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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>2026-04-19T23:55:39.752+00:00</pubDate>
        <ttl>60</ttl>
        <item>
        <guid isPermaLink="true">https://www.por-journal.com/articles/10.3389/pore.2026.1612402</guid>
        <link>https://www.por-journal.com/articles/10.3389/pore.2026.1612402</link>
        <title><![CDATA[Case Report: Thigh anastomotic hemangioma]]></title>
        <pubdate>2026-04-14T00:00:00Z</pubdate>
        <category>Case Report</category>
        <author>Li Chen</author><author>Xia Gao</author><author>Qiang Zhang</author>
        <description><![CDATA[Anastomotic hemangioma (AH) is a rare benign vascular tumor primarily occurring in the genitourinary tract; however, only two cases have been reported in the thigh. In this report, a 42-year-old female patient presented to the hospital for examination due to “a subcutaneous mass on the lateral aspect of the left thigh discovered 9 months ago, which has been gradually enlarging.” Subsequently, the lump was removed via local surgery. Histological examination reveals: At low magnification, the tumor was situated within the superficial subcutaneous fascia layer, presenting a loose lobular structure. Most of its margins were well - defined, while a small portion displayed expansile infiltrative changes. There were well - differentiated vascular lumens arranged in a communicating or anastomosing pattern, along with pseudopapillary structures. At high magnification, tumor cells were oval or short spindle - shaped, with vacuoles in the cytoplasm that contain red blood cells or homogeneously red - stained glassy globules. Moderate atypia was present, and mitotic activity was frequent, with hot spots averaging approximately 4/mm2. PCR-GNAQ mutation detection result: detected a missense mutation at codon 209 in exon 5 (c.627A>T, p. Q209H). Follow-up revealed tumor recurrence 10 months after surgery. Given the rarity of AH occurring on skin surfaces, coupled with the high proliferative activity observed in this case and its recurrence following excision, we report the diagnostic and therapeutic process along with the clinical and pathological features of this AH case. This aims to enhance the understanding of this disease among clinicians and pathologists.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.por-journal.com/articles/10.3389/pore.2026.1612375</guid>
        <link>https://www.por-journal.com/articles/10.3389/pore.2026.1612375</link>
        <title><![CDATA[Novel MYH11::GLI3 fusion in ileal leiomyoma]]></title>
        <pubdate>2026-04-13T00:00:00Z</pubdate>
        <category>Brief Research Report</category>
        <author>Ioannis Panagopoulos</author><author>Ingvild Lobmaier</author>
        <description><![CDATA[BackgroundLeiomyomas of the gastrointestinal tract (GI) are benign smooth muscle neoplasms with limited genetic characterization. Molecular investigations may improve diagnostic classification and enhance understanding of their biological behavior.MethodsRNA sequencing using multiple fusion-detection algorithms was performed on an ileal leiomyoma. Key findings were validated by RT-PCR and Sanger sequencing.ResultsA MYH11::GLI3 fusion was identified. Additional chimeric transcripts were detected but interpreted as secondary events based on limited read support. The biological relevance of MYH11::GLI3 relates to smooth muscle specific MYH11 expression and GLI3-mediated Hedgehog signaling.ConclusionThis study reports, for the first time, the identification of a MYH11::GLI3 chimera in gastrointestinal leiomyoma, thereby expanding the molecular spectrum of these tumors. Deregulation of GLI3 may represent an alternative mechanism of Hedgehog pathway perturbation in this neoplasm. The frequency and clinical significance of GLI3-rearranged gastrointestinal smooth muscle tumors remain to be determined.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.por-journal.com/articles/10.3389/pore.2026.1612408</guid>
        <link>https://www.por-journal.com/articles/10.3389/pore.2026.1612408</link>
        <title><![CDATA[Correction: Diagnostic performance of intracystic carcinoembryonic antigen (CEA) versus glucose in differentiation of mucinous and non-mucinous pancreatic cysts]]></title>
        <pubdate>2026-03-27T00:00:00Z</pubdate>
        <category>Correction</category>
        <author>György Gyimesi</author><author>Bánk Keczer</author><author>Péter Rein</author><author>Miklós Horváth</author><author>Ákos Szűcs</author><author>Tamás Marjai</author><author>Attila Szijártó</author><author>István Hritz</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.por-journal.com/articles/10.3389/pore.2026.1612281</guid>
        <link>https://www.por-journal.com/articles/10.3389/pore.2026.1612281</link>
        <title><![CDATA[The uterine secretome initiates growth of gynecologic tissues in ectopic locations: re-evaluating the evidence]]></title>
        <pubdate>2026-03-10T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Jan Sunde</author><author>K. A. Pennington</author>
