Histology and histopathology最新文献

{"title":"Xinnaotongluo liquid protects H9c2 cells against hypoxic damage through IRF2/HIF-1α-mediated oxidation, inflammation, and apoptosis.","authors":"Jiankun Cui, Hui Liu, Yanmei Feng","doi":"10.14670/HH-18-855","DOIUrl":"https://doi.org/10.14670/HH-18-855","url":null,"abstract":"<p><p>Myocardial ischemia is the primary reason for ischemic heart disease. Xinnaotongluo liquid has been reported to have an improving effect on cardiovascular diseases. In our study, we detected the effects of Xinnaotongluo liquid on H9c2 cell oxidation, inflammation, and apoptosis induced by hypoxia stimulation. H9c2 cells were exposed to hypoxia and/or Xinnaotongluo liquid stimulation. Cell viability, oxidation, inflammation, and apoptosis, along with HIF-1α expression were measured. Subsequently, si-HIF-1α was transfected into H9c2 cells to detect whether HIF-1α depletion was involved in the effect of Xinnaotongluo liquid on H9c2 cells stimulated by hypoxia. Then, the regulatory effect of IRF2 on HIF-1α was detected. Hypoxia exposure induced H9c2 cell viability reduction, oxidation, inflammation, and apoptosis. Xinnaotongluo liquid alleviated the H9c2 cell viability reduction, oxidation, inflammation, and apoptosis induced by hypoxia. HIF-1α was activated in hypoxia-exposed H9c2 cells, and the knockdown of HIF-1α strengthened the effects of Xinnaotongluo liquid on hypoxia-exposed H9c2 cells. Additionally, HIF-1α was transcriptionally regulated by IRF2, and IRF2 was associated with the upregulation of HIF-1α in hypoxia-exposed H9c2 cells. Xinnaotongluo liquid alleviated H9c2 cell apoptosis and inflammation induced by hypoxia, which might be achieved by regulating IRF2/HIF-1α expression.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18855"},"PeriodicalIF":2.5,"publicationDate":"2024-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142846577","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":"Effects of combustible cigarettes and electronic nicotine delivery systems on the regenerative properties of mesenchymal stem cells derived from periodontal ligament (PDL-MSCs).","authors":"Nikolina Kastratovic, Olivera Milosevic-Djordjevic, Carl Randall Harrell, Valentin Djonov, Vladislav Volarevic","doi":"10.14670/HH-18-854","DOIUrl":"https://doi.org/10.14670/HH-18-854","url":null,"abstract":"<p><strong>Introduction: </strong>Periodontal ligament-derived mesenchymal stem cells (PDL-MSCs) are promising cells with crucial roles in maintaining and repairing periodontal tissue. However, their regenerative capacity can be influenced by various factors, including cigarette smoke and electronic nicotine delivery system (ENDS) aerosols. Smoking and vaping can impair their regenerative potential, and even though ENDS are perceived as safer tobacco products, there is a lack of evidence to guarantee this assumption.</p><p><strong>Material and methods: </strong>Changes in the viability and proliferation of PDL-MSCs will be investigated after smoke and aerosol generation and cell exposure. In addition, the effects of smoke and aerosols on the immunomodulatory capacity of PDL-MSCs co-cultured with T lymphocytes will be further determined via the evaluation of cytokine profiles and flow cytometry analysis of T-cell phenotypes.</p><p><strong>Results: </strong>Combustible cigarettes (CCs) induced more severe impairment in the viability and proliferation of PDL-MSCs compared with ENDS. Also, CCs promoted a proinflammatory immune response that could cause tissue damage to progress. On the other hand, ENDS had the potential to generate an immunosuppressive response that would prevent further cell decay.</p><p><strong>Discussion: </strong>The regenerative capacity of PDL-MSCs decreased after treatment with both cigarette smoke and ENDS-aerosols. Even though the results demonstrate less severe effects with ENDS, further research is essential to evaluate their safety and impact on the capacity of PDL-MSCs to prevent and restore oral injuries caused by chronic exposure to aerosols.