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        <title>Pathology and Oncology Research | New and Recent Articles</title>
        <link>https://www.por-journal.com/journals/pathology-and-oncology-research</link>
        <description>RSS Feed for Pathology and Oncology Research | New and Recent Articles</description>
        <language>en-us</language>
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        <pubDate>2026-11-12T13:14:40.694+00:00</pubDate>
        <ttl>60</ttl>
        <item>
        <guid isPermaLink="true">https://www.por-journal.com/articles/10.3389/pore.2026.1612573</guid>
        <link>https://www.por-journal.com/articles/10.3389/pore.2026.1612573</link>
        <title><![CDATA[Morphologic variants in PanNETs: clinicopathologic and prognostic associations]]></title>
        <pubdate>2026-11-12T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Neslihan Berker</author><author>Melek Büyük</author><author>Beslen Göksoy</author><author>Kürşat Rahmi Serin</author><author>Mine Güllüoğlu</author>
        <description><![CDATA[BackgroundPancreatic neuroendocrine tumors (PanNETs) exhibit morphologic heterogeneity, including uncommon variant patterns that create diagnostic challenges and whose clinicopathologic significance remains incompletely defined.MethodsWe retrospectively analyzed 82 resected, well-differentiated PanNETs to identify non-classical morphologic variants and evaluate their clinicopathologic and survival associations. Morphologic variants were classified using literature-based criteria. Overall survival and recurrence-free survival were assessed using Kaplan-Meier and Cox models.ResultsMorphologic variants were identified in 20 tumors (24%), including eosinophilic (oncocytic-hepatoid), dyscohesive/plasmacytoid-rhabdoid, lipid-rich, peliotic/angiomatoid, paraganglioid, and pseudoglandular patterns. Variants previously classified as aggressive (n = 14) were significantly associated with higher Ki-67 indices (p = 0.044) and higher WHO grades (p = 0.007). No significant associations were observed between variant status and pathologic stage, nodal status, or metastatic disease at diagnosis. Aggressive variants showed a trend toward shorter overall survival, although this did not reach statistical significance (p = 0.086). In multivariable Cox models for recurrence-free survival, nodal involvement remained independently associated with recurrence risk. The Ki-67 index showed a trend toward increased recurrence risk, although this did not reach statistical significance, whereas morphologic variant status did not show an independent prognostic impact.ConclusionMorphologic variants constitute an important component of the histologic spectrum of PanNETs and are associated with adverse histopathologic features. Recognition of these patterns is important in diagnostic practice, especially in limited biopsy or metastatic settings where they may mimic other neoplasms. Given the limited number of variant cases and survival events in this single-institution cohort, their independent prognostic significance remains unproven, and non-classical morphologies should be interpreted cautiously alongside established parameters, such as nodal status and proliferation index.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.por-journal.com/articles/10.3389/pore.2026.1612568</guid>
        <link>https://www.por-journal.com/articles/10.3389/pore.2026.1612568</link>
        <title><![CDATA[Death plasticity in cancer: a network perspective on regulated cell death pathways and their therapeutic exploitation]]></title>
        <pubdate>2026-11-10T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Muhammet Volkan Bülbül</author><author>Turan Demircan</author>
        <description><![CDATA[For most of the twentieth century, apoptosis was regarded as the principal—if not sole—regulated route to cellular self-destruction, and cancer therapy was designed accordingly. Over the past decade, however, the discovery of mechanistically distinct regulated cell death (RCD) modalities—ferroptosis, pyroptosis, necroptosis, cuproptosis, disulfidptosis, PANoptosis, and a broader non-canonical landscape encompassing autophagy-dependent death, anoikis, entosis, parthanatos, and lysosomal cell death—has reframed resistance to cell death as a composite phenotype rather than a single evaded pathway. This review synthesizes the molecular executors, cancer-specific evasion mechanisms, and immunological consequences of each RCD modality, before shifting to the network level to examine the master regulatory axes (phosphoinositide 3-kinase (PI3K)–AKT–mechanistic target of rapamycin (mTOR), nuclear factor erythroid 2-related factor 2 (NRF2)–Kelch-like ECH-associated protein 1 (KEAP1), p53, and Wnt/β-catenin) and metabolic reprogramming events (the Warburg shift) through which single oncogenic alterations confer broad-spectrum death resistance. Particular attention is given to the immunogenicity of different death modalities within the tumor microenvironment, where lytic pathways that release damage-associated molecular patterns (DAMPs), such as necroptosis, pyroptosis, and cuproptosis, can convert immunologically cold tumors into those responsive to checkpoint blockade, in contrast to the immunologically silent execution of apoptosis. The review concludes by identifying the principal barriers to clinical translation—context-dependent death sensitivity, a scarcity of validated pharmacological probes for non-apoptotic pathways, contradictory immunological findings, tumor metabolic heterogeneity, and the absence of standardized clinical biomarkers—and outlines emerging directions, including proteolysis-targeting chimera (PROTAC)-based degradation of resistance nodes, composite multi-pathway death signatures, and single-cell/spatial approaches capable of resolving death competence at cellular resolution. Understood as a plastic, network-level capability rather than a switch to be thrown, cancer cell death offers a substantially larger and more combinable therapeutic target space than the apoptosis-centric paradigm alone.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.por-journal.com/articles/10.3389/pore.2026.1612665</guid>