        <description><![CDATA[The origin of ectopic gynecologic lesions has been debated since 1927, when Sampson first proposed retrograde menstruation as the underlying cause of endometriosis. Reproduction in mammals is an unusually permissive process, enabling the implantation of tissue genetically distinct from the mother in which leukemia inhibitory factor (LIF) is known to be a pleiotropic master transcription factor affecting multiple gene pathways such as adhesion and immune tolerance. Herein we review the uterine secretome theory, and how the initial step in ectopic lesion development is implantation. The uterine secretome, which typically cycles every 28–35 days to prepare the endometrium for potential embryo implantation and does so for decades, can be hijacked by free floating cells to implant ectopically when pregnancy does not occur. This review will focus on this emerging theory and its ability to reconcile longstanding gaps in our understanding of both benign and malignant ectopic lesion initiation.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.por-journal.com/articles/10.3389/pore.2026.1612367</guid>
        <link>https://www.por-journal.com/articles/10.3389/pore.2026.1612367</link>
        <title><![CDATA[Clinicopathological and molecular features of solid pseudopapillary neoplasms: a retrospective series including a small subset of aggressive cases]]></title>
        <pubdate>2026-03-09T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Erdem Comut</author><author>Ahmet Celik</author><author>Alper Uguz</author><author>Orkan Ergun</author><author>Simge Baran</author><author>Asuman Argon</author><author>Deniz Nart</author><author>Funda Yilmaz</author><author>Nese Calli Demirkan</author>
        <description><![CDATA[Solid pseudopapillary neoplasms (SPNs) are rare pancreatic tumors that are indolent but occasionally present with metastatic or locally invasive disease. Although recurrent CTNNB1 exon 3 mutations define their molecular background, the clinicopathological and molecular features associated with these less common presentations remain incompletely characterized. This retrospective study included 62 patients diagnosed with SPN between 2000 and 2025. Clinicopathological and immunohistochemical features, including β-catenin, progesterone receptor (PR), androgen receptor (AR), and BAP1, were evaluated. Targeted sequencing was performed in a subset of cases with metastatic or locally invasive disease (n = 5). Patients showed a wide age range (8–71 years), female predominance (54/62, 87.1%), and a mean tumor size of 7.2 cm. Lymphovascular invasion was rare (1/59, 1.7%). Metastatic or locally invasive SPNs (n = 8) more frequently showed higher Ki-67 values (median, 5%; range, 1%–15%), increased mitotic activity (2/8, 25%), and capsular/parenchymal invasion (6/8, 75%), while perineural invasion was absent. All tumors demonstrated nuclear β-catenin expression, with PR and AR positivity (50/59, 84.7% and 47/57, 82.5%, respectively). PR expression was higher in AR-positive cases (43/47, 91.5% vs. 6/10, 60%). BAP1 loss was identified in 13/57 cases (22.8%). Targeted sequencing consistently identified CTNNB1 exon 3 mutations. Additional low-frequency molecular alterations affecting genes involved in cell cycle regulation, chromatin remodeling, and signaling pathways, including CDKN2A and BAP1, were observed. During a mean follow-up of 97.2 months, distant metastasis occurred in 4/62 patients (6.5%) and locally invasive disease in 4/62 (6.5%), with an overall survival rate of 95%. Overall, these findings highlight the biological heterogeneity of SPNs and indicate that, despite a shared molecular background, aggressive behavior is not defined by a single reproducible pathological or molecular feature.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.por-journal.com/articles/10.3389/pore.2026.1612333</guid>
        <link>https://www.por-journal.com/articles/10.3389/pore.2026.1612333</link>
        <title><![CDATA[Prognostic and predictive factors of immune checkpoint inhibitor therapy in urinary bladder cancer]]></title>
        <pubdate>2026-03-02T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Melinda Váradi</author><author>Balázs Magyar</author><author>Ádám Széles</author><author>Sára Korda</author><author>Bernadett Németh</author><author>Barbara Simon</author><author>Henning Reis</author><author>Csilla Oláh</author><author>Orsolya Horváth</author><author>Bálint Dér</author><author>Péter Nyirády</author><author>Tibor Szarvas</author>
        <description><![CDATA[Immune checkpoint inhibitor (ICI) therapy has become a firmly integrated component of the systemic treatment repertoire for locally advanced and metastatic urothelial bladder cancer (UBC). Over the past decade, multiple ICIs have demonstrated meaningful clinical activity, and their indications have expanded across treatment lines, including second-line therapy after platinum, first-line therapy for cisplatin-ineligible disease, avelumab maintenance following chemotherapy, and, more recently, combination strategies such as pembrolizumab plus enfortumab vedotin. Despite these advances, patient responses to ICIs remain highly heterogeneous. While a subset of patients achieves substantial tumor regression and long-term survival, a considerable proportion derives little or no benefit. The rapidly evolving therapeutic landscape - encompassing antibody-drug conjugates, targeted agents, and perioperative ICI approvals - further emphasizes the need to identify which patients are most likely to respond to immunotherapy. Given the marked variability in therapeutic sensitivity and the increasing availability of alternative effective treatments, accurate prediction of ICI efficacy is becoming increasingly crucial for personalized treatment selection. In this review, we provide a comprehensive overview of currently established and emerging biomarkers of ICI response in UBC, including PD-L1 immunohistochemistry, serum inflammatory markers, tumor mutational burden, histology and molecular subtypes, gene expression patterns and microbiome features. We discuss their strengths, limitations, and potential translational relevance, highlighting ongoing challenges and future directions.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.por-journal.com/articles/10.3389/pore.2026.1612298</guid>
