{"title":"[Sentinel lymph node mapping in colorectal and anal tumors from the beginning until now].","authors":"Kornél Vajda","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Introduction: </strong>Sentinel lymph node biopsy in colorectal cancer remains controversial. Lymph node metastasis is the most important prognostic factor, and even in the absence of lymph node metastasis, the risk of local recurrence is 15-20%.</p><p><strong>Methods: </strong>The sentinel lymph node was identified in vivo by subserosal injection of blue dye or indocyanine green (ICG), and ex vivo by submucosal or subserosal injection. Stained lymph nodes were examined by the pathologist conventionally with hematoxylin-eosin staining, and in cases of negativity, with serial sectioning and immunohistochemistry and/ or RT-PCR.</p><p><strong>Results: </strong>Despite the high detection rate of 70-99%, sensitivity for macrometastasis is low (33-93.1%), but improves with the detection of micrometastasis. Stage migration based on micrometastasis detection ranged between 5-15%. Aberrant lymphatic drainage occurs in 3.9-7.1% of cases.</p><p><strong>Conclusions: </strong>At present, the sensitivity of colorectal sentinel lymph node identification is not suitable for guiding treatment, as the false negative rate is high. This is due to the lack of standardization, inadequate patient selection, and the large number of T3-4 stage tumors. Several authors recommend investigating early T1-2 stage tumors, the incidence of which is increasing due to screening.</p>","PeriodicalId":94127,"journal":{"name":"Magyar onkologia","volume":"70 3","pages":"249-257"},"PeriodicalIF":0.0,"publicationDate":"2026-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13577722/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148957771","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Ten years of translational innovation in HER2-targeted immune cell therapy - A comprehensive review of the work of the University of Debrecen Cell and Molecular Therapy Research Group.","authors":"György Vereb, Árpád Szöőr","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>HER2-targeted therapies have improved outcomes in solid tumors, but their efficacy is often limited by resistance and tumor microenvironmental barriers. Over the past decade, the University of Debrecen Cell and Molecular Therapy Research Group has focused on developing CAR-engineered immune cell strategies to address these challenges. Our work spans advances in CAR-T cell design, including optimization of costimulatory signaling, development of modular targeting systems, and expansion toward off-the-shelf platforms such as CAR-NK cells. Collectively, these efforts highlight the potential of engineered immune cells to overcome key limitations of conventional therapies and support the continued evolution of CAR-based approaches for solid tumors.</p>","PeriodicalId":94127,"journal":{"name":"Magyar onkologia","volume":"70 2","pages":"151-156"},"PeriodicalIF":0.0,"publicationDate":"2026-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13233018/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148102368","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Péter Nagy, Anna Kamilla Kis, Eszter Bajtai, Ines Lidia Haffaressas, Balázs Gombos, Dóra Bereczki, Kornélia Szebényi, Gergely Szakács, Szilárd Tóth, András Füredi
{"title":"Reframing cancer drug resistance: transporters, persister cells, senescence, and emerging therapeutic strategies.","authors":"Péter Nagy, Anna Kamilla Kis, Eszter Bajtai, Ines Lidia Haffaressas, Balázs Gombos, Dóra Bereczki, Kornélia Szebényi, Gergely Szakács, Szilárd Tóth, András Füredi","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Cancer drug resistance remains one of the greatest barriers to durable therapeutic success. Here, we reframe resistance as a dynamic landscape shaped by transporter‑mediated efflux, reversible drug‑tolerant persister states, and therapy‑induced senescence. This review highlights areas where our group has made substantial contributions, with a particular focus on our own experimental and conceptual advances. We show how P‑glycoprotein (P-gp) overexpression, traditionally viewed as an obstacle sustaining cancer multidrug resistance (MDR), creates exploitable metabolic vulnerabilities, enabling the development of MDR‑selective compounds. We demonstrate that persister cells rely on transient P‑gp-mediated detoxification, revealing a therapeutic window during drug‑free intervals. We further show that senescence is not a terminal fate but a relapse‑initiating state requiring targeted intervention. Finally, we illustrate how pharmacokinetics and dosing schedules can be harnessed to reshape tumor evolution, culminating in LiPyDau, a next‑generation liposomal anthracycline with durable activity against resistant tumors. Together, these insights outline a unified strategy for anticipating, intercepting, and ultimately overcoming cancer drug resistance.</p>","PeriodicalId":94127,"journal":{"name":"Magyar onkologia","volume":"70 2","pages":"118-127"},"PeriodicalIF":0.0,"publicationDate":"2026-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13233020/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148102355","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Zsófia Gábriel, Fatime Szalai, Viktória Varga, Henrik Wehn Olsen, Nóra Förhécz, Bálint Csikós, Gábor Petővári, Ildikó Krencz, Dorottya Moldvai, Anna Sebestyén