        <link>https://www.por-journal.com/articles/10.3389/pore.2026.1612665</link>
        <title><![CDATA[Retraction: Semaphorin 5A, an axon guidance molecule, enhances the invasion and metastasis of human gastric cancer through activation of MMP9]]></title>
        <pubdate>2026-11-09T00:00:00Z</pubdate>
        <category>Retraction</category>
        
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.por-journal.com/articles/10.3389/pore.2026.1612560</guid>
        <link>https://www.por-journal.com/articles/10.3389/pore.2026.1612560</link>
        <title><![CDATA[A retrospective analysis of cetuximab efficacy based on the comprehensive RAS/RAF mutation profiles of colorectal cancer]]></title>
        <pubdate>2026-11-03T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>József Tímár</author><author>Erzsébet Rásó</author><author>Tamás Barbai</author><author>Marcell Baranyi</author><author>István Kenessey</author><author>Zsuzsanna Pápai</author><author>Andrea Uhlyarik</author>
        <description><![CDATA[BackgroundIn colorectal cancer the most frequently analyzed markers are RAS/RAF mutations which have negative predictive role for anti-EGFR antibody therapy. Although the hotspot mutations of the K- and NRAS exon 2-4 are well defined, the predictive role of rare mutations of other codons are questionable and the current guidelines are less precise in this respect.MethodsWe have retrospectively re-analyzed the full spectrum of RAS/RAF mutations by next-generation sequencing (NGS) in a small cohort of nineteen cetuximab treated metastatic colorectal cancer patients whose enrollment was based on KRAS exon 2 mutation analysis.ResultsWe have detected 13 rare RAS/RAF mutations where 5 occurred together with hotspot (HSP) mutations. In the five non-HSP mutant cases we have detected 8 rare/non-HSP RAS/RAF mutations: KRAS-E37.,C51Y, NRAS-D57N,E62K,G60E/V14I, HRAS-P34L and BRAF-G464R. Kaplan-Meier analysis indicated that the progression free survival (PFS) of non-HSP cases ran parallel with wild type (WT) cases separately from the HSP mutant cases without statistical significance (p = 0.156). However, the combination of WT group with non-HSP cases resulted in a near significant survival difference from HSP cases (p = 0.057, HR = 3.501). Kaplan-Meier analysis of the overall survival (OS) again demonstrated that the survival curve of WT cases ran parallel with non-HSP cases, clearly separated from the HSP cases (p = 0.024). Overall survival of WT cases was significantly different as compared to HSP cases (p = 0.005) with HR of 6.362 (CI 1.496–27.055) as expected, while it was not statistically different from non-HSP cases (p = 0.092) with a HR of 0.891 (CI 0.248–3.205).ConclusionIn this small retrospective study we showed that the analyzed non-HSP mutations of RAS/RAF in colorectal cancer treated with cetuximab do not have negative effect on the efficacy. Since our cohort is very small and do not have accordingly the necessary statistical power of the survival analyses, therefore can only be considered as hypothesis generating one of the issue of the predictive role of non-hotspot RAS mutations on cetuximab efficacy.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.por-journal.com/articles/10.3389/pore.2026.1612579</guid>
        <link>https://www.por-journal.com/articles/10.3389/pore.2026.1612579</link>
        <title><![CDATA[Analysis of clinical and pathological characteristics of 10 cases of fetal lung adenocarcinoma]]></title>
        <pubdate>2026-11-02T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Ying Qiu</author><author>Wenyao Liu</author><author>Qianxiu Jin</author><author>Xiangjun Sun</author><author>Yilin Wang</author><author>Naichun Zhang</author>
        <description><![CDATA[BackgroundFetal adenocarcinoma of the lung (FLAC) is a rare subtype of lung adenocarcinoma resembling the developing fetal lung at the pseudoglandular stage (8–16 weeks of gestation). This study investigates the clinicopathological features, along with key diagnostic and treatment considerations for FLAC.MethodsClinical data from 10 FLAC patients diagnosed at Linyi People’s Hospital between January 2017 and December 2024 were retrospectively analyzed. Their clinicopathological characteristics were summarized in conjunction with relevant literature.ResultsThe cohort comprised low-grade FLAC (L-FLAC, 6 cases) and high-grade FLAC (H-FLAC, 4 cases). Pathological examinations indicated higher frequencies of pleural invasion (3/4) and lymph node metastasis (1/4) in H-FLAC, which exhibited marked nuclear atypia and abundant mitoses, while L-FLAC demonstrated mild cellular atypia and morular structures. Immunohistochemistry revealed universal positivity for TTF-1. Napsin A expression was noted in both L-FLAC (3/3) and H-FLAC (2/4). In L-FLAC, β-catenin showed nuclear/cytoplasmic or nuclear expression in the vast majority of cases while H-FLAC displayed only membranous expression. Molecular testing detected an EGFR exon 19 deletion in one H-FLAC case and a KRAS G12C mutation in another. No recurrence was observed during follow-up, which ranged from 4 to 93 months.ConclusionFLAC exhibits distinctive morphological features and immunophenotypes, necessitating differential diagnosis from primary pulmonary tumors and metastatic malignancies. Surgical resection remains the primary therapeutic strategy. No disease recurrence was observed during follow-up from 4 to 93 months, although some patients had a shorter follow-up period of 4–6 months.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.por-journal.com/articles/10.3389/pore.2026.1612553</guid>