        <link>https://www.por-journal.com/articles/10.3389/pore.2026.1612298</link>
        <title><![CDATA[The effect of the COVID-19 pandemic on TNM status among head and neck cancer patients in Hungary]]></title>
        <pubdate>2026-02-20T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Benedek Besenczi</author><author>Angéla Horváth</author><author>Imre Uri</author><author>Kornél Dános</author>
        <description><![CDATA[PurposeHungary ranks among the countries with both the highest incidence and mortality of head and neck cancers worldwide. The COVID-19 pandemic, caused by the SARS-CoV-2 virus placed a significant burden on the healthcare system. Our study aims to investigate its impact on Hungarian head and neck cancer patients by analyzing changes in stage at presentation, patient delay and overall survival due to the viral pandemic.MethodsA retrospective cohort study was performed analyzing patients’ medical records from a tertiary head and neck surgical center in Hungary. The inclusion criteria required the tumor to be a squamous cell carcinoma of the oral cavity, oropharynx, hypopharynx, or larynx. Based on the timing of restrictive measures due to the pandemic, patients were divided into two groups: Group A: “pre-COVID-19” (3 September 2012 – 11 March 2020) and Group B: “post-COVID-19 onset” (12 March 2020 – 5 December 2022) The latter group was further subdivided into Group C: “during-COVID-19” (12 March 2020 – 13 June 2021) and Group D: “post-COVID-19” (14 June 2021 – 5 December 2022).Results620 patients met the inclusion criteria. Group A had 427 patients, Group B had 193, Group C had 69, and Group D had 124. Compared to Group A (54.1%), there was a higher proportion of N+ status patients in Group B (69.6%), Group C (63.8%), and Group D (73.0%), with a significant difference throughout. Changes in T status and patient delay time was not present. Analyzing symptoms, there was a significant increase in delay time for patients with hemoptysis (from 2.1 to 16.3 weeks). No significant difference in overall survival was observed between the study groups.ConclusionThere are limited publications available on this topic in Europe, particularly in Hungary, especially studies that compare the periods before, during, and after the COVID-19 pandemic. Head and neck cancer patients were found to have more advanced clinical nodal disease after the COVID-19 onset, despite no changes in patient delay time and overall survival. Our findings highlight the importance of further studies on how viral infections and pandemics affect oncology care pathways to improve preparedness for future public health crises.]]></description>
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        <guid isPermaLink="true">https://www.por-journal.com/articles/10.3389/pore.2026.1612238</guid>
        <link>https://www.por-journal.com/articles/10.3389/pore.2026.1612238</link>
        <title><![CDATA[Germline BRCA testing in routine clinical practice: a single-center experience]]></title>
        <pubdate>2026-02-20T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Aliz Nikolényi</author><author>Ágnes Dobi</author><author>Dóra Sántha</author><author>Renáta Kószó</author><author>Máté Iványi</author><author>Emese Horváth</author><author>Márton Zsolt Enyedi</author><author>Katalin Priskin</author><author>Bernadett Csányi</author><author>Attila Patócs</author><author>Henriett Butz</author><author>János Papp</author><author>Zoltán Varga</author><author>Rozália Tóth</author><author>Judit Oláh</author><author>Zsuzsanna Kahán</author>
        <description><![CDATA[The identification of gBRCA1/2 mutations in breast cancer patients is crucial. Successful identification of the mutations has the potential to alter disease treatment and healthcare management of patients whose relatives harbor pathogenic/likely pathogenic (P/LP) variants. In this retrospective analysis, patient- and disease-specific medical data were analyzed in a cohort of breast cancer patients with a known gBRCA1/2 status who were treated between 2019–2021. The prevalence and type of gBRCA1/2 P/LP variants, and their relation to the histopathological data of the cancers, were studied. The presence of one or more clinical criteria leading to germline testing, the outcome of patient management, and family member outcomes were collected. Germline variants were found in 67/259 cases and included 61 P/LP alterations and six “variants of unknown significance” (VUS) of the BRCA1/2 genes. A spectrum of 31 different variants was detected; eight of them occurred in more than one patient, of which three (detected in 26 cases) belonged to the mutations most prevalently detected by the previously used technology in Hungary. The likelihood of revealing a pathogenic gBRCA1/2 mutation increased with the number of risk criteria for germline testing. The presence of three or more risk criteria was predictive for carrying a gBRCA1/2 mutation with an odds ratio (OR) of 10.65 (95% CI 5.20–21.80, p < 0.001). Among the histopathology data, a higher rate of grade 3 or triple negative breast cancer was found among gBRCA1/2 P/LP variant carriers as compared to that in non-carriers. For ultimately revealing a gBRCA1/2 P/LP variant, a positive family history (OR 6.69, 95% CI 1.82–24.64, p = 0.003) and triple negative breast cancer (OR 5.65, 95% CI 2.73–11.71, p < 0.001) were the strongest independent predictive factors. Knowing of gBRCA1/2 alterations meant healthcare management was modified in 86.9% of cases. Germline testing for breast cancer patients, guided by current protocols, is essential for optimizing patient care. Adhering to established clinical criteria facilitates effective patient selection while preventing the unnecessary expansion of testing to average-risk populations. Keywords: BRCA1/2, breast cancer, cancer susceptibility genes, germline testing, medical genetics.