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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>
        <generator>Frontiers Feed Generator,version:1</generator>
        <pubDate>2026-05-12T21:09:45.923+00:00</pubDate>
        <ttl>60</ttl>
        <item>
        <guid isPermaLink="true">https://www.por-journal.com/articles/10.3389/pore.2026.1612303</guid>
        <link>https://www.por-journal.com/articles/10.3389/pore.2026.1612303</link>
        <title><![CDATA[Magnetic resonance imaging based radiomics for predicting pathogenetic features and survival in rectal cancer]]></title>
        <pubdate>2026-05-07T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Bertalan Toth</author><author>Marcell Mesterházi</author><author>Istvan Szabo</author><author>Tamas Mersich</author><author>Erika Toth</author><author>Janos Szoke</author><author>Andras Benczur</author><author>Csaba Kerepesi</author><author>David Laszlo Tarnoki</author><author>Adam Domonkos Tarnoki</author>
        <description><![CDATA[BackgroundPrediction of pathologic features and outcome in patients with rectal cancer is challenging as a result of lack of a significant biomarker and heterogeneity between and within tumors. This study aims to evaluate the potential of Magnetic Resonance Imaging (MRI)-based radiomics in predicting key pathological features and long-term survival outcomes in patients.MethodsA retrospective study was conducted on 510 rectal cancer patients treated between 2015 and 2019. The inclusion criteria required pre-therapeutic MRI performed on a Discovery MR750W 3.0T machine and known KRAS mutation status. Forty-seven patients met the criteria. MRI sequences included T1-weighted, T2-weighted fat-saturated (T2FS), high-resolution T2-weighted (T2HR), and diffusion-weighted imaging (DWI). Radiomic features were extracted using PyRadiomics, and machine learning models were developed using XGBoost and LightGBM classifiers. Feature selection was performed using Sequential Feature Selector (SFS) and Minimum Redundancy Feature Selection (mRMR).ResultsThe model for KRAS mutation status achieved an Area Under the ROC curve (AUC) of 0.7475 (training) and 0.75 (testing). Lymph node invasion prediction had an AUC of 0.7892 (training) and 0.7984 (testing). Vascular invasion prediction yielded an AUC of 0.6989 (training) and 0.7143 (testing). The 5-year survival prediction model showed an AUC of 0.7848 (training) and 0.7750 (testing). Metastasis prediction achieved an AUC of 0.6627 (training) and 0.6857 (testing).ConclusionMRI-based radiomics demonstrates significant potential in predicting key pathological features and long-term survival outcomes in rectal cancer patients. Integrating multimodal imaging data and clinical information, along with automated segmentation techniques, could further enhance model accuracy and clinical utility.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.por-journal.com/articles/10.3389/pore.2026.1612302</guid>
        <link>https://www.por-journal.com/articles/10.3389/pore.2026.1612302</link>
        <title><![CDATA[Postpartum acquired hemophilia A: immunopathogenesis, diagnostic challenges, and treatment with the CyDRi protocol]]></title>
        <pubdate>2026-05-04T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Ágnes Szappanos</author><author>Hajnalka Andrikovics</author><author>Péter Varga</author><author>Mónika Fekete</author><author>Vince Fazekas-Pongor</author><author>Márk Lehoczki</author><author>Viktória Király</author><author>Beáta Vilimi</author><author>Gábor Mikala</author><author>Imre Bodó</author><author>Andrea Ceglédi</author>
        <description><![CDATA[Acquired hemophilia A (AHA) is a rare, potentially life-threatening autoimmune bleeding disorder characterized by the development of inhibitory autoantibodies against factor VIII (FVIII). While most commonly diagnosed in the elderly, AHA can also occur in the postpartum period, where it presents unique diagnostic and therapeutic challenges. This review provides a comprehensive overview of the pathogenesis, clinical features, diagnostic approaches, and current therapeutic strategies for postpartum AHA. We highlight the immunological shifts during pregnancy and the postpartum period that may contribute to the breakdown of immune tolerance and the emergence of FVIII autoantibodies. Key aspects of laboratory diagnosis are outlined, including the role of coagulation screening, mixing studies, and inhibitor assays. We compare the efficacy and safety of established immunosuppressive regimens, with a particular focus on the CyDRi protocol—a combination of cyclophosphamide, dexamethasone, and rituximab—which has demonstrated high rates of complete remission with a favorable toxicity profile. To illustrate clinical application, we describe a case of severe postpartum AHA managed successfully with the CyDRi protocol, followed by an uneventful subsequent pregnancy. With timely diagnosis and appropriately tailored immunosuppressive therapy, postpartum AHA can be effectively treated, and favorable hematologic and reproductive outcomes are achievable.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.por-journal.com/articles/10.3389/pore.2026.1612388</guid>