        <link>https://www.por-journal.com/articles/10.3389/pore.2026.1612553</link>
        <title><![CDATA[Prognosis and tumor grading in bladder urothelial carcinomas with intratumoral grade heterogeneity]]></title>
        <pubdate>2026-10-05T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Gökhan Veli Alkan</author><author>Kutsal Doğan</author><author>Meltem Türk Alkan</author><author>Evrim Önder</author>
        <description><![CDATA[AimsGrade heterogeneity is one of the most debated issues in the grading of urothelial carcinomas. The 2022 WHO classification states that approximately one-third of urothelial carcinomas exhibit grade heterogeneity and suggests that the presence of ≥5% high-grade component may justify classification as high-grade. Nevertheless, the need for further evidence was also emphasized. This study aimed to evaluate the prognostic impact of the high-grade component in urothelial carcinomas with grade heterogeneity and to determine a threshold value for high-grade proportion that is clinically meaningful for grading.MethodsThis retrospective study included 180 cases of non-muscle-invasive urothelial carcinoma with grade heterogeneity, diagnosed between January 2019 and August 2022 on TUR specimens, with available clinical data. Recurrence and survival time were assessed. Cases with >90% high-grade component were excluded.ResultsRecurrence was observed in 26.7% of cases. The two-year survival rate was 73.3%. While no significant association was found between recurrence and the proportion of high-grade component, survival time significantly decreased as the proportion of high-grade component increased. ROC curve analysis identified 27.5% as the cut-off value associated with adverse prognosis.ConclusionIn non-muscle-invasive urothelial carcinomas, the proportion of high-grade component showed a strong association with survival. Together with literature findings, our results suggest that a threshold higher than 5% may be more appropriate for assigning tumors to the high-grade category. Nonetheless, risk stratification incorporating tumor size and extent remains essential for prognostic evaluation.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.por-journal.com/articles/10.3389/pore.2026.1612588</guid>
        <link>https://www.por-journal.com/articles/10.3389/pore.2026.1612588</link>
        <title><![CDATA[A Letter to the Editor regarding the article “gastric epithelial neoplasm of fundic-gland mucosa lineage: representative of the low atypia differentiated gastric tumour and Ki67 may help in their identification”]]></title>
        <pubdate>2026-09-30T00:00:00Z</pubdate>
        <category>Letter to the Editor</category>
        <author>Houqiang Li</author><author>Lanqing Zheng</author><author>Guodong Zhong</author><author>Linying Chen</author><author>Xin Chen</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.por-journal.com/articles/10.3389/pore.2026.1612543</guid>
        <link>https://www.por-journal.com/articles/10.3389/pore.2026.1612543</link>
        <title><![CDATA[Impact of p53 status on recurrence patterns and oncologic outcomes in non-invasive high-grade endometrial cancer]]></title>
        <pubdate>2026-08-31T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Eduardo Paulino</author><author>Thiago Branco</author><author>Guilherme Gomes de Mesquita</author><author>Andreia Cristina de Melo</author>
        <description><![CDATA[ObjectiveThis retrospective study evaluated the impact of p53-abnormal (p53abn) status on recurrence patterns and outcomes among patients with non-invasive, high-grade endometrial cancer (EC) treated at the Brazilian National Cancer Institute (INCA) between 2010 and 2025.MethodsEligible patients had high-grade histologies—including endometrioid grade 3 (ECG3), serous (USC), clear cell (CC), carcinosarcoma (CS), mixed, or undifferentiated tumors—without myometrial invasion. Clinical, surgical, and pathological characteristics, as well as recurrence and survival data, were reviewed. Immunohistochemical analysis of p53 expression was performed, and p53 status was correlated with clinical outcomes, particularly recurrence rate.ResultsFifty-nine patients met the inclusion criteria, with a mean age of 65 years. Most underwent total hysterectomy with or without bilateral salpingo-oophorectomy (59.3%); 40.7% also received lymphadenectomy or omentectomy. Histologic distribution was mainly endometrioid (39.0%) and serous (39.0%). Forty-six (78%) and 13 (22%) had p53 abnormal and normal tumors. Seven patients (11.9%) received chemotherapy and 15 (25.4%) received radiotherapy. Three patients had already disease outside uterus. Among 56 patients with FIGO stage IC disease, recurrence occurred in 16.1%, predominantly at extra-pelvic sites (33.3% abdominal, 22.2% distant). Five-year recurrence was 23.2% for p53abn tumors versus 0% for wild-type, and 12.5% of patients died—mostly within the p53abn subgroup.ConclusionThe findings suggest that even in non-invasive high-grade EC, p53 abnormalities confer higher recurrence risk and poorer outcomes, while wild-type tumors show excellent prognosis. These results support individualized treatment approaches and highlight the need for larger, prospective validation studies.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.por-journal.com/articles/10.3389/pore.2026.1612550</guid>