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.por-journal.com/articles/10.3389/pore.2026.1612284</guid>
        <link>https://www.por-journal.com/articles/10.3389/pore.2026.1612284</link>
        <title><![CDATA[Isolated signals in BCL2, MYC, BCL6, and DDIT3 FISH: implications for genetic alterations and protein dysregulation]]></title>
        <pubdate>2026-02-11T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Zongchen Wei</author><author>Qiuyue Chen</author><author>Zhenbo Feng</author><author>Fang Tang</author>
        <description><![CDATA[ObjectivesFluorescence in situ hybridization (FISH) break-apart probes are widely employed to detect gene rearrangements in malignant tumors. Notwithstanding their utility, the complex genetic alterations in tumors frequently give rise to isolated signals, the mechanisms underlying which remain poorly understood. This study aimed to elucidate the genetic causes of isolated FISH signals in lymphoma and myxoid liposarcoma samples, providing a more accurate basis for interpreting FISH results.MethodsSix cases of lymphoma and myxoid liposarcoma, which showed isolated signals for BCL2, MYC, BCL6, or DDIT3 in FISH detection, were carefully screened. Whole genome resequencing (WGR) was employed to analyze the genetic variations present in these samples. In addition, immunohistochemistry was used to assess the expression levels of the corresponding proteins in these samples.ResultsWGR results revealed that all six cases with isolated signals harbored target gene translocations, with 5′and 3′probe-binding region deletions or inversions detected in BCL2, MYC, and BCL6, and in the 5′probe-binding region of DDIT3. Additionally, overexpression of the corresponding proteins was present in samples with isolated BCL2, MYC, and BCL6 signals.ConclusionDeletions or inversions in the probe-binding sequence regions may disrupt probe recognition and binding, leading to isolated FISH signals for BCL2, MYC, BCL6, and DDIT3. Notably, in cases with isolated BCL2, MYC, or BCL6 signals, translocations involving these genes were associated with increased expression of their encoded proteins. These findings improve the understanding of FISH signal interpretation in tumor gene rearrangement detection and provide a valuable reference for clinical diagnosis.]]></description>
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        <guid isPermaLink="true">https://www.por-journal.com/articles/10.3389/pore.2026.1612311</guid>
        <link>https://www.por-journal.com/articles/10.3389/pore.2026.1612311</link>
        <title><![CDATA[Sample adequacy in bronchoscopic ROSE: comparison between laboratory specialist and pathologist]]></title>
        <pubdate>2026-02-03T00:00:00Z</pubdate>
        <category>Brief Research Report</category>
        <author>Gergő Szűcs</author><author>Judit Pápay</author><author>Eszter Regős</author><author>Ildikó Krencz</author><author>Márton Sághi</author><author>Péter Horváth</author>
        <description><![CDATA[Rapid on-site evaluation (ROSE) during bronchoscopy provides the opportunity to assess the adequacy of the sampling site, thus enabling diagnosis. The rapid evaluation of smears is typically performed by cytopathologists, but this is not always feasible. At our institution, a university-trained clinical biochemist performs the evaluation of ROSE smears. Our aim was to compare ROSE evaluations conducted by a laboratory specialist and a cytopathologist. We assessed the adequacy of lymph node samples from 78 patients using ROSE: 37 samples were obtained via EBUS-TBNA and 41 via TBNA. All smears were examined by the laboratory specialist, and simultaneously prepared parallel smears from the same needle passes were sent to the Department of Pathology for evaluation. Of the 78 samples, both the laboratory specialist and the pathologist team deemed 63 samples adequate and 8 samples inadequate. In 7 cases, there was a disagreement between the pathologist team and laboratory specialist. This resulted in a 92.3% agreement. The Cohen’s kappa value was 0.71, indicating strong and Gwet’s AC1 value was 0.90 corresponding to almost perfect agreement. The diagnostic performance was also excellent. Our conclusion is that ROSE performed by a laboratory specialist is a suitable alternative to on-site evaluation by a pathologist. It may help to overcome the resource shortage of interventional pulmonologists and cytopathologists.]]></description>
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        <guid isPermaLink="true">https://www.por-journal.com/articles/10.3389/pore.2026.1612324</guid>
        <link>https://www.por-journal.com/articles/10.3389/pore.2026.1612324</link>
        <title><![CDATA[Editorial: Cytometry in oncology]]></title>
