Histology and histopathology, Vol.40, Nº11, (2025)

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Open Access
Challenging diagnosis in pulmonary NUT carcinoma: A report of two cases with different histopathologic and molecular features and a novel SPECC1 :: NUTM1 gene fusion
(Universidad de Murcia, Departamento de Histología e Histopatología, 2025) Xie Ling; Chen Jie; Ke Fei; Zheng YanYing; Li Hui; Biología Celular e Histología
Background. NUT carcinoma (NC), formerly known as NUT midline carcinoma, is a rare but highly aggressive cancer. It is a poorly differentiated carcinoma characterized by rearrangements of the NUTM1 (nuclear protein in Testis) gene with a member of the bromodomain-containing protein (BRD) family gene, usually BRD4. There is limited knowledge about primary pulmonary NC till now. It is probably underestimated or underdiagnosed because of its poorly differentiated character, misleading immunophenotype, and wide range of differential diagnoses. Method. We report here two cases of pulmonary NC with different clinicopathological and molecular presentations to draw attention to some atypical clinicopathologic features that can help clinicians and pathologists consider this rare entity. Results. The first case shows a nested pattern with small, uniform, blue epithelioid cells and aberrant expression of neuroendocrine markers, which has a known BRD3::NUTM1 fusion accompanied by a novel IGR (downstream ROR2)::NUTM1 fusion. The second case demonstrates solid sheets and cords of eosinophilic epithelioid-polygonal cells with a mucoid stroma and TTF1 expression, which has a novel SPECC1::NUTM1 gene fusion accompanied by TP53 and JAK1 gene oncogenic variants. Conclusion. As a result, our study contributes to expanding the variant spectrum of the NUTM1 gene. NUT carcinoma with different fusion partners seems to have unique clinicopathological characteristics, yet more cases need to accumulate experience
Open Access
Ion channels and actin: A tale of two friends
(Universidad de Murcia, Departamento de Histología e Histopatología, 2025) Sesti Federico; Forzisi Elena; Biología Celular e Histología
An increasing number of studies highlight ion channels as multifunctional proteins involved in diverse cellular processes, including proliferation, differentiation, adhesion, migration, morphology, and programmed cell death (apoptosis). Given these broad roles, it is not surprising that ion channels interact closely with actin, a ubiquitous cytoskeletal component that participates in a vast array of biological functions. Ion channels depend on the actin cytoskeleton for essential activities such as trafficking to and from the plasma membrane. Conversely, actin dynamics are often modulated by ion channels during various cellular events. In this review, we provide an overview of the field and discuss key examples that reveal emerging patterns in the bidirectional interactions between ion channels and the actin cytoskeleton
Open Access
Histological and transcriptomic analysis of paravaginal and central defects in anterior vaginal wall prolapse: Insights from DeLancey's pelvic floor theory
(Universidad de Murcia, Departamento de Histología e Histopatología, 2025) Zhang Chun; Tang Qingxia; Zhou Yan; Fu Xuemei; Hu Pan; Liu Lubin; Biología Celular e Histología
Background. This study aimed to pre-liminarily explore the differences between paravaginal and central defect types of anterior vaginal wall prolapse based on DeLancey's pelvic floor theory. Methods. Seventy-eight patients with normal, paravaginal, or central defect vaginal wall tissues were collected and stained using hematoxylin and eosin (HE) and immunofluorescence staining to analyze and identify the expression of vimentin and phosphohistone H3 (PH3). Ribonucleic acid from fresh tissues was extracted for transcriptome sequencing to analyze differences between paravaginal and central defect types of anterior vaginal wall prolapse. Results. Significant differences were found in age, menopausal status, body mass index, pregnancy, and delivery among the control, paravaginal, and central defect groups. Histological analysis revealed that the distribution of interstitium in the normal HE staining group was compact and continuous. In the paravaginal defect interstitium, fiber morphology was altered, while central defect