        <link>https://www.por-journal.com/articles/10.3389/pore.2026.1612550</link>
        <title><![CDATA[Association of selected ELAC2, MSR1, RNASEL and KLK3 polymorphisms with prostate cancer susceptibility in a Hungarian cohort]]></title>
        <pubdate>2026-08-28T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Sebestyen Kovacs</author><author>Renata Szalai</author><author>Laszlo Barati</author><author>Kinga Hadzsiev</author>
        <description><![CDATA[BackgroundProstate cancer (PCa) remains a leading malignancy among men worldwide, with inherited genetic susceptibility playing a pivotal role in its pathogenesis. Although numerous single nucleotide polymorphisms (SNPs) within immune response, inflammatory, and apoptotic pathways have been linked to PCa risk, these associations often exhibit substantial inconsistency across diverse populations. This study aimed to evaluate the association of selected polymorphisms within the RNASEL, ELAC2, MSR1, and KLK3 genes with PCa susceptibility in a Hungarian cohort.MethodsThis case-control study included 103 histologically confirmed prostate cancer patients and 103 healthy controls recruited at the University of Pécs Department of Urology. Genotyping of selected polymorphisms was performed by PCR and Sanger sequencing at the Department of Medical Genetics. Statistical associations were evaluated using chi-square tests, odds ratios, and logistic regression.ResultsA statistically nominally significant association with prostate cancer susceptibility was observed for the RNASEL rs486907 polymorphism, demonstrating a potential protective effect under the dominant model in the studied population (OR = 0.53, 95% CI: 0.30–0.92, p = 0.025). In the age-adjusted logistic regression analysis, this association remained statistically significant (OR = 0.56, 95% CI: 0.32–0.99, p = 0.046), suggesting that the observed effect was independent of age. In contrast, no statistically significant associations were identified between prostate cancer risk and the investigated polymorphisms in the KLK3, MSR1, or ELAC2 genes.ConclusionThe present study demonstrated a significant association between the RNASEL rs486907 polymorphism and prostate cancer susceptibility in a Hungarian cohort, suggesting a potential protective effect of this variant. These findings support the possible role of inherited genetic factors in prostate cancer development and highlight the importance of population-specific genetic association studies. Further investigations involving larger cohorts are warranted to validate these observations.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.por-journal.com/articles/10.3389/pore.2026.1612490</guid>
        <link>https://www.por-journal.com/articles/10.3389/pore.2026.1612490</link>
        <title><![CDATA[Beyond animal models: using human pluripotent stem cell-derived stem and progenitor cells to predict cytotoxicity in normal tissues]]></title>
        <pubdate>2026-08-20T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Katalin Vincze</author><author>Nóra Varga</author><author>Szilárd Tóth</author><author>Anna Kamilla Kis</author><author>Rita Béres</author><author>János Miklós Réthelyi</author><author>Zoltán János Veréb</author><author>Zsuzsa Erdei</author><author>Balázs Sarkadi</author><author>Ágota Apáti</author>
        <description><![CDATA[BackgroundThe clinical efficacy of anticancer drugs is often limited by dose-dependent toxicity to normal cells, particularly to rapidly dividing stem and progenitor cell populations. Traditional preclinical toxicity screening relies on animal models or primary human cells/immortalized lines, both of which have significant limitations regarding scalability, reproducibility, genetic diversity, and translational relevance.ObjectiveThis study aims to establish and validate a human pluripotent stem cell -based platform for profiling the toxicity of cytostatic drugs on healthy, dividing cell populations, and to compare their sensitivity to that of cancer cell lines.MethodsTwo hiPSC lines (male and female) were reprogrammed from umbilical cord blood cells, fully characterized, and differentiated into neural progenitors and mesenchymal derivatives. Dose–response curves were generated using a dilution series of four anticancer drugs and four other pharmacologically active compounds based on cell viability. Toxic half-maximal values (IC50) were determined for each cell type and compared to those obtained from conventional cancer cell lines.ResultsThe highest sensitivity to DNA-damaging agents was exhibited by pluripotent stem cells, followed by neural progenitors, with mesenchymal derivatives being the least sensitive. Notably, except for mesenchymal cells, both pluripotent stem cells and their differentiated derivatives were more sensitive to cytostatics than cancer cell lines.ConclusionHuman iPSC-derived stem/progenitor cells recapitulate the in vivo sensitivity of healthy dividing cell populations to chemotherapy. This platform offers unlimited, genetically consistent, and reproducible access to human cells, rendering it as a powerful complementary approach or even an alternative to animal models and primary human cells for early-phase drug safety profiling.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.por-journal.com/articles/10.3389/pore.2026.1612565</guid>