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18854"},"PeriodicalIF":2.5,"publicationDate":"2024-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142835530","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":"Tumor necrosis factor receptor-associated protein 1 promotes aerobic glycolysis and cisplatin resistance by regulating the Wnt/β-catenin signaling pathway in lung cancer.","authors":"Ruijie Li, Mengguo Lv, Juan Liu, Qian Sun","doi":"10.14670/HH-18-853","DOIUrl":"https://doi.org/10.14670/HH-18-853","url":null,"abstract":"<p><p>In this study, we investigated the effects of tumor necrosis factor receptor-associated protein 1 (TRAP1) on aerobic glycolysis in cisplatin-resistant lung cancer cells and explored the underlying mechanism. TRAP1 expression levels were determined in cisplatin-resistant lung cancer tissues and A549/CDDP cells. Subsequently, TRAP1 expression in A549/CDDP cells was silenced via small interfering RNA transfection. Moreover, changes in lactate content, glucose consumption, expression levels of lactate dehydrogenase A (LDHA), hexokinase 2 (HK2), and pyruvate kinase M2 (PKM2), and sensitivity to cisplatin were analyzed. Specifically, the Wnt/β-catenin signaling pathway was examined using the Wnt/β-catenin activator, BML-284. TRAP1 expression levels were higher in cisplatin-resistant tissues and A549/CDDP cells than in cisplatin-sensitive tissues and A549 cells (<i>P</i><0.05). Moreover, the lactate content, glucose consumption, LDHA, HK2, PKM2 expression levels, and half-maximal inhibitory concentration of cisplatin were all significantly decreased after <i>TRAP1</i> silencing (<i>P</i><0.05). Compared with A549 cells, the Wnt/β-catenin pathway was activated in A549/CDDP cells, which was inhibited via <i>TRAP1</i> silencing. BML-284 reversed the effects of <i>TRAP1</i> silencing on the aerobic glycolysis and cisplatin sensitivity of A549/CDDP cells. Our findings suggest that TRAP1 affects the cisplatin resistance of lung cancer, possibly by regulating aerobic glycolysis via the Wnt/β-catenin pathway.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18853"},"PeriodicalIF":2.5,"publicationDate":"2024-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142828393","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":"Modulation of the malignant behavior of tongue squamous cell carcinoma cells by matrix metallopeptidase 25 through the NF-κB pathway.","authors":"Shuang Bai, Shao-Kang Sun, Zhen-Qi Xu, Ying-Bin Yan","doi":"10.14670/HH-18-852","DOIUrl":"https://doi.org/10.14670/HH-18-852","url":null,"abstract":"<p><strong>Objective: </strong>Accumulating evidence has implicated matrix metalloproteinases (MMPs) in the progression of human cancers. Matrix metallopeptidase 25 (MMP25) is a membrane-type MMP whose role in tumorigenesis and cancer development is not well understood. Here, we investigated the functions of MMP25 in tongue squamous cell carcinoma (TSCC).</p><p><strong>Methods: </strong>Gene expression was measured using real-time PCR and western blot. CCK-8 and Transwell assays were used to determine the proliferation, migration, and invasion of TSCC cells. An NK cell co-culture experiment was performed to evaluate the killing of TSCC cells by NK cells.</p><p><strong>Results: </strong>MMP25 had higher expression levels in TSCC tissues than in adjacent non-cancerous tissues. MMP25-overexpressing and MMP25-silenced TSCC cell lines were established by lentiviral transduction. Overexpression of MMP25 promoted proliferation, migration, and invasion of TSCC cells, whereas knockdown of MMP25 had opposite effects. MMP25 modulated the levels of proliferation- and apoptosis-related proteins (PCNA, cyclin D, cyclin B1, p27, and cleaved caspase 3 and 9) and upregulated two invasion-related MMPs (mature MMP2 and MMP9). Additionally, MMP25 promoted tumor growth of TSCC cells in athymic nude mice. Notably, MMP25 upregulated PD-L1 in TSCC cells, attenuated NK cell killing of TSCC cells, and inhibited the secretion of anti-tumor cytokines (TNF-α and IFN-γ). Furthermore, MMP25 promoted the nuclear translocation of NF-κB p65, suggesting that activation of NF-κB signaling may mediate the pro-tumor functions of MMP25 in TSCC.</p><p><strong>Conclusion: </strong>This study revealed a novel role for MMP25 in TSCC, highlighting the potential of MMP25 as a therapeutic target in TSCC.