interstitial fibers were fragmented. PH3 expression was significantly lower in the central defect type than in the normal and paravaginal defect groups, suggesting degenerative lesions in the vaginal mucosa with central defects. Vimentin distribution in the normal group was tightly packed and continuous, whereas, in the paravaginal defect interstitium, vimentin filaments were fragmented into small spots and micro-aggregates. In the central defect interstitium, vimentin micro-aggregates exhibited altered coalescence and cell shape, appearing punctate. These findings indicated degenerative lesions in the anterior vaginal interstitium of both paravaginal and central defect types. KEGG enrichment analysis of differential genes revealed their involvement in proteinaceous extracellular matrix (ECM)-related signaling pathways, with increased expression of matrix metalloproteinase 13 (MMP13), MMP3, MMP12, and MMP7 in the paravaginal defect type compared with the central defect type. Conclusion. The differences between paravaginal and central defect types of anterior vaginal wall prolapse may be related to the expression of MMP-related proteins; KEGG enrichment analysis of differential genes indicated that they were closely related to the protein ECM pathway. Moreover, delineative lesions appeared in the paravaginal defect interstitium, and degenerative lesions appeared in the central defect mucosa and interstitium, which further enriched the DeLancey three-level theory
Open Access
Extracellular vesicles derived from different brain tissue cells: A potential therapeutic measure for hypoxic-ischemic brain injury in immature brains
(Universidad de Murcia, Departamento de Histología e Histopatología, 2025) Guan Yitong; Yang Lijun; Cui Hong; Biología Celular e Histología
Neonatal hypoxic-ischemic encephalopathy/ neonatal hypoxic-ischemic brain damage and neonatal acute ischemic stroke are common causes of hypoxic-ischemic brain injury (HIBI) in the neonatal period, which may lead to permanent neurological sequelae. It is difficult to distinguish the two in the early stage. As a timely brain protection measure, hypothermia is still the standard treatment, but its efficacy in the treatment of immature brain injury is still controversial. The underlying pathophysiological mechanisms and effective treatment strategies of neonatal HIBI have been an active area of research. Extracellular vesicles (EVs), a class of nanoscale membranous structures, play a critical role in intercellular communication by facilitating the transfer of bioactive molecules or engaging in receptor-mediated interactions. Recent studies have demonstrated that various cell types within brain tissue, including neurons, astrocytes, microglia, endothelial cells, and stem cells, secrete substantial amounts of EVs. These vesicles carry diverse cargo, such as microRNAs, DNA, and proteins, which exert regulatory effects on recipient cells within the brain, thereby mediating neuroprotective effects. These effects include enhancing synaptic plasticity, modulating neuroinflammation, promoting angiogenesis, and regulating cellular autophagy, collectively contributing to neuroprotection. This review aims to summarize the functional characteristics of EVs derived from different cell types within the brain and to highlight recent advancements in this field. By providing insights into the role of EVs in HIBI, it seeks to provide novel insights and references for understanding the pathogenesis of neonatal HIBI and exploring innovative therapeutic approaches
Open Access
PlGF/Flt-1/MMP-1 axis in gingival carcinoma bone invasion
(Universidad de Murcia, Departamento de Histología e Histopatología, 2025) Nguyen Phuong Thao; Miyauchi Mutsumi; Subarnbhesaj Ajiravudh; Ogawa Ikuko; Chea Chanbora; Takata Takashi; Biología Celular e Histología