        <pubdate>2026-01-29T00:00:00Z</pubdate>
        <category>Special Issue Editorial</category>
        <author>Gábor Barna</author><author>József Dudás</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.por-journal.com/articles/10.3389/pore.2026.1612325</guid>
        <link>https://www.por-journal.com/articles/10.3389/pore.2026.1612325</link>
        <title><![CDATA[Commentary: CVM-1118 (foslinanib), a 2-phenyl-4-quinolone derivative, promotes apoptosis and inhibits vasculogenic mimicry via targeting TRAP1]]></title>
        <pubdate>2026-01-27T00:00:00Z</pubdate>
        <category>Commentary</category>
        <author>Mary J. C. Hendrix</author><author>Elisabeth A. Seftor</author><author>Richard E. B. Seftor</author><author>Yi-Wen Chu</author><author>Du-Shieng Chien</author><author>Yen-Ling Chen</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.por-journal.com/articles/10.3389/pore.2026.1612297</guid>
        <link>https://www.por-journal.com/articles/10.3389/pore.2026.1612297</link>
        <title><![CDATA[Microsatellite status and its correlation with clinicopathological features in gastric carcinoma: insights from a retrospective study in Northern Pretoria]]></title>
        <pubdate>2026-01-23T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Ntebogeng Kgokong</author><author>Michelle McCabe</author><author>Lucia N. Mhlongo</author><author>Thato Nkwagatse</author><author>Moshawa C. Khaba</author>
        <description><![CDATA[Introduction/backgroundGastric carcinomas (GC) are heterogeneous malignancies characterised by distinct histological and molecular subtypes. The microsatellite instability (MSI) molecular subtype, resulting from deficient DNA mismatch repair (dMMR), accounts for approximately 22% of global GC cases. Empirical evidence indicates differences in clinicopathological features, demographics, and treatment response in MSI GC compared to microsatellite stable (MSS) GC. MSI status has emerged as a potential biomarker for advanced GC, and this study aimed to determine the MSI prevalence of histopathologically confirmed GC cases at our centre.Method and materialThis was a retrospective cross-sectional analysis of GC cases from 2018 to 2022, which were retrieved from the laboratory information system. DNA from these cases was isolated and assessed for MSI using a pentaplex PCR panel and confirmatory IHC on MSI-H was performed. Samples with no allelic size variation in the 5 microsatellite markers were classified as microsatellite stable (MSS), variation in 1 marker as microsatellite instability low (MSI-L), and variation in 2 or more microsatellite markers as MSI-H.ResultsThe study consisted of 64 cases with a MSI prevalence of 21.9% (n = 14) displaying a male predominance (n = 10; 71.4%) and a mean age of 62.7 years. Among these 14 MSI cases, 42.9% (n = 6) were classified as MSI-H with a mean age of 59.3 years. Half (n = 3) of these cases presented with upper gastrointestinal bleeding, with a majority of them diagnosed with moderately differentiated adenocarcinomas (66.7%). Microsatellite instability low was seen in 57.1% (n = 8) of the cases with a mean age of 65.3 years, and of these, patients presented with vomiting, epigastric pain and dysphagia with equal frequency at 25% (n = 2 respectively).ConclusionThe frequency of MSI cases in this study is congruent with global trends, highlighting the importance of microsatellite status in GC for understanding clinicopathological differences between MSI and MSS patients. These findings support the potential of MSI status as a biomarker.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.por-journal.com/articles/10.3389/pore.2026.1612253</guid>
        <link>https://www.por-journal.com/articles/10.3389/pore.2026.1612253</link>
        <title><![CDATA[Assessment of the prevalence and consistency of microvascular flow imaging patterns in focal nodular hyperplasia]]></title>
        <pubdate>2026-01-23T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Boglárka Zsély</author><author>Aladár Dávid Rónaszéki</author><author>Marco Himsel</author><author>Zita Zsombor</author><author>Gabriella Győri</author><author>Anikó Folhoffer</author><author>Dorottya Mühl</author><author>Viktor Bérczi</author><author>Byung-So Park</author><author>Damján Pekli</author><author>Oszkár Hahn</author><author>András Kiss</author><author>Pál Maurovich-Horvat</author><author>Pál Novák Kaposi</author>
        <description><![CDATA[ObjectivesTo identify characteristic vascular features of focal nodular hyperplasia (FNH) on microvascular flow imaging (MVFI) and assess the utility of MVFI in FNH diagnosis.MethodsThis retrospective study included B-mode ultrasound (US) and MVFI scans of 41 FNHs, 21 hepatocellular carcinomas (HCCs), 20 metastases (METs), 10 hepatocellular adenomas (HCAs), and eight hemangiomas (HEMs) from 80 patients. Diagnoses were confirmed by contrast-enhanced imaging or histology. Two independent observers evaluated vascular patterns on MVFI. Interobserver agreement was calculated, and logistic regression models using either B-mode or MVFI features were developed to differentiate FNH from other focal liver lesions (FLLs).ResultsInterobserver agreement for MVFI patterns was substantial (κ = 0.641, p < 0.001). The spoke-wheel pattern (OR = 51.53 and 35.28) and central artery (OR = 4.96 and 1.95) were strongly associated with FNH. However, the spoke-wheel pattern also appeared in subsets of HCAs (20%–30%), HCCs (14%–19%), and METs (5%–15%). Rim vascularity was common but nonspecific. The MVFI-based model (AUC = 0.891, p < 0.001) outperformed the B-mode model (AUC = 0.814) in distinguishing FNH. For lesions ≥3 cm, MVFI accuracy was even higher (AUC = 0.944, p < 0.001).ConclusionMVFI enhances the diagnostic confidence of US for FNH, particularly in asymptomatic patients at low risk for malignancy. However, given the potential overlap with certain malignant FLLs, MVFI findings should be interpreted with caution.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.por-journal.com/articles/10.3389/pore.2025.1612248</guid>