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18852"},"PeriodicalIF":2.5,"publicationDate":"2024-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142817920","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":"The prognostic value of H3 K27me3 in meningiomas: A review on current evidence and methodological challenges.","authors":"Alberto Pietrantoni, Valeria Barresi","doi":"10.14670/HH-18-851","DOIUrl":"https://doi.org/10.14670/HH-18-851","url":null,"abstract":"<p><p>Meningiomas are the most common primary intracranial neoplasms. Although they mostly exhibit a benign course, some cases recur after surgery and show high morbidity and mortality rates. In addition to currently established prognostic factors, such as the extent of surgical resection and tumor grade assessed according to World Health Organization (WHO) criteria, the prognostic significance of the immunohistochemical loss of Histone 3 trimethylation in Lysine 27 (H3 K27me3) has emerged in meningiomas. This review examined original studies that analyzed the immunohistochemical expression of H3 K27me3 in meningiomas and its correlation with various features, including overall survival (OS), recurrence-free survival (RFS), and WHO grade. A literature search was conducted in PubMed for English-language publications up to July 8, 2024. Sixteen studies were included in this review. In summary, current evidence indicates that H3 K27me3 loss is more frequent in tumors exhibiting higher biological aggressiveness, as reflected by a significant association with a higher WHO grade, proliferative index, and prognostically unfavorable methylation classes. In addition, published studies consistently indicate a negative prognostic significance for progression-recurrence-free survival (PFS/RFS) in WHO grade 2 meningiomas and OS in WHO grade 3 tumors. However, the lack of a standardized definition for H3 K27me3 loss significantly hampers the incorporation of the H3 K27me3 immunohistochemical assay into routine practice to establish the prognosis of meningiomas.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18851"},"PeriodicalIF":2.5,"publicationDate":"2024-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142812931","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 inhibits the activation of microglia and cough sensitivity of guinea pigs exposed to PM2.5.","authors":"Shu Zhang, Li Long, Senlin Chai, Mingtong Lin, Hankun Lu, Xuemei Liu, Yaowei He, Rong Dong, Zhe Chen","doi":"10.14670/HH-18-850","DOIUrl":"https://doi.org/10.14670/HH-18-850","url":null,"abstract":"<p><strong>Objective: </strong>The study aimed to examine the impact of melatonin on mitigating brain inflammation and cough sensitivity resulting from exposure to particulate matter 2.5 (PM2.5).</p><p><strong>Methods: </strong>Guinea pigs were randomly assigned to the blank control group, normal saline group, PM2.5 exposure group, and PM2.5 exposure + melatonin group. The PM2.5 exposure and PM2.5 exposure + melatonin groups were given intranasal instillations of PM2.5 suspension twice daily for 28 consecutive days. Starting on day 21, the PM2.5 exposure + melatonin group was treated with an intraperitoneal injection of melatonin at 10 pm. Cough sensitivity to citric acid, microglia activation, IL-1β and TNF-α levels in the airway and dorsal vagal complex (DVC), and ultrastructural changes in neurons within the DVC were assessed.</p><p><strong>Results: </strong>The PM2.5 exposure group exhibited a significantly higher cough count to citric acid challenge (29.1±5.7 coughs) compared with the PM2.5 exposure + melatonin group (18.8±4.1 coughs), normal saline group (8.4±2.1 coughs), and blank control group (7.7±1.8 coughs). In addition, cough latency was shorter in the PM2.5 exposure group (26.9±6.5 seconds) than in the PM2.5 exposure + melatonin group (36.6±12.4 seconds), normal saline group (43.4±14.7 seconds), and blank control group (47.0±13.0 seconds). The PM2.5 exposure + melatonin group showed significantly reduced IL-1β (105.3±14.3 pg/ml) and TNF-α levels (113.0±23.5 pg/ml) in the DVC, as well as in the bronchoalveolar lavage fluid (IL-1β: 24.92±5.14 pg/ml, TNF-α: 12.72±3.99 pg/ml) compared with the PM2.5 exposure group (in the DVC: IL-1β: 132.7±17.6 pg/ml, TNF-α: 143.8±30.4 pg/ml; in the bronchoalveolar lavage fluid: IL-1β: 34.0±5.3 pg/ml; TNF-α: 15.8±0.8 pg/ml). Microglia in the DVC were less activated in the PM2.5 exposure + melatonin group (25.1±5.4) than in the PM2.5 exposure group (54.6±9.9). Furthermore, the PM2.5 exposure group exhibited an impaired blood-brain barrier in the DVC, which tended to alleviate the PM2.5 exposure + melatonin group.</p><p><strong>Conclusions: </strong>Exposure to PM2.5 induces airway inflammation, central facilitation, and heightened cough sensitivity in guinea pigs. Melatonin significantly inhibits microglia activation and reduces airway and DVC inflammation, which might contribute to attenuated cough hypersensitivity.