Background. Gingival squamous cell carcinoma (SCC) frequently invades adjacent bone tissue, leading to significant morbidity and mortality. Understanding the molecular mechanisms driving bone invasion is crucial for developing targeted therapies. We investigated the role of placental growth factor (PlGF) in this process, focusing on its interaction with RANKL and MMP-1. Methods. We examined the role of PlGF in bone invasion of gingival SCC through analysis of patient samples (n=55) and various in-vitro assays, including an in-vitro bone-cell coculture system. We investigated the molecular mechanisms underlying PlGF-mediated bone invasion and its relationship with RANKL and MMP-1 expression. Results. Our findings demonstrate that gingival SCC-secreted PlGF promotes local bone invasion through two possible ways: 1) direct induction of RANKL expression, activating osteoclast formation and bone resorption, and 2) indirect upregulation of RANKL via MMP-1 signaling. PlGF secretion by tumor cells triggered RANKL and MMP-1 production and significantly stimulated migration and osteoclastogenesis (p<0.05). Furthermore, PlGF is highly expressed in gingival SCC and significantly correlated with bone invasion. Finally, we also confirmed the significantly positive correlation between expression levels of MMP-1 with PlGF and Flt-1 expression. Conclusion. This study identifies PlGF as a key regulator of osteoclastogenesis in gingival SCC through both direct and MMP-1-mediated pathways. Therefore, targeting PlGF activity may represent a potential therapeutic strategy for inhibiting bone invasion in gingival SCC
Open Access
Astragaloside IV suppression of chronic atrophic gastritis by upregulating PAR-1 in vitro and in vivo
(Universidad de Murcia, Departamento de Histología e Histopatología, 2025) Duan Bensong; Bao Zhewei; Yang Jingya; Wang Zhenzhen; Li Aoxiang; Yang Jin; Lv Mengke; Zhang Haibin; Biología Celular e Histología
Background. Astragaloside IV (AS-IV) has demonstrated a protective effect against gastrointestinal tract injury induced by various factors. However, its potential mechanism against chronic atrophic gastritis (CAG) remains unknown. Purpose. The objective of the present study was to investigate the impact of AS-IV on CAG and elucidate its molecular mechanism. Methods. The mRNA and protein levels of protease-activated receptor-1 (PAR-1) and related proteins were assessed using reverse transcription-polymerase chain reaction and western blot analyses, respectively. In addition, the levels of inflammatory factors were measured via enzyme-linked immunosorbent assay in GES-1 cells following treatment with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). The CAG model was established in rats induced with MNNG and concurrently treated with AS-IV for 10 weeks. Subsequently, serum samples were collected to assess the expression levels of proteins reflecting inflammatory markers. The gastric tissue sections were used for hematoxylin and eosin staining, immunohistochemical analysis, and the assessment of p-NF-κB p65 and PAR-1 signaling. Results. In-vitro experiments demonstrated that the mRNA levels of PAR-1 were upregulated following treatment with AS-IV and MNNG. Conversely, inhibition of PAR-1 expression reversed the therapeutic effects of AS-IV on MNNG-treated GES-1 cells, leading to increased expression of cyclooxygenase-2 and p-NF-κB p65. In addition, PAR-1 inhibition notably reversed MNNG-induced inflammatory factors, including IL increase. In-vivo experimental validation further confirmed that the upregulation of PAR-1 expression following treatment with AS-IV exerted a protective effect on the gastric mucosa of CAG rats. Conclusion. In conclusion, the findings of the present study suggested that AS-IV exhibited therapeutic efficacy against CAG induced by MNNG; its mechanism may be closely associated with the thrombin/PAR-1 signaling pathway. The present study provides a theoretical foundation for further exploration of the pharmacological effects of AS-IV on the treatment of human CAG
Open Access
Chelerythrine-mediated targeting of NF-κB and Nrf2 pathways alleviates liver injury in a carbon tetrachloride-induced liver fibrosis mouse model
(Universidad de Murcia, Departamento de Histología e Histopatología, 2025) Ding Yisong; Li Xiaoming; Qi Ruixing; Su Yingshi; Wang Xiaoli; Biología Celular e Histología