        <link>https://www.por-journal.com/articles/10.3389/pore.2025.1612248</link>
        <title><![CDATA[Digitally derived Ki-67 proliferation index for GastroEnteroPancreatic neuroendocrine neoplasms]]></title>
        <pubdate>2026-01-07T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Tamás Micsik</author><author>Lilla Csellár</author><author>Árpád V. Patai</author><author>Anna Jakab</author><author>Viktor Jónás</author><author>Béla Molnár</author>
        <description><![CDATA[Ki-67 proliferation indices (PIs) define the grading of GastroEnteroPancreatic NeuroEndocrine Neoplasms (GEPNENs) and are crucial for therapeutic decisions. The precise Ki-67 assessment relies on manual counting, which is time-consuming, hardly accessible during routine pathological signout and thus usually replaced by the easier eye-estimation/balling method prone to interobserver variability and differences originating from the hot-spot size, localisation and tumor heterogeneity. These discrepancies can significantly affect the final PI resulting in misgrading of GEPNENs with potential adverse patient outcomes. In the era of digital pathology more and more applications are available to overcome this problem. In our retrospective study of 60 surgically resected GEPNEN cases, we tested the equivalence of traditional clinical (C) grading, manual counting with a MarkerCounter (MC) application and automatic grading with tumor recognition PatternQuant application with subsequent NuclearQuant (NQ) PI-assessment within 3DHistechs digital pathology platform. We found almost perfect agreement between the various grading methods (Spearman rank-order correlations: C vs. MC: ρ = 0.912, C vs. NQ: ρ = 0.883, MC vs NQ: ρ = 0.953) without clinically significant misgradings. Also the numerical values of the PIs derived with the various methods showed close correlations (Linear regression: C vs. MC: r = 0.952, C vs. NQ: r = 0.925, MC vs NQ: r = 0.978). The automated PI-assessment involved a mean 5-fold more tumor cells, better approximating the global/total Ki-67 PI, which was earlier shown to deliver more robust prognostic power and decreased interobserver variability. Furthermore, G3 tumors differed from G2 and G1 tumors in their cytomorphological parameterers: high grade tumors had significantly larger and more polymorphic, less regular tumor cell nuclei, which parameters could be also utilized for grading and/or prognostication purposes. Our study applied a simple, quick, easy-to-use, Machine Learning-based method that could be incorporated into routine digital pathology signout alleviating pathologists’ workload and increasing precision and recall rate.]]></description>
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        <guid isPermaLink="true">https://www.por-journal.com/articles/10.3389/pore.2025.1612202</guid>
        <link>https://www.por-journal.com/articles/10.3389/pore.2025.1612202</link>
        <title><![CDATA[Valosin containing protein (VCP/p97) expression in laryngeal squamous cell carcinoma: clinical evaluation and implications for targeted therapy]]></title>
        <pubdate>2025-11-21T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Inga M. C. Seuthe</author><author>Hanna C. Hunsicker-Biederbeck</author><author>Markus Ruwe</author><author>Julius Knierer</author><author>Eric Ehrke-Schulz</author><author>Eren Erdogan</author><author>Sabine Eichhorn</author><author>Jonas J.-H. Park</author>
        <description><![CDATA[PurposeValosin-containing protein (VCP/p97) is a key regulator of proteostasis and cellular stress response and has been linked to tumor progression and poor prognosis in various malignant diseases. However, data on its role in laryngeal squamous cell carcinoma (LSCC) are lacking.MethodsIn this retrospective single-center study, VCP/p97 protein expression was analyzed by immunohistochemistry in a cohort of 100 LSCC patients. Expression levels were semi-quantitatively assessed with H-Score, compared to normal tissue if possible and correlated with clinicopathological parameters. Survival analyses were evaluated by Cox regression.ResultsVCP/p97 was expressed in all tumors. Most LSCC (77.0%) showed a uniform staining pattern. 46 of these tumors (59.7%) exhibited a staining intensity of 2–3. Among the tumors with a non-homogeneous staining pattern (n = 23), two tumors showed a predominance to lower staining (staining intensity 1). In 13 samples a comparison to normal epithelium was possible. In these samples, 9 (69.2%) samples showed higher VCP/p97 expression compared to the normal epithelium and 4 (30.8%) showed lower expression. VCP/p97 H-Score was not significantly associated with tumor stage, grade, lymph node status or patient survival.ConclusionAlthough VCP/p97 expression is not prognostic in LSCC, its consistent expression may suggest a potential role as a molecular target. Further functional and translational studies are warranted to explore the therapeutic utility of VCP/p97 inhibition in LSCC.]]></description>
