,"publicationDate":"2024-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142371657","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tetrahydropalmatine promotes macrophage autophagy by inhibiting the AMPK/mTOR pathway to attenuate atherosclerosis.","authors":"Hui Wang, Ke Ding, Jiaqi He, Jiahong Wang","doi":"10.14670/HH-18-809","DOIUrl":"10.14670/HH-18-809","url":null,"abstract":"<p><strong>Background: </strong>Atherosclerosis (AS) is a chronic progressive arterial disease that is associated with macrophage autophagy and AMP-activated protein kinase (AMPK)/mechanistic target of the rapamycin (mTOR) pathway. Tetrahydropalmatine (THP) can activate AMPK-dependent autophagy. We aim to study the mechanism of macrophage autophagy mediated by THP in the treatment of AS via the AMPK/mTOR pathway.</p><p><strong>Methods: </strong>High-fat diet apolipoprotein E-deficient mice and ox-LDL-induced RAW264.7 cells were used to mimic the AS model, then THP was administered. Cell viability was detected by MTT. Pathological aorta lesions were detected using Hematoxylin and Eosin, Masson, and oil red staining. Lipid metabolism indices and inflammatory factors were measured using ELISA. A transmission electron microscope was used to observe autophagosomes. Autophagy and AMPK/mTOR pathway protein expression was detected by immunofluorescence and Western blot. The AMPK inhibitor 9-β-d-Arabinofuranosyl Adenine (Ara-A) was used to validate the effect of THP. The mRNA expression of <i>Beclin-1</i> and <i>MCP-1</i> was detected by q-PCR.</p><p><strong>Results: </strong>THP administration regulated lipid metabolism by lowering total cholesterol, triacylglycerol, low-density lipoprotein, and high-density lipoprotein levels, and suppressed aortic damage. THP suppressed aortic damage and regulated lipid metabolism by altering serum lipid levels. THP reduced inflammation and macrophage CD68 expression. Twenty μg/mL THP reduced cell viability. THP decreased cholesterol uptake and increased efflux, promoting autophagy. THP increased autophagosome number, LC3B expression, and autophagy markers p-AMPK/AMPK and LC3-II/LC3-I. THP also decreased p-mTOR/mTOR and P62. THP increased <i>Beclin-1</i> mRNA expression and decreased <i>MCP-1</i> mRNA expression. Ara-A reversed THP's effects.</p><p><strong>Conclusion: </strong>THP promotes macrophage autophagy by inhibiting the AMPK/mTOR pathway to attenuate AS.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18809"},"PeriodicalIF":2.5,"publicationDate":"2024-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142365102","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Morphological features and genetic background in ectomesenchymal chondromyxoid tumor: A systematic review.","authors":"Raquel Helena Junia de Souza, Fernanda Aragão Felix, Flávia Martins Vasconcelos Filiú, Witalo Pereira de Jesus, Felipe Paiva Fonseca, Ricardo Santiago Gomez, Lucas Guimarães Abreu, Sílvia Ferreira de Sousa","doi":"10.14670/HH-18-808","DOIUrl":"https://doi.org/10.14670/HH-18-808","url":null,"abstract":"<p><strong>Background: </strong>Ectomesenchymal chondromyxoid tumor (EMCMT) is a rare neoplasm that mainly affects the tongue and harbors recurrent, although not exclusive, gene fusions. Owing to its rarity, overlapping features with other tumors may lead to challenges in the microscopic diagnosis. We aimed to perform a systematic review focusing on the histomolecular findings of EMCMT of the oral and maxillofacial region and to evaluate the possible association between microscopic features with the genetic background.</p><p><strong>Methods: </strong>An electronic search was made on PubMed, Web of Science, Scopus, Ovid, and Embase. Clinicopathological, immunohistochemical, and molecular data were retrieved.</p><p><strong>Results: </strong>Overall, 114 cases from 53 articles on EMCMT were analyzed. Histologically, EMCMT was described as demarcated (84.2%), lobulated (66.7%), reticulated (51.8%), and arranged in sheets, cords, and strands (42.9%), with 73.7% of lesions with spindle-shaped cells. Myxoid stroma (88.6%), chondroid areas (60.5%), chondromyxoid stroma (57.0%), and fibrous septae (42.9%) were also tumor-outlined features. The most expressed markers were vimentin (100.0%), cyclin D1 (100.0%), GFAP (88.5%), NSE (87.5%), S100 (86.5%), CD56 (76.9%), and CD57 (76.5%). The <i>RREB1-MRTFB</i> fusion was detected in 91.0% of the cases investigated and <i>EWSR1</i> rearrangements in 17.4%. The presence of the fusion <i>RREB1::MRTFB</i> or chromosome alterations in the <i>EWSR1</i> gene were not highly specific to the morphological features of EMCMT.</p><p><strong>Conclusion: </strong>This study provides a comprehensive summary of the clinicopathological, immunohistochemical, and molecular characteristics of EMCMT, aiding in a more accurate microscopic diagnosis of this rare tumor.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18808"},"PeriodicalIF":2.5,"publicationDate":"2024-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142345763","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}