Background and Aims. This study aimed to investigate the mechanism and efficacy of chelerythrine (CHE) in treating carbon tetrachloride (CCl4)-induced liver fibrosis, with a particular focus on the nuclear factor-erythroid-related factor-2 (Nrf2) and nuclear factor-kappa-B (NF-κB) signaling pathways. Methods. Mice were induced with CCl4 for eight weeks and categorized into the control group, CCl4 model group, and CHE low (7 mg/kg/d, ig,), medium (14 mg/kg/d, ig), and high-dose (28 mg/kg/d, ig) groups with 10 animals in each group. Following CHE treatment, liver sample morphology was assessed using multiple immunohistochemistry, and serum biochemical indicators were measured. ELISA was used to determine IL-10, IL-1β, and TNF-α contents. Western blotting and RT-PCR were employed to analyze protein and mRNA levels of α-SMA, Col-I, fibronectin, Nrf2, HO-1, NQO1, GCLc, GCLm, NF-κB, p-NF-κB, IκBα, and p-IκBα. Nrf2 knockout mice were used to assess the impact of CHE on the Nrf2 signaling pathway. Results. The findings demonstrated that CHE significantly ameliorated oxidative damage, inflamma-tory response, and liver fibrosis in CCl4-induced mice. CHE treatment increased Nrf2 expression and its target proteins, including HO-1 and GCLc, an effect not observed in Nrf2 knockout mice. In addition, CHE reduced NF-κB expression levels. Conclusions. These results suggest that CHE can alleviate liver fibrosis in CCl4-induced mice by modulating NF-κB/IκBα and Nrf2 signaling pathways. These findings propose CHE as a potential novel anti-liver fibrosis drug
Open Access
Sheng-Jiang-Yi-You decoction inhibits the inflammatory response by down-regulating the p38MAPK signaling pathway to alleviate Helicobacter pylori-associated gastritis
(Universidad de Murcia, Departamento de Histología e Histopatología, 2025) Li Ze; Chen Ruirui; Tang Weihong; Zheng Xiaoya; Jin Xuefeng; Wang Zhongmin; Wu Qiao; Biología Celular e Histología
Background. Helicobacter pylori (HP)-associated gastritis is an important factor in development of stomach cancer. Components of Sheng-Jiang-Yi-You decoction (SJYYD) exert gastroprotective effects. However, the effects and mechanism of SJYYD in HP-associated gastritis remain uncertain. Methods. HP bacterial solution (1×109 CFU/mL) was gavaged every other day for 14 days to construct an HP-associated gastritis mouse model. Male BALB/c mice were randomized into Sham, HP, HP+Standardized triple therapy (HP+Triplet), HP+SJYYD (0.4 mL/20 g), HP+Triplet+SJYYD, HP+anisomycin (ANI) (2.5 mg/kg/d, p38MAPK agonist, HP+ANI), and HP+ SJYYD+ANI groups (n=6). Gastric mucosal injury detection and rapid urease test for HP infection were conducted. HE staining for pathological damage and ELISA for pro-inflammatory factors and immuno-globulin G (IgG) content were performed. Measurement of p38 mitogen-activated protein kinase (p38MAPK) pathway-related factor expression was performed by qRT-PCR and western blot. Results. The increased IgG content and HP colonization rate indicated successful modeling. SJYYD caused attenuated gastric mucosal damage, with decreased ulcer index (UI), HP colonization rate, inflammatory cell infiltration, tumor necrosis factor-α (TNF-α), interleukin (IL)-6, and IL-1β levels in HP-associated gastritis mice. Moreover, SJYYD reduced p38MAPK, c-Jun N-terminal kinase (JNK), and extracellular regulated protein kinase (ERK) mRNA expression, as well as p-p38MAPK/p38MAPK, p-JNK/JNK, and p-ERK/ERK protein expression in gastric mucosa tissues of HP-associated gastritis mice. The above effects were reversed by further ANI treatment. Conclusion. SJYYD may attenuate HP-associated gastritis by inhibiting inflammatory response by down-regulating p38MAPK pathway, providing scientific evidence for clinical application of SJYYD in HP-associated gastritis treatment and promoting the development of therapeutic approaches in HP-associated gastritis
Open Access
Venous vasculature drives neovascularization and stroma formation in pancreatic neuroendocrine tumors via intussusceptive angiogenesis and vein intravasation
(Universidad de Murcia, Departamento de Histología e Histopatología, 2025) Díaz-Flores Lucio; Gutiérrez Ricardo; Pino García Maria; González-Gómez Miriam; Carrasco Jose Luis; Madrid Juan Francisco; Díaz-Flores Varela Lucio; Biología Celular e Histología