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        <guid isPermaLink="true">https://www.por-journal.com/articles/10.3389/pore.2025.1612266</guid>
        <link>https://www.por-journal.com/articles/10.3389/pore.2025.1612266</link>
        <title><![CDATA[Comprehensive genomic profiling for homologous recombination deficiency guides PARP inhibitor therapy recommendations in ovarian cancer]]></title>
        <pubdate>2025-11-13T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Alp Inci</author><author>Isabell Witzel</author><author>Holger Moch</author><author>Sepehr Rahmani-Khajouei</author><author>Martin Zoche</author><author>Eleftherios Pierre Samartzis</author>
        <description><![CDATA[ObjectiveTo evaluate the technical performance and clinical integration of FoundationOne®CDx (F1CDx) for high-grade serous ovarian cancer (HGSOC), focusing on its role in guiding PARP inhibitor (PARPi) therapy recommendations in a tertiary oncology center.MethodsWe conducted a retrospective analysis of 178 F1CDx tests performed on 168 HGSOC patients with unknown BRCA mutation status between January 2019 and August 2024. Molecular findings, including BRCA1/2 mutations, homologous recombination deficiency (HRD) status, loss of heterozygosity (LOH) scores, and HRR-related gene alterations, were correlated with tumor board recommendations and decisions for PARPi therapy. Laboratory turnaround time (TAT), assay performance, and integration into clinical workflows were assessed.ResultsThe F1CDx assay successfully generated comprehensive molecular profiles in 174 samples, with minimal limitations due to computational tumor content or inconclusive HRD readout. BRCA1/2 mutations were detected in 13.1% of patients, and 39.5% of tumors were HRD-positive (LOH ≥16%). In the internal cohort, 81.8% of patients received PARPi therapy recommendations, all directly informed by F1CDx results. PARPi selection differed by HRD status, with niraparib favored in HR-proficient and olaparib in HRD-positive tumors. The mean laboratory TAT was 8.4 days (standard deviation ±3.8), with 92.2% of tests completed within 14 days. No additional profiling was required for PARPi therapy recommendation, and no incidental findings beyond the scope of HRD testing were detected.ConclusionMolecular profiling with F1CDx proved to be a technically feasible, clinically impactful, and time-efficient assay, demonstrating its value in supporting molecular-guided PARPi therapy recommendations in the routine care of HGSOC patients.]]></description>
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        <guid isPermaLink="true">https://www.por-journal.com/articles/10.3389/pore.2025.1612252</guid>
        <link>https://www.por-journal.com/articles/10.3389/pore.2025.1612252</link>
        <title><![CDATA[Trop2 expression, p16 expression status, and histologic subtype in carcinoma of the uterine cervix]]></title>
        <pubdate>2025-11-07T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Grit Gesine Ruth Hiller</author><author>Benjamin Wolf</author><author>Mirjam Forberger</author><author>Annekathrin Freude</author><author>Christine Elisabeth Brambs</author><author>Svenja Droste</author><author>Lars-Christian Horn</author><author>Anne Kathrin Höhn</author>
        <description><![CDATA[IntroductionThe antibody-drug conjugate (ADC) Sacituzumab-Govitecan (SG), a humanized anti-Trop2 monoclonal antibody linked to the cytotoxic topoisomerase I inhibitor SN38, achieved promising results in the treatment of various solid tumors. Treatment approaches with SG requires the expression of Trop2 within tumor cells. The present study explored immunohistochemical Trop2 expression in cervical carcinomas in correlation with histologic subtypes and p16 expression status.Material and methodsUsing an immunoreactive score (IRS), immunohistochemical Trop2 expression in surgically treated cervical carcinoma specimens was evaluated by comparing squamous cell carcinomas and adenocarcinomas, and the expression status of p16 as a surrogate marker for high-risk HPV infection.ResultsA total of 101 cases were included in this study. Of these 75% were squamous cell carcinomas, and 25% were adenocarcinomas, and 5% showed negative immunoexpression for p16, indicating HPV-independent carcinoma. All tumors showed at least weak Trop2 expression. There were no differences in the mean Trop2 IRS-scores comparing histological subtype [squamous: 8.5 (3–9) vs. adeno: 6 (1–9); p = 0.8] and p16 expression status [positive: 9 (6–9) vs. negative: 8 (6–9; p = 0.6]. No differences in Trop2 expression were observed when post-surgical tumor stage, pelvic lymph node status and peritumoral stromal remodelling (desmoplastic response and peritumoral infiltrating lymphocytes) were analysed.ConclusionRegardless of the histologic tumor type and p16 expression status, cervical carcinomas show high Trop2 expression and, therefore, may represent a promising therapeutic target. Clinical trials exploring Trop2 directed ADCs such as Sacituzumab-Govitecan are warranted in this cancer type, including the prognostically poor HPV-independent (p16 negative) tumors, mainly adenocarcinomas.SignificanceRegardless of the histologic tumor type and p16-expression status, cervical carcinomas show high Trop2 expression, which may therefore represent a promising therapeutic target in these tumors.]]></description>
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        <guid isPermaLink="true">https://www.por-journal.com/articles/10.3389/pore.2025.1612161</guid>