        <link>https://www.por-journal.com/articles/10.3389/pore.2026.1612388</link>
        <title><![CDATA[Case Report: The molecular profile of granular cell astrocytoma predicts aggressive clinical behavior, independent of morphology]]></title>
        <pubdate>2026-05-04T00:00:00Z</pubdate>
        <category>Case Report</category>
        <author>Melanie Jensen</author><author>Pranoy Das</author><author>Oliver Wroe-Wright</author><author>Oscar MacCormac</author><author>Francesco Marchi</author><author>Ali Elhag</author><author>Yasir A. Chowdhury</author><author>Ross Laxton</author><author>Rebecca Ellmers</author><author>Omar Al-Salihi</author><author>Keyoumars Ashkan</author><author>Ranjeev Bhangoo</author><author>Francesco Vergani</author><author>Istvan Bodi</author><author>Zita Reisz</author><author>Jose Pedro Lavrador</author>
        <description><![CDATA[BackgroundGranular cell astrocytoma (GCA) is a rare, morphologically distinct variant of IDH-wildtype glioblastoma that can appear deceptively low-grade yet behave aggressively. Its molecular features remain poorly defined, and no methylation-based classification has previously been reported.MethodsTwo GCAs diagnosed in our clinical neuropathology department were described with the integration of clinical, intraoperative, histopathological, and molecular data, including DNA methylation profiling, a targeted next-generation sequencing panel, and, in one case, whole genome sequencing (WGS).ResultsThe patients were aged 63 and 54 years old, respectively, both presenting with supratentorial tumors showing granular cell morphology. Case 1 showed a densely cellular tumor composed entirely of bland-appearing granular cells without a conventional astrocytic component. Case 2 showed low-grade granular cell areas transitioning into high-grade astrocytic regions with mitoses, microvascular proliferation, and necrosis. Despite these morphological differences, both cases matched the methylation class “Glioblastoma, IDH-wildtype, mesenchymal subtype” and shared molecular features typical of glioblastoma, including chromosome +7/−10 and CDKN2A/B deletion. Both patients harbored oncogenic NF1 variants. WGS in Case 2 also revealed homozygous MTAP loss and chromoanasynthesis on chromosome 9. Case 1 received Stupp protocol chemoradiotherapy, recurred after 3 months of treatment, and died 11 months after diagnosis. Case 2 has progressed with a new posterior fossa lesion while on adjuvant temozolomide.ConclusionThese cases demonstrate that GCAs span a morphological spectrum yet molecularly correspond to the mesenchymal subtype of IDH-wildtype glioblastoma. Integrated molecular testing is therefore essential for accurate diagnosis and for guiding clinical management, including consideration for potential clinical trial enrollment.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.por-journal.com/articles/10.3389/pore.2026.1612328</guid>
        <link>https://www.por-journal.com/articles/10.3389/pore.2026.1612328</link>
        <title><![CDATA[Multimodal prehabilitation for upper gastrointestinal tumors: effects on postoperative morbidity and mortality – a meta-analysis of randomized controlled trials]]></title>
        <pubdate>2026-04-28T00:00:00Z</pubdate>
        <category>Systematic Review</category>
        <author>Csenge Papp</author><author>Armand Csontos</author><author>Daniel Kehl</author><author>Lili Dora Sindler</author><author>Andras Vereczkei</author><author>Andras Papp</author>
        <description><![CDATA[BackgroundPatients suffering from upper gastrointestinal (UGI) cancers often present with malnutrition and frailty before undergoing major surgical procedures, which significantly elevates the risk of postoperative complications. Prehabilitation focuses on optimizing a patient’s functional capacity before surgery to improve postoperative outcomes. Our goal was to synthesize the effects of prehabilitation on the postoperative outcomes of UGI cancer patients undergoing major surgical intervention using a systematic review and meta-analysis.MethodsA comprehensive systematic search was conducted across the PubMed, Embase, Cochrane, and Scopus databases to identify relevant randomized controlled trials (RCTs). Ten RCTs, encompassing data from 878 patients, were included in the analysis. Pooled risk ratios (RRs) were calculated for dichotomous variables (e.g., incidence of complications), and weighted mean differences were