{"title":"3D bioprinted in vitro models in cancer metabolism research.","authors":"Zsófia Gábriel, Fatime Szalai, Viktória Varga, Henrik Wehn Olsen, Nóra Förhécz, Bálint Csikós, Gábor Petővári, Ildikó Krencz, Dorottya Moldvai, Anna Sebestyén","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Cancer metabolism is a central field in oncology, strongly serving as critical adaptation mechanism driving tumour progression, therapeutic response, and patient prognosis. The complexity of tumour metabolism remains difficult to mimic using conventional experimental conditions. Preclinical models, including in vitro 2D cultures and in vivo animal models, often fail to accurately reproduce the dynamic tissue alterations. Increasing evidence highlights the crucial role of the tumour microenvironment, nutrient availability, hypoxia, extracellular matrix components, and metabolic crosstalk between cancer, stromal, and immune cells in shaping tumour metabolic rewiring. Consequently, advanced 3D culture systems have gained significant attention, offering new perspectives for modelling cellular complexity and metabolic heterogeneity. This review summarises metabolic adaptation mechanisms influenced by microenvironment, and discusses the evolution of current modelling. Furthermore, through our own research in 3D bioprinting, we highlight the emerging role of 3D bioprinted models in tumour biology, cancer metabolism research and drug sensitivity studies.</p>","PeriodicalId":94127,"journal":{"name":"Magyar onkologia","volume":"70 2","pages":"95-116"},"PeriodicalIF":0.0,"publicationDate":"2026-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13233023/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148102342","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"[Investigating tumor cell motility under hypoxia and therapeutic resistance in cancer models].","authors":"Eszter Sára Surguta","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Aim: </strong>This study aimed to investigate the role of the tumor microenvironment in two key aspects of cancer progression: regulation of tumor cell motility and development of resistance to targeted therapy.</p><p><strong>Methods: </strong>In vitro lung adenocarcinoma cell lines were used to assess the effects of hypoxia on cell migration, proliferation, signaling pathway activity, and expression of epithelial- mesenchymal transition (EMT) markers.</p><p><strong>Results: </strong>Hypoxia reduced single-cell motility and proliferation while promoting collective invasion and inducing cell line-specific EMT-related changes. Hypoxia-mimicking CoCl2 treatment failed to reproduce the effects of true hypoxic conditions. In the second part of the study, a patient- derived tumor xenograft (PDTX) model of BRAF V600E mutant melanoma was established to investigate acquired resistance to vemurafenib. Bulk RNA sequencing identified potential resistance-associated markers, however, protein- level validation was inconclusive.</p><p><strong>Conclusions: </strong>Our results highlight that both hypoxia and therapeutic pressure modulate tumor progression in a complex, context-dependent manner.</p>","PeriodicalId":94127,"journal":{"name":"Magyar onkologia","volume":"70 2","pages":"176-178"},"PeriodicalIF":0.0,"publicationDate":"2026-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148102319","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Premedication with steroids in breast cancer - supportive treatment or tumour growth promotion?","authors":"Henriett Butz, Anna Oláh, Attila Patócs","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Glucocorticoids, most commonly dexamethasone, are widely used alongside breast cancer therapy to alleviate adverse effects of chemotherapy, particularly allergic reactions and nausea. However, growing evidence shows that the activation of the glucocorticoid receptor (GR) has context-dependent effects on tumour biology, with both tumour-suppressive and tumour-promoting consequences. This review summarises the molecular basis of GR signalling in breast cancer and its prognostic relevance across molecular subtypes. Particular emphasis is placed on ligand-dependent and ligand-independent GR activation, crosstalk with the oestrogen receptor and GR-regulated transcriptional programmes associated with tumour cell migration and therapy resistance. Overall, the available evidence suggests that the use of glucocorticoids in triple-negative breast cancer is not biologically neutral. Assessment of GR using methods such as routine immunohistochemistry may add future value for patient's stratification for GR-targeted therapy and could inform more personalised supportive treatment and follow-up strategies; however, these approaches require prospective validation before clinical implementation.</p>","PeriodicalId":94127,"journal":{"name":"Magyar onkologia","volume":"70 2","pages":"137-148"},"PeriodicalIF":0.0,"publicationDate":"2026-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13233022/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148102329","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Anna Kiss, Tamás Pintér, Mónika Révész, Esztella Mikolás, Erika Tóth, Kinga Lakatos, Domonkos Ádám Tárnoki, Attila Patócs
{"title":"[Successful selpercatinib treatment of metastatic medullary thyroid cancer carrying rare RET variant].","authors":"Anna Kiss, Tamás Pintér, Mónika Révész, Esztella Mikolás, Erika Tóth, Kinga Lakatos, Domonkos Ádám Tárnoki, Attila Patócs","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Aim: </strong>Medullary thyroid carcinoma (MTC) is a rare neuroendocrine malignancy in which serum calcitonin plays a pivotal role in early diagnosis, surgical planning, guidance of systemic therapy, and monitoring of treatment response. This case highlights the importance of laboratory diagnostics during selpercatinib therapy in a patient with disseminated MTC harboring a rare RET pathogenic variant.</p><p><strong>Methods: </strong>A cervical vertebral fracture in a young, asymptomatic male revealed MTC metastasis with distant dissemination and markedly elevated serum CEA and calcitonin levels. Tumor tissue and circulating DNA analysis identified the rare p.Glu632_Leu633del RET mutation. No germline alteration was detected. First-line systemic therapy comprised the selective RET tyrosine kinase inhibitor selpercatinib combined with denosumab.