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18850"},"PeriodicalIF":2.5,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142806916","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":"Hsa_circ_0088036 promotes tumorigenesis and chemotherapy resistance in hepatocellular carcinoma via the miR-140-3p/KIF2A axis.","authors":"Zhong Wang, Lei Wang, Guoqing Yin, Heng Li, Rong Zhang, Yuan Feng, Wen Chang","doi":"10.14670/HH-18-849","DOIUrl":"10.14670/HH-18-849","url":null,"abstract":"<p><strong>Background: </strong>Hepatocellular carcinoma (HCC) is a cancer with high morbidity and mortality. There are limited treatment options, particularly for chemotherapy-resistant HCC patients. Circular RNA hsa_circ_0088036 was associated with the development of bladder cancer and non-small cell lung cancer. However, whether it might be a potential therapeutic target for HCC remains elusive.</p><p><strong>Methods: </strong>Hsa_circ_0088036 expression was detected in HCC tumor tissues and cell lines using real-time PCR. The influences of hsa_circ_0088036 on proliferation and invasion as well as chemotherapy sensitivity in HCC cells were investigated by gain- and loss-of-function analyses. Associations among hsa_circ_0088036, miR-140-3p, and KIF2A were validated by real-time PCR, miRNA pull-down assay, dual-luciferase reporter assay, and western blot. Furthermore, a rescue experiment using KIF2A overexpression was performed to evaluate the regulatory mechanism of hsa_circ_0088036 in HCC cells. Additionally, the effect and mechanism of hsa_circ_0088036 were confirmed in a xenograft mouse model.</p><p><strong>Results: </strong>Hsa_circ_0088036 was highly expressed in HCC tissues and cells, with even higher expression in oxaliplatin-resistant cells. This expression was positively correlated with tumor size and TNM stage of the patients. Overexpression of hsa_circ_0088036 promoted the proliferation and invasion of HCC cells, while silencing mediated the opposite effects. Meanwhile, knockdown of hsa_circ_0088036 enhanced chemotherapy sensitivity, including oxaliplatin, doxorubicin, and sorafenib, in HCC cells. Furthermore, hsa_circ_0088036 silencing inhibited tumor growth and increased oxaliplatin sensitivity <i>in vivo</i>. Mechanically, hsa_circ_0088036 functioned via the miR-140-3p/KIF2A axis with the activation of PI3K/Akt and Notch signaling pathways.</p><p><strong>Conclusions: </strong>Hsa_circ_0088036 promoted HCC tumorigenesis and chemotherapy resistance by activating the PI3K/Akt and Notch pathways through regulating miR-140-3p/KIF2A signaling. Thus, hsa_circ_0088036 may be a potential therapeutic target in chemotherapy-resistant HCC.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18849"},"PeriodicalIF":2.5,"publicationDate":"2024-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142716150","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":"Assessing the expression of Nectin-4 in solid tumors by immunohistochemistry - what do we know?","authors":"Christine Sanders, Glen Kristiansen","doi":"10.14670/HH-18-848","DOIUrl":"https://doi.org/10.14670/HH-18-848","url":null,"abstract":"<p><p>Antibody-Drug Conjugates (ADCs) represent a promising class of anti-cancer substances that combine the specificity of monoclonal antibodies with the potency of cytotoxic drugs, hence they enable a new approach of targeted therapy. The use of the ADC Entfortumab Vedotin (EV), which targets the viral receptor Nectin-4, showed an impressive clinical response in metastatic urothelial carcinoma. In this review, we present what is known about the expression of Nectin-4 in various tumor entities, focusing on immunohistochemistry as a diagnostic venue to detect positive expression, as this inexpensive technique is readily available in pathology laboratories. Various studies demonstrated expression of Nectin-4 in many solid tumor entities with the highest expression rates in urothelial carcinomas and breast cancer. To date, the relevance of the subcellular compartment of immunoreactivity (membranous vs. cytoplasmic) is still unclear in respect of its predictive value for EV therapy, which ought to be clarified in further studies.