        <link>https://www.por-journal.com/articles/10.3389/pore.2025.1612161</link>
        <title><![CDATA[Examination of histopathological growth patterns of liver metastases in a retrospective, consecutive, single-center, cohort study]]></title>
        <pubdate>2025-10-30T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Anita Sejben</author><author>Parsa Abbasi</author><author>Boglárka Pósfai</author><author>Tamás Lantos</author>
        <description><![CDATA[ObjectiveHistopathological growth patterns (HGPs) were identified as prognostic factors for colorectal adenocarcinomas; however, they have been examined in a consecutive setting with controversial results. Our study aimed to examine HGPs’ association with clinicopathological factors in a retrospective, consecutive, single-center, cohort study.MethodsOur study comprised the data of patients who were treated for liver metastases from 2011 to 2023. In all cases, general clinicopathological data were registered. The histological slides of all metastatic foci were individually evaluated. Statistical analyses were carried out by using the Kruskal-Wallis and Fisher’s exact test. P-values less than 0.05 were considered significant.ResultsAltogether 336 liver metastases from 205 patients have been included in our retrospective, consecutive, single-center, cohort study. The male-to-female ratio was 116:89, and the average age of patients was 68 years (median: 69.5; range: 27-93). Most examined cases were of colorectal origin (n = 164). Replacement pattern was found to be the most common (n = 99). The 163 colorectal adenocarcinoma metastasis cases reflected a similar order of magnitude of replacement type (n = 78) and desmoplastic (n = 68) HGPs. The majority (70%) of neuroendocrine tumours (n = 10) showed pushing HGP, while 3 of 5 non-epithelial tumours were associated with replacement-type HGP. A significant association was found between HGPs and histological subtype (p < 0.001), grade (p = 0.002), the presence of venous spread (p = 0.02), and the largest diameter of liver metastasis (p = 0.023).ConclusionEven though our study highlights the HGPs’ association with several clinicopathological parameters that might influence prognosis, their role in the treatment process of colorectal or other carcinomas remains controversial.]]></description>
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        <guid isPermaLink="true">https://www.por-journal.com/articles/10.3389/pore.2025.1612227</guid>
        <link>https://www.por-journal.com/articles/10.3389/pore.2025.1612227</link>
        <title><![CDATA[Case Report: From teratoma to adenocarcinoma: molecular insights into somatic-type malignancy in testicular germ cell tumors - two case reports and review of the literature]]></title>
        <pubdate>2025-10-28T00:00:00Z</pubdate>
        <category>Case Report</category>
        <author>Tímea Rozsvai</author><author>Boglárka Pósfai</author><author>László Torday</author><author>Emőke Borzási</author><author>György Lázár</author><author>Judit Oláh</author><author>Bence Radics</author><author>István Előd Király</author><author>István Papos</author><author>Márton Balázsfi</author><author>Zsombor Melegh</author><author>Levente Kuthi</author><author>Anikó Maráz</author>
        <description><![CDATA[Testicular germ cell tumors (TGCTs), though typically responsive to therapy, may rarely develop somatic-type malignancy (STM), a transformation associated with poor prognosis and chemoresistance. This study presents two cases of postpubertal-type teratoma with intestinal-type adenocarcinoma as STM, offering insights into their clinical, histopathological, immunophenotypic, and molecular profiles. The first patient, a 63-year-old male, presented with pulmonary and retroperitoneal metastases and underwent orchiectomy, revealing an intratesticular intestinal-type adenocarcinoma. Molecular testing confirmed 12p overrepresentation and pathogenic mutations in CTNNB1, STK11, and MDM2. The second patient, initially diagnosed at age 35 with a mixed TGCT, developed STM as a late recurrence 16 years post-orchiectomy, manifesting as a retroperitoneal mass with vertebral invasion. Histology again confirmed intestinal-type adenocarcinoma, and molecular testing revealed amplification of ERBB2, KRAS, along with mutations in TP53 and PIK3CA. Both cases were managed with capecitabine-oxaliplatin plus bevacizumab, followed by maintenance therapy, achieving disease stabilization for at least 9 months. These cases illustrate the diagnostic and therapeutic complexities of STM, particularly with adenocarcinoma morphology that may mimic primary gastrointestinal neoplasms. Accurate diagnosis required exclusion of alternate primary sites and demonstration of chromosome 12 aberrations using FISH and next-generation sequencing. Our findings emphasize the importance of long-term follow-up in TGCT patients, particularly those with teratomatous elements, and highlight the value of cytogenetic and molecular profiling in confirming STM and identifying potential therapeutic targets. Given the rarity of STM, especially in metastatic or recurrent settings, there is an urgent need for standardized diagnostic protocols and evidence-based treatment strategies. These cases support the use of tumor-specific chemotherapy regimens guided by the histological and molecular characteristics of STM.]]></description>
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