</p><p><strong>Results: </strong>Rapid clinical improvement occurred without significant adverse effects. Serum calcitonin levels normalized within four weeks, and imaging revealed marked tumor regression.</p><p><strong>Conclusion: </strong>This case underscores the value of liquid biopsy detected mutations in guiding targeted therapy. Clinical, biochemical, and radiological findings support the potential use of selective RET tyrosine kinase inhibitors for this rare mutation. Serum calcitonin serves as a reliable quantitative biomarker of therapeutic efficacy.</p>","PeriodicalId":94127,"journal":{"name":"Magyar onkologia","volume":"70 2","pages":"169-174"},"PeriodicalIF":0.0,"publicationDate":"2026-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13233019/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148102328","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"[Psychological distress and cancer: facts and myths in the light of scientific evidence].","authors":"Tamás Szekeres, Péter Kovács","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Psychological stress and cancer are frequently framed in causal narratives in public discourse; however, current scientific evidence does not support such assumptions. Epidemiological and prospective cohort studies indicate that psychological stress cannot be established as an independent carcinogenic factor, and population-level associations between stress and cancer incidence are consistently absent. Certain psychosocial variables, including maladaptive coping strategies or persistent high-level distress, show moderate and inconsistent associations with clinical outcomes (e.g., survival, recurrence), but these findings are heterogeneous and subject to methodological limitations. Psycho-oncological interventions effectively reduce psychological distress and improve quality of life, while direct causal effects on tumor progression remain unproven. Accordingly, psychosocial care is clinically warranted, contributing to patient well-being and adaptive coping, while clearly distinguishing these effects from biological causal pathways.</p>","PeriodicalId":94127,"journal":{"name":"Magyar onkologia","volume":"70 2","pages":"161-167"},"PeriodicalIF":0.0,"publicationDate":"2026-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13233016/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148102338","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"[Targeting tumor hypoxia in combined therapeutic strategies in breast and ovarian cancer].","authors":"Laura Svajda","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Aim: </strong>Tumor hypoxia is a major driver of tumor progression and metastasis. Hypoxic adaptation is regulated by hypoxiainducible factor-1 (HIF-1), which controls the transcription of genes promoting malignant behavior. HIF-1 inhibitors have failed as monotherapies in clinical trials, highlighting the need for combination-based strategies. This study aimed to develop hypoxia-targeted combination therapies for breast and ovarian cancers.</p><p><strong>Methods: </strong>Using established in vitro and in vivo hypoxia models, we evaluated acriflavine, a HIF-1 inhibitor, in combination with paclitaxel and an epithelial-mesenchymal transition targeting agent.</p><p><strong>Results: </strong>Acriflavine exerted potent antiproliferative effects, particularly in triple-negative breast cancer cell lines, and proteomic profiling indicated modulation of migration, proliferation, and cellular metabolism. The acriflavine-paclitaxel combination showed synergistic antitumor and antimetastatic activity, which was further enhanced by rolipram.</p><p><strong>Conclusions: </strong>Overall, our findings support hypoxia-targeted combination approaches and provide a biological rationale for combining HIF-1 inhibition with immune checkpoint blockade in breast cancer.</p>","PeriodicalId":94127,"journal":{"name":"Magyar onkologia","volume":"70 2","pages":"180-182"},"PeriodicalIF":0.0,"publicationDate":"2026-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148102346","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Beáta Biri-Kovács, Katalin Úri, Attila Andor, Mahendravarman Mohanraj, Attila Kolonics, Zsuzsanna Anna Pató, Elias S J Arnér
{"title":"Context‑dependent targeting of thioredoxin reductase 1 in cancer: a mechanistic review.","authors":"Beáta Biri-Kovács, Katalin Úri, Attila Andor, Mahendravarman Mohanraj, Attila Kolonics, Zsuzsanna Anna Pató, Elias S J Arnér","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Targeting the cytosolic selenoprotein thioredoxin reductase 1 (TrxR1, also named TXNRD1) has emerged as a promising strategy to exploit redox vulnerabilities in cancer. However, both preclinical observations and recent mechanistic studies indicate that TrxR1 inhibition can have context‑dependent outcomes. This article synthesizes a mechanistic framework linking cytosolic redox buffering, proteostasis, receptor tyrosine kinase (RTK) signaling, and immune surveillance with treatment responses. It highlights the dual functional roles of the TrxR1-substrate TXNL1 (also named TRP32), discusses intracellular transcriptional crosstalk shaping treatment sensitivity, and outlines potential combination strategies with RTK modulators.</p>","PeriodicalId":94127,"journal":{"name":"Magyar onkologia","volume":"70 2","pages":"128-135"},"PeriodicalIF":0.0,"publicationDate":"2026-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13233021/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148102349","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}