        <link>https://www.por-journal.com/articles/10.3389/pore.2026.1612565</link>
        <title><![CDATA[Retraction: Knockdown of Sox2 inhibits OS cells invasion and migration via modulating Wnt/β-catenin signaling pathway]]></title>
        <pubdate>2026-08-13T00:00:00Z</pubdate>
        <category>Retraction</category>
        
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.por-journal.com/articles/10.3389/pore.2026.1612537</guid>
        <link>https://www.por-journal.com/articles/10.3389/pore.2026.1612537</link>
        <title><![CDATA[Case Report: Pancreatic amphicrine-like carcinoma with acinar differentiation harboring a KANK4-RAF1 gene fusion]]></title>
        <pubdate>2026-08-11T00:00:00Z</pubdate>
        <category>Case Report</category>
        <author>Sabrina Kammerer</author><author>Peter Bode</author><author>Heide Schreiber</author><author>Guacimara Ortega Sanchez</author>
        <description><![CDATA[Pancreatic amphicrine-like carcinoma (ALC) is an exceptionally rare neoplasm characterized by simultaneous exocrine and endocrine differentiation within the same tumour cells. These tumours represent a diagnostic challenge because they must be distinguished from mixed neuroendocrine–non-neuroendocrine neoplasms (MiNENs), which consist of morphologically distinct tumour components. We report a case of pancreatic ALC with acinar differentiation harboring a KANK4::RAF1 fusion identified by comprehensive genomic profiling. Histologically, the tumour demonstrated acinar differentiation with expression of trypsin and BCL10 together with neuroendocrine differentiation characterized by synaptophysin and INSM1 expression within the same neoplastic population. Molecular analysis revealed a RAF1 rearrangement, a potentially actionable alteration previously described in a subset of pancreatic acinar carcinomas. The patient showed rapid disease progression despite systemic chemotherapy. Treatment with the MEK inhibitor trametinib was initiated based on the presence of a RAF1 fusion but was discontinued after 1 month because of toxicity, preventing assessment of therapeutic efficacy. This case expands the molecular spectrum of pancreatic ALC with acinar differentiation and highlights the importance of comprehensive molecular profiling in rare pancreatic neoplasms to identify potentially actionable genomic alterations.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.por-journal.com/articles/10.3389/pore.2026.1612448</guid>
        <link>https://www.por-journal.com/articles/10.3389/pore.2026.1612448</link>
        <title><![CDATA[SPOCK1 overexpression suggests poor prognosis in head and neck squamous cell carcinomas]]></title>
        <pubdate>2026-08-06T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Noemi Piroska Jakob</author><author>Matyas Majoros</author><author>Imre Uri</author><author>Helga Szakadati</author><author>Ede Birtalan</author><author>Kornelia Baghy</author><author>Zoltan Kelemen</author><author>Laszlo Tamas</author><author>Kornel Danos</author><author>Tibor Krenacs</author>
        <description><![CDATA[Head and neck squamous cell carcinomas (HNSCCs) are mostly associated with smoking, alcohol intake, and/or human papillomavirus HPV16 and/or HPV18 infection. However, most tumors are diagnosed at an advanced stage. In the search for biomarkers of HNSCC, we studied the prognostic role of SPOCK1, a heparan sulfate proteoglycan. In HNSCC, SPOCK1 expression was tested both at in silico mRNA level using the Kaplan-Meier Plotter and at in situ protein level after SPOCK1 immunohistochemistry after whole slide digitalization. Protein expression results were analyzed using H-Scores, both by eye-control testing and with a machine-learning-based automated image analysis tool, DensitoQuant. SPOCK1 mRNA expression was found to be significantly higher in oral carcinomas than in the normal oral mucosa (log-rank p = 5.76e-06). Elevated SPOCK1 mRNA expression was consistently associated with a strongly reduced overall survival (OS; HR = 1.57 (1.2–2.06); log-rank p = 0.001) in HNSCC. This was particularly true for tumors with high (log-rank p = 0.00085) vs. low (log-rank p = 0.55) neoantigen (NeoAG) levels, at median antigen level stratification. Both the Cox-regression analysis and the log-rank test revealed elevated SPOCK1 protein levels in association with significantly reduced OS in our 97 HNSCC patients (both p = 0.002), which was supported by automated image analysis testing (p = 0.008 and p = 0.044, respectively). Our findings suggest that SPOCK1 can be a candidate adverse prognostic biomarker also in HNSCC. Therefore, SPOCK1 overexpression may specify a group of oral cancers with aggressive tumor biology.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.por-journal.com/articles/10.3389/pore.2026.1612465</guid>
        <link>https://www.por-journal.com/articles/10.3389/pore.2026.1612465</link>
        <title><![CDATA[Molecular classification of endometrial carcinoma: clinical utility of an NGS panel with targeted detection of 116 cancer-related genes]]></title>