The microenvironment of pancreatic neuroendocrine tumors (PanNETs) has been extensively studied; however, research on their venous vasculature has largely focused on tumor invasion and metastasis. This study aims to (a) evaluate the role of veins/venules in PanNET neovascularization, tumor intravasation, and stromal tract (trabecula) formation, including the potential involvement of intussusceptive angiogenesis (IA); and (b) compare the trabeculae observed in PanNETs with those found in hepatic cavernous hemangiomas (HCHs) where IA in veins plays an important role. To achieve these objectives, we conducted an integrated morphological approach encompassing primary PanNETs (n=42), hepatic metastases of PanNETs (n=4), and HCHs (n=11). Our findings in both primary and metastatic PanNETs reveal (a) the involvement of veins/venules in tumor neovascularization, with IA acting synergistically with sprouting angiogenesis, through the formation of pillars, meshes, and complex meshes (vessels that encapsulate tumor clusters-endothelium-coated tumor clusters); (b) the development of connective tissue around the neo-vasculature, potentially involving adventitial CD34-positive stromal cells/telocytes; and (c) a notable architectural resemblance between the trabeculae of PanNETs and those of HCHs. In conclusion, this work highlights the pivotal role of the preexisting venous vasculature in PanNET neovascularization, tumor intravasation, and stroma formation, with active participation of IA. These findings provide a pathophysiological foundation for future in-depth molecular investigations and may pave the way for new studies on therapeutic strategies targeting angiogenic mechanisms
Open Access
Pinocembrin ameliorates non-alcoholic fatty liver disease by activating Nrf2/HO-1 and inhibiting the NF-κB signaling pathway
(Universidad de Murcia, Departamento de Histología e Histopatología, 2025) Chen Weina; Xue Diming; Feng Xia; Zhong Yinhang; Li Quanqing; Zhang Weihang; Jiang Guojun; Biología Celular e Histología
Objectives. The high intake of high-fat diets and changes in sedentary lifestyles have led to an increase in non-alcoholic fatty liver disease (NAFLD). This study aimed to investigate the effect and mechanism of Pinocembrin (Pin) on NAFLD in vivo and in vitro. Methods. The pharmacodynamics of Pin alone or in combination with ML385 was assessed in high-fat diet (HFD)-mediated NAFLD mice. HepG2 cells were treated with palmitic acid (PA)/oleic acid (OA) (1:2) as an in vitro model to study the effect of Pin on lipid deposition and oxidative stress. The roles of Pin in glucose and lipid metabolism, inflammation, oxidative stress, and the Nrf2/HO-1/NF-κB pathway were measured. Results. Pin alleviated lipid deposition, inflam-matory response, and oxidative stress in HFD-induced NAFLD mice and PA/OA-induced HepG2 cells. Moreover, ML385 partly attenuated the protection of Pin on inflammatory response and oxidative stress in vivo and in vitro. More importantly, feeding with an HFD significantly decreased the expression of Nrf2 and HO-1, but treatment with Pin increased their expression, accompanied by an increased nuclear transposition of Nrf2. Conclusion. Taken together, these results indicated that Pin alleviated glucose and lipid metabolism disorders, inflammation, and oxidative stress in NAFLD by activating the Nrf2/HO-1 signaling pathway and restraining the NF-κB pathway
Open Access
Engineering vascular grafts from decellularized plants: Advances and challenges
(Universidad de Murcia, Departamento de Histología e Histopatología, 2025) Merna Nick; Biología Celular e Histología
Small-caliber vascular grafts (<6 mm diameter) are critical for coronary and peripheral bypass surgeries, yet developing functional substitutes remains challenging. Autologous vessels are ideal but often unavailable or of poor quality. Synthetic grafts, such as expanded polytetrafluoroethylene (ePTFE) and Dacron, have high failure rates at small diameters due to thrombosis, intimal hyperplasia, and compliance mismatch. Tissue-engineered vascular grafts (TEVGs) aim to overcome these issues by providing a biocompatible scaffold with an endothelial lining. Decellularized plant tissues have recently gained attention as natural scaffolds for TEVGs due to their structural similarity to human vasculature. Leaves and stems provide an extracellular matrix (ECM) primarily composed of cellulose, which is biocompatible, porous, and non-thrombogenic. These scaffolds are cost-effective, scalable, and ethically uncontroversial. Decellularized parsley stems or leatherleaf leaves, for instance, can be recellularized with endothelial and smooth muscle cells (SMCs) to create small-diameter grafts that support endothelialization and withstand physiological pressures. Perfusion bioreactors further enhance the functionality