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18848"},"PeriodicalIF":2.5,"publicationDate":"2024-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142710034","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":"Phosphorylated protein kinase R (PKR)-like endoplasmic reticulum kinase (PERK) expression in breast cancer is correlated with malignant proliferation and histological grading.","authors":"Xiaosi Yang, Shuqiang Duan, Jie Zha, Tao Jiang, Chun Ye, Shuihong Yu","doi":"10.14670/HH-18-847","DOIUrl":"https://doi.org/10.14670/HH-18-847","url":null,"abstract":"<p><p>This study aims to detect the expression of phosphorylated PERK in breast cancer using immunohistochemistry and explore its significance. We examined 134 cases of formalin-fixed and paraffin-embedded breast cancer tissues. It was found that the expression of phosphorylated PERK in ductal carcinoma was higher than that in lobular carcinoma, and the difference between them was statistically significant, suggesting that phosphorylated PERK played different roles in the occurrence and development of different types of breast cancer. Compared with Ki-67-negative breast cancer tissues, phosphorylated PERK has higher expression in Ki-67-positive tissues and is positively correlated with Ki67 expression, indicating that phosphorylated PERK plays an important role in breast cancer's malignant proliferation and progression. We also found a positive correlation between phosphorylated PERK expression and the histological grading of invasive ductal carcinoma, indicating that phosphorylated PERK plays an important role in the differentiation of invasive ductal carcinoma. Our study revealed the differential expression of phosphorylated PERK in subtypes of breast cancer. It contributed to the malignant proliferation of breast cancer and tissue differentiation of invasive ductal carcinoma of the breast.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18847"},"PeriodicalIF":2.5,"publicationDate":"2024-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142686897","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":"Identification of new tissue markers for the monitoring and standardization of penile cancer according to the degree of differentiation.","authors":"Carlos Casanova-Martín, Diego Liviu Boaru, Oscar Fraile-Martinez, Cielo Garcia-Montero, Diego De Leon-Oliva, Patricia De Castro-Martinez, Maria José Gimeno-Longas, Julia Bujan, Natalio García-Honduvilla, Luis G Guijarro, Raquel Gragera, Laura Lopez-Gonzalez, Miguel A Saez, Connie Ferrara-Coppola, Víctor Baena-Romero, Raul Diaz-Pedrero, Melchor Alvarez-Mon, María Val Toledo-Lobo, Miguel A Ortega","doi":"10.14670/HH-18-846","DOIUrl":"https://doi.org/10.14670/HH-18-846","url":null,"abstract":"<p><p>Penile cancer is an uncommon disease compared with other urological tumors and is more common in low- and middle-income countries. Risk factors include age, ethnicity, smoking, hygiene, and human papillomavirus infection. Although carcinoma of the penis can be cured in up to 80% of cases if detected early, late diagnosis drastically reduces survival rates, especially in metastatic cases. More than 95% of cases are squamous cell carcinomas, and the degree of cell differentiation is a key histopathological factor, distinguishing between poorly (P), moderately (M), and well-differentiated (W) carcinomas, with verrucous carcinoma (V) having the best prognosis due to its low metastatic capacity. This study analyses the differential expression of several biomarkers related to cell proliferation and cell cycle, inflammation, epigenetics, and autophagy (cell cycle (IRS-4, Ki-67, RB1, CDK4, cyclin D1, ERBB2, β-catenin, and MAGE-A), inflammation (COX2, NLRP3, and AIF-1), epigenetics (HAT-1) and autophagy (ULK-1 and ATG9A) in penile carcinoma according to the degree of differentiation. Immunohistochemical techniques were performed on 34 penile squamous cell carcinoma (PSCC) samples classified into subtype V (N=6), and groups P (N=9), M (N=9), and W (N=10). The findings suggest a differential expression of molecules according to the degree of cell differentiation, with a higher differential expression of molecules according to the degree of cell differentiation, suggesting that the proteins studied could have predictive value. The study highlights the complexity of PSCC and the need for future studies to explore translational applications and search for new biomarkers to improve clinical management and understanding of this disease.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18846"},"PeriodicalIF":2.5,"publicationDate":"2024-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142728157","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}