        <pubdate>2026-07-28T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Lingfeng Chen</author><author>Zhijie You</author><author>Xunbin Yu</author><author>Yijuan Wu</author><author>Xin Chen</author><author>Jie Lin</author>
        <description><![CDATA[BackgroundThis study aimed to evaluate the efficacy of a single-test, targeted DNA next-generation sequencing (NGS) panel in classifying endometrial carcinoma (EC) into molecular subtypes and to compare its performance with that of the established Sanger sequencing + immunohistochemistry (Sanger + IHC) molecular classification.MethodsTargeted DNA NGS was performed on 131 samples using the clinically validated AmoyDx® Comprehensive Panel, and a commercially available targeted AmoyDx EC Panel covering POLE, TP53, and MSI was used for 63 samples.ResultsThe concordance between the NGS and Sanger + IHC classifications was 93.8% (182/194 cases), with a kappa value of 0.908. The exclusion of seven discordant POLE mutations improved concordance to 97.4% (kappa = 0.962). NGS identified 30 POLE mutations compared to 23 detected by Sanger sequencing, which missed low-frequency variants. Microsatellite instability (MSI) analysis and mismatch repair (MMR) immunohistochemistry (IHC) results were highly concordant (97.9%). However, NGS-based TP53 mutation detection showed moderate agreement with the p53 IHC results (kappa = 0.688). Mutations associated with targeted therapy trials, including PTEN (76.3%), PIK3CA (50.4%), and ARID1A (35.9%), were found in 131 EC samples.ConclusionThese findings indicate that NGS-based molecular classification aligns well with Sanger + IHC molecular classification and offers higher sensitivity than Sanger sequencing, thereby improving the identification of mutations associated with targeted therapy trials. This enhances the prognosis and treatment planning for patients with advanced EC.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.por-journal.com/articles/10.3389/pore.2026.1612374</guid>
        <link>https://www.por-journal.com/articles/10.3389/pore.2026.1612374</link>
        <title><![CDATA[TRK immunohistochemistry in pediatric rhabdomyosarcomas: diagnostic and prognostic utility and limitations]]></title>
        <pubdate>2026-07-17T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Renáta Lajti</author><author>Katalin Dezső</author><author>Zoltán Sápi</author><author>Gergő Papp</author><author>Anna Mohás</author><author>Bence Bukovszky</author><author>Sándor Szabó</author><author>Luca Felkai</author><author>Monika Csóka</author>
        <description><![CDATA[Rhabdomyosarcoma is the third most common extracranial solid tumor in childhood. Treatment of patients is multimodal, based on systemic chemotherapy and local therapy by surgery and/or radiotherapy. Although standard therapies result in an overall survival of more than 75% for patients in the low-risk group, the prognosis for high-risk patients remains poor. For this reason, new therapeutic alternatives are needed. One such option is the use of specific Tropomyosin receptor kinase (TRK) inhibitors, which provides the opportunity of targeted therapeutic treatment for patients carrying Neurotrophic Receptor Tyrosine Kinase (NTRK) translocations. As the frequency of these aberrations is not yet known in rhabdomyosarcomas, the aim of this study was to map the pan-TRK expression profile of rhabdomyosarcomas by an affordable method and to investigate the link between the expression and the clinicopathological features. We studied samples of patients diagnosed with rhabdomyosarcoma at the Pediatric Center, Semmelweis University, Budapest, Hungary. Using immunohistochemistry, we found that pan-TRK expression was detected in 38% of the cases studied. The expression was present in a significantly higher proportion of samples in the unfavorable, alveolar histological subtype. However, no NTRK fusion was detected in the 17 TRK expressing samples.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.por-journal.com/articles/10.3389/pore.2026.1612491</guid>
        <link>https://www.por-journal.com/articles/10.3389/pore.2026.1612491</link>
        <title><![CDATA[Extensive-stage small cell lung cancer in Hungary: a real-world analysis (2013–2022)]]></title>
        <pubdate>2026-07-16T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Krisztina Bogos</author><author>András Bajcsay</author><author>Gabriella Gálffy</author><author>Lilla Tamási</author><author>Zsolt Pápai-Székely</author><author>Veronika Sárosi</author><author>Anikó Maráz</author><author>Regina Pálföldi</author><author>Lilla Horváth</author><author>Judit Hoffer</author><author>Szilvia Szécsényi</author><author>Kata Kirschner</author><author>Celia Blasszauer</author><author>Dániel Reibl</author><author>Ida Komka</author><author>Anna A. Ascsillán</author><author>Lajos V. Kemény</author><author>Gyula Ostoros</author>