calculated for continuous variables using a random-effects model. Study quality was assessed using the RoB2 and GRADE approaches.ResultsThe meta-analysis showed a trend toward a lower incidence of minor postoperative complications (Clavien–Dindo Grade I–II) in the prehabilitation group. While the common effect model showed significance, the certainty of evidence remains low to very low for most outcomes, suggesting these results should be interpreted with caution. However, a significant reduction was found in Grade III complications when using a common effect model, although no significant differences were detected in Grade IV complications or mortality. Cardiovascular complications and hospital readmission rates also showed no significant disparity.ConclusionThe implementation of prehabilitation in UGI cancer patients is safe and shows a positive trend toward reducing minor postoperative complications, thereby enhancing patient comfort and potentially accelerating recovery time. While the certainty of evidence remains low, further high-quality RCTs with larger patient cohorts are warranted, especially to explore the role of multimodal prehabilitation.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.por-journal.com/articles/10.3389/pore.2026.1612362</guid>
        <link>https://www.por-journal.com/articles/10.3389/pore.2026.1612362</link>
        <title><![CDATA[Surgical management of ulcerative colitis-associated colorectal cancer in a 20-year period, a single-centre study]]></title>
        <pubdate>2026-04-22T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>János Tajti</author><author>László Libor</author><author>Szabolcs Ábrahám</author><author>Zsolt Simonka</author><author>Anikó Maráz</author><author>Attila Paszt</author><author>Tamás Molnár</author><author>Judit Oláh</author><author>György Lázár</author>
        <description><![CDATA[IntroductionThe incidence of inflammatory bowel disease is on the rise. Inflammation that persists for years or decades may involve the risk of malignant transformation. Indeed, it is the cause of death in 15% of the UC patient population. Proctocolectomy followed by ileal pouch-anal anastomosis is the accepted surgical procedure.AimOur study objective was to retrospectively assess the occurrence and surgical treatment of UC-associated colorectal cancer cases in our institute and analyse survival data.Materials and methodsIn our department, 39 patients (12 female and 27 male patients) underwent surgery for UC-associated colorectal cancer between 1 January 2005 and 1 January 2025. Their mean age was 55 ± 13.4 years. Risk factors for the disease, examination results, types of surgery, perioperative and long-term surgical results, and survival measures were assessed retrospectively. The latter were determined using the Kaplan–Meier analysis.ResultsThirty-nine patients were diagnosed with UC at a mean age of 35.7 ± 16.7 years, and an average of 19.4 ± 12.3 years passed between the diagnosis of UC and the first surgical intervention. Regular endoscopies were performed in only 66% of our patients. Preoperative staging confirmed distant metastases in 12 patients (30.7%). Patients underwent 34 elective and 5 emergency surgeries. The mean follow-up duration was 40.2 ± 51.7 months. Only 7 patients (17.9%) had a T1 lesion. Lymph node involvement was confirmed in 17 cases (44.5%), whereas 12 patients (30.7%) showed dissemination. Adjuvant chemotherapy was administered in 23 cases (58.9%), and follow-up was recommended for 13 patients (33.3%). During the study period, 17 of the 39 patients died. The mean survival after the surgical procedure was 98.6 months (8.2 years). Survival was significantly shorter in patients who had undergone emergency surgery, were active smokers, suffered from PSC, and lacked gastroenterological follow-up.ConclusionBased on our experience, it is especially important for UC patients to receive close gastroenterological follow-up in specialised centres and undergo regular colonoscopies and for staff to evaluate biopsy samples properly and perform the appropriate surgical procedures in due time, preferably proctocolectomy and creation of IPAA with a minimally invasive method.]]></description>
      </item><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.2026.1612238</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.2026.1612298</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>
      </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.2026.1612253</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>
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        <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>
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        <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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