of plant-based grafts by simulating physiological conditions. Pulsatile flow and pressure stimulate endothelial cell alignment, reducing thromb-ogenicity, while mechanical stimulation promotes SMC maturation and ECM deposition, improving graft strength and compliance. This review summarizes recent advances in plant-based vascular grafts and perfusion bioreactor conditioning, compares their performance to conven-tional grafts, and highlights remaining challenges. Decellularized plant scaffolds, with their inherent vascular architecture and biocompatibility, show promise as natural templates for small-caliber vascular grafts. However, further research is needed to address key challenges such as standardization, mechanical optimization, and long-term in vivo validation to facilitate their clinical application
Open Access
Deregulation and delocalization of the m6A demethylase FTO and aberrant m6A levels in ccRCC tissue samples
(Universidad de Murcia, Departamento de Histología e Histopatología, 2025) Tito Claudia; Rosa Paolo; Sorrentino Veronica; Magnanti Martina; Innocenti Angelica; Zaccaria Lorenzo; Costantini Manuela; Laiza Alessia; Bastianelli Daniela; Masciarelli Silvia; Pastore Antonio Luigi; Simone Giuseppe; Carbone Antonio; Fatica Alessandro; Petrozza Vincenzo; Fazi Francesco; Biología Celular e Histología
N6-methyladenosine (m6A) is one of the most abundant mRNA modifications established by the activity of three classes of enzymes: writers, readers, and erasers. The relevance of m6A in the regulation of gene expression implies its key role in normal biological processes and cancer development. Given the little knowledge about the involvement of m6A in clear cell Renal Carcinoma (ccRCC), our analysis should be regarded as a pilot study aimed at investigating the expression of m6A enzymes in tissues and urine specimens of ccRCC patients. The expression of m6A enzymes was validated by quantitative reverse-transcription PCR and immuno-histochemistry, comparing normal and tumoral tissues. Quantification of m6A levels in urine specimens of healthy and cancer patients was performed by colorimetric Urine m6A assay. We observed the upregulation and nuclear localization of the m6A demethylase FTO in tumoral tissues compared with their respective normal counterparts. The nuclear expression of FTO decreases with an increase in tumor grade. Moreover, we identified a decrease in m6A levels in cancer samples. These findings might represent novel evidence to further investigate the issue, to reveal new diagnostic markers for tumorigenesis, leading to a potential m6A-targeted therapy in ccRCC
Open Access
Liver morphology and histological alterations related to reproductive phases of female silver croaker Plagioscion squamosissimus (Acanthuriformes, Sciaenidae)
(Universidad de Murcia, Departamento de Histología e Histopatología, 2025) Horas Do Nascimento Yane Caroline; Pereira dos Santos Silva Amanda; Kotz Kliemann Bruna Caroline; Paiva Ramos Igor; Franceschini Lidiane; Delariva Rosilene Luciana; De Oliveira Manoel Letícia; Belancieri Souza Cristieli Fernanda; Ninhaus Silveira Alexandre; Veríssimo-Silveira Rosicleire; Biología Celular e Histología
This study describes the morphology of the liver tissue, histological alterations, and their relationships with the reproductive phases of the female silver croaker Plagioscion squamosissimus. We tested the hypothesis that histological alterations in liver tissue can occur at the expense of the reproductive phase of the female and that climatic factors, such as rainfall, interfere with the reproductive phases and, consequently, promote histological alterations. Histological analysis of the liver showed liver tissue with hepatocytes, bile ducts, blood vessels, sinusoids, intrahepatic pancreas, and phagocytic cells. The histological alterations observed were cytoplasmic vacuolization and degeneration, aggregates of melanomacrophages, hyperemia, and vascular congestion, with cytoplasmic vacuolization, cytoplasmic degeneration, and vascular congestion being the most frequent. We observed that the frequency of cytoplasmic vacuolization increased throughout gonadal development with a decrease in the spawning-capable phase, and that cytoplasmic degeneration and vascular congestion were more frequent in the suitable spawning phase. In addition, relationships