        <description><![CDATA[This study provides a comprehensive nationwide analysis of extensive-stage small cell lung cancer (ES-SCLC) in Hungary, examining incidence rates, demographic trends, treatment patterns, and survival outcomes. We used data from the National Health Insurance Fund (NHIF) covering the period of 2013–2022, and we analyzed 8,104 ES-SCLC patients who received first-line (1L) etoposide-platinum (EP) chemotherapy, all of whom were confirmed to not have received concomitant chemoradiotherapy or curative thoracic surgery and had histology results in line with SCLC. We evaluated epidemiology, regional distribution, radiotherapy use, and subsequent treatment pathways. For the efficacy analysis, we narrowed the cohort to 5,576 patients who initiated EP within 1 year of their first C34-coded lung cancer diagnosis between 2013 and 2019, enabling 3-year follow-up. Key endpoints included overall survival (OS) and progression-free survival (PFS), the latter of which was inferred using time to first subsequent therapy (TFST). Our results revealed a shifting age distribution toward the age group above 70 years, while the male-to-female ratio gradually evened out. Treatment patterns showed the increasing use of carboplatin over cisplatin and frequent short course radiotherapy. Among those who underwent subsequent therapy, EP rechallenge was most widespread. Despite high initial response rates, survival outcomes remained poor: median PFS was 6.5 months (6-month: 52.9%, 1-year: 19%, 3-year: 5.2%), and median OS was 9.3 months (6-month: 69.8%, 1-year: 37.5%, 3-year: 9.2%). These results were in line with international real-world evidence and clinical trial data. Our findings highlight the aggressive nature of ES-SCLC and provide insight to the limited efficacy of chemotherapy-based therapies, underscoring the need to improve existing 1L and subsequent-line treatments and to introduce novel options. As Hungary transitions into the immunotherapy era, future studies with extended follow-up that incorporate staging, radiotherapy intent, comorbidities, and progression data will be essential for optimizing therapeutic strategies.]]></description>
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        <guid isPermaLink="true">https://www.por-journal.com/articles/10.3389/pore.2026.1612480</guid>
        <link>https://www.por-journal.com/articles/10.3389/pore.2026.1612480</link>
        <title><![CDATA[Association between the histopathologic measurement of tumor–visceral peritoneal distance and prognosis in T3 colon adenocarcinoma]]></title>
        <pubdate>2026-07-13T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Özgecan Hamdemir</author><author>Semin Ayhan</author><author>Ömer Atmış</author><author>Ömer Acar</author>
        <description><![CDATA[ObjectiveTo investigate the relationship between microscopic tumor–visceral peritoneal distance (T-VPD) and histopathological markers of aggressiveness in pT3 colon adenocarcinoma and to assess its prognostic significance.MethodsA total of 329 resection specimens were retrospectively analyzed. T-VPD was defined as the shortest distance between the deepest invasive tumor front and the true serosal surface. Cut-off values of ≤0.01 cm, ≤0.05 cm, ≤0.1 cm, and ≤0.5 cm were evaluated. Associations with adverse histopathological features were examined using multivariable logistic regression. Overall survival (OS) and disease-free survival (DFS) were analyzed in 181 patients with available follow-up using Kaplan–Meier curves and Cox regression.ResultsT-VPD ≤0.5 cm was independently associated with lymphovascular invasion, whereas T-VPD ≤0.05 cm correlated with poor differentiation and tumor deposits. In OS analysis, advanced age, nodal metastasis, lymphovascular invasion, and perineural invasion were adverse prognostic factors, while a strong peritumoral lymphocytic response was protective. Tumor deposits predicted worse DFS, and peritumoral lymphocytic response remained protective. T-VPD was not an independent predictor of survival.ConclusionT-VPD reflects aggressive tumor behavior but lacks independent prognostic value. Combined with established adverse features, it may provide additional information for risk stratification in pT3 colon cancer.]]></description>
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        <guid isPermaLink="true">https://www.por-journal.com/articles/10.3389/pore.2026.1612455</guid>
        <link>https://www.por-journal.com/articles/10.3389/pore.2026.1612455</link>
        <title><![CDATA[Frequency and clinicopathological features of somatic neoplasms arising in ovarian mature teratomas: a single-center experience]]></title>
        <pubdate>2026-07-10T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Şenay Yıldırım</author><author>Gül Alkan Bülbül</author><author>Döndü Nergiz</author><author>Hülya Tosun Yıldırım</author><author>Arif Hakan Önder</author><author>Işın Üreyen</author>
        <description><![CDATA[ObjectiveSomatic neoplasms arising in mature teratomas (SN-MT) are rare clinical entities that pose significant diagnostic and therapeutic challenges. This study aims to determine the frequency of SN-MT and evaluate the clinicopathological characteristics that distinguish these cases from uncomplicated mature teratomas (MT).MethodsWe retrospectively reviewed 500 cases of presumed ovarian mature teratomas evaluated at a single center between 2006 and 2021. After strict exclusion criteria, 385 patients were included. All histopathological slides underwent systematic pathological re-evaluation by expert pathologists. Clinical, radiological, and laboratory data were compared between the MT and SN-MT groups.ResultsThe overall incidence of somatic neoplasms (benign and malignant) was 3.1% (n = 12), with a malignant transformation rate of 2.07% (n = 8). The histological spectrum was highly heterogeneous and comprised both benign and malignant entities. Benign tumors identified in MTs included paraganglioma, choroid plexus papilloma, and adnexal tumor, whereas malignant tumors included squamous cell carcinoma (SCC), glioblastoma, anaplastic astrocytoma, adult-type granulosa cell tumor, and mixed carcinoma. The SN-MT group exhibited significantly larger mean tumor diameters compared to the MT group (9.45 ± 4.22 cm vs. 6.67 ± 3.32 cm, p < 0.05). On gross examination, mixed solid–cystic architecture was a powerful predictor of neoplasia (83.3% in SN-MT vs. 22.3% in MT, p < 0.0001). Preoperative serum tumor markers (CA 125, CA 19-9, and CEA) showed no significant discriminatory value. False-negative findings on intraoperative frozen section analysis may be attributable to the focal distribution of these lesions.ConclusionSN-MT is a rare but histologically diverse condition. Large tumor size and the presence of solid components on macroscopic examination should raise suspicion of somatic transformation. Given the limitations of frozen section analysis and serum markers, rigorous macroscopic sampling and expert pathological examination remain the gold standard for diagnosis. While early-stage disease carries a favorable prognosis, the heterogeneity of subtypes necessitates individualized management.]]></description>
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        <guid isPermaLink="true">https://www.por-journal.com/articles/10.3389/pore.2025.1612113</guid>
        <link>https://www.por-journal.com/articles/10.3389/pore.2025.1612113</link>
        <title><![CDATA[Evaluating an RNA-based test for proliferation assessment and recurrence prediction in early HR+/HER2− breast cancer]]></title>
        <pubdate>2026-07-08T00:00:00Z</pubdate>
        <category>Brief Research Report</category>
        <author>Marcus Vetter</author><author>Elena Diana Chiru</author><author>Anna Gasior</author><author>Joanna Gorniak</author><author>Sara Rollinson</author><author>Leanne Gough</author><author>Mathew Harrison</author><author>Martina Sonderegger-Stalder</author><author>Matthias Matter</author><author>Simone Muenst</author><author>Christian Kurzeder</author>
        <description><![CDATA[Multigene signatures like Oncotype DX and Prosigna Prediction Analysis of Microarray 50 (PAM50) help estimate distant recurrence risk in patients with luminal breast cancer receiving endocrine therapy. Determining the benefit of adjuvant chemotherapy, tests are costly and not always supported through reimbursement. We aimed to assess the utility of the APIS Breast cancer subtyping kit (BCSK) and its proliferation score (PS), as a potential prognostic assay. We analysed 141 adult patients with early luminal HER2- breast cancer diagnosed between 2020 and 2022 at Cantonal Hospital Basel-Land and Basel University Hospital. All patients had a valid OncotypeDX® Recurrence Score (RS) and received at least one line of adjuvant therapy. Molecular subtype and PS were obtained using the APIS BCSK. We performed the Prosigna PAM50 risk of recurrence (ROR) test on a subset of 59 patients. Our findings showed high concordance at the single marker level (estrogen receptor -ESR1, progesterone receptor - PGR, human epidermal growth factor receptor 2 - ERBB2 and marker of proliferation Ki-67 - MKI67), and between the BCSK and PAM50 subtype (overall percent agreement, OPA-71.2%). Notably, BCSK showed stronger agreement with immunohistochemistry (IHC)-based subtypes (OPA: 71.2%) than PAM50 with IHC (OPA: 54.2%). The BCSK PS correlated moderately with Prosigna PAM50 ROR (ρ = 0.4787) and more weakly with Oncotype DX RS (ρ = 0.4006). The correlation between ROR and RS was weak (ρ = 0.2255). In this preliminary comparison, the APIS BCSK and PS demonstrate promising potential as an initial molecular subtyping and risk stratification tool for breast cancer patients.]]></description>
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        <guid isPermaLink="true">https://www.por-journal.com/articles/10.3389/pore.2026.1612376</guid>
        <link>https://www.por-journal.com/articles/10.3389/pore.2026.1612376</link>
        <title><![CDATA[Obesity from the perspective of the liver]]></title>
        <pubdate>2026-07-07T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Miklós Csala</author><author>József Mandl</author>
        <description><![CDATA[Glucose is at the center of liver metabolism, and together with NADPH, it is an essential factor in hepatic regulation and adaptation to different metabolic states. The liver plays a fundamental role in the development of obesity. Excess food intake, particularly excess glucose, primarily burdens liver metabolism. The hepatocyte-specific glycogenoreticular system, a functional unit based on the tight interaction between glycogen particles and the ER, is central to the storage and distribution of glucose throughout the body. Additionally, the liver converts excess glucose into ketogenic molecules. The liver is the most important site for glucogenic to ketogenic conversion in the body. However, the escape route offered by unrestricted fatty acid synthesis and deposition takes its toll in the long run. An NADPH pool is also a pivotal connection among intermediary metabolism, redox homeostasis, and drug metabolism in hepatocytes. Preservation and recovery of excess glucose is a commitment, which presents a potential pitfall. Overfeeding can lead to pathological consequences by disrupting regulatory mechanisms. The fulfillment of metabolic goals by the liver plays a significant role in the development of various pathological conditions, such as fatty liver, obesity, insulin resistance, and metabolic syndrome.]]></description>
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