between histological alterations, hepatosomatic index, gonadosomatic index, reproductive phases, and rainfall were also observed, showing that alterations were more frequent in periods with higher rainfall and reproductive phases when females were ready to reproduce. In short, histological alterations may be subject to the reproductive phases of females, which are influenced by rainfall, as observed in many studies. Thus, this study presents the morphology of the liver tissue of P. squamosissimus, and the results shed light on the importance of considering the reproductive phases in studies evaluating histological alterations in the liver
Open Access
A low nuclear-to-cytoplasmic ratio of VDR expression is an independent prognostic marker in breast cancer
(Universidad de Murcia, Departamento de Histología e Histopatología, 2025) Schubert Charlotte; Vilsmaier Theresa; Batz Falk; Cavaillès Vincent; Sixou Sophie; Kolben Thomas; Meister Sarah; Buschmann Christina; Hagemann Friederike; Biología Celular e Histología
The aim of this retrospective study was to analyze the prognostic value of cytoplasmic versus nuclear expression of the vitamin D receptor (VDR) in breast cancer (BC) tissue samples and to relate the results to clinicopathological parameters. VDR expression was assessed in 319 primary breast cancer patients using the Remmele and Stegner immunoreactive scoring (IRS) system. Follow-up data were obtained from the Munich Cancer Registry. The correlation with overall survival (OS) and disease-free survival (DFS) was calculated using univariate and multivariate analyses. Correlation analysis revealed a correlation between nuclear VDR expression and improved outcomes for both OS (p=0.004) and DFS (p=0.001). Conversely, cytoplasmic VDR expression was significantly associated with a shorter OS (p=0.003) and DFS (p<0.001). Additionally, both cytoplasmic and nuclear VDR expression were found to be independent markers of DFS (p<0.001; p=0.021) when examined alongside clinicopathological parameters. Moreover, nuclear VDR expression was positively associated with lower lymph node invasion (pN; p=0.01). For triple-negative patients, cytoplasmic VDR expression was found to have a significant inverse correlation with DFS (p<0.001). Lastly, the ratio of VDR nuclear/cytoplasmic was identified as an auxiliary independent marker of DFS and OS. These findings strongly indicate that the subcellular localization of VDR is crucial in determining BC prognosis. The expression of nuclear VDR appears to have a protective effect, while cytoplasmic VDR is associated with a more aggressive disease course. The data may help identify subgroups of patients with high-risk BC, possibly leading to specific options for targeted tumor therapy
Open Access
Salivary gland carbonic anhydrases
(Servicio de Publicaciones, Departamento de Histología e Histopatología, 2025) Redman Robert S.; Biología Celular e Histología
Carbonic anhydrases (CA) are zinc metalloenzymes that catalyze the reversible conversion of carbon dioxide and water to bicarbonate. For most mammalian cells, this reaction is essential to maintaining intracellular physiological pH. For salivary glands, it also has an important role in the regulation of the pH and buffering capacity of their secretory product, saliva, which is central to the activity of salivary digestive enzymes. This review is a chronological narrative of the discovery and distribution of CA and its isoenzymes in mammalian salivary glands and saliva and the role of CA in regulation of salivary pH via secretion of the salivary CA isoenzyme and the secretion and reabsorption of bicarbonate from the ductal lumen. The interaction of sodium/bicarbonate co-transporters and other factors in these processes is briefly described. The distribution of CA among mammalian species, salivary glands, and gland cells as determined by CA activity in saliva and gland extracts, enzyme histochemistry, and immunohistochemistry is presented in tables. The importance of salivary CA to oral health is underscored by the reduction in salivary gland and salivary CA activity by nutritional zinc deficiency and genetic variants of two of the CA isoenzymes, which cause dysgeusia and hyposalivation and are associated with increased dental caries

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