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<title>Faculty of Medicine in Pilsen</title>
<link>https://hdl.handle.net/20.500.14178/904</link>
<description/>
<pubDate>Sun, 14 Jun 2026 11:38:20 GMT</pubDate>
<dc:date>2026-06-14T11:38:20Z</dc:date>
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<title>Evolving Concepts in Salivary Duct Carcinoma: A Narrative Review</title>
<link>https://hdl.handle.net/20.500.14178/3827</link>
<description>Evolving Concepts in Salivary Duct Carcinoma: A Narrative Review
Masalunga, Marvin C; Bradley, Patrick J; van Herpen, Carla; Nagao, Toshitaka; Stenman, Göran; Vander Poorten, Vincent; Hellquist, Henrik; Di Palma, Silvana; Bradová, Martina; Leivo, Ilmo; Ferlito, Alfio; Skálová, Alena
Salivary duct carcinoma (SDC) is an aggressive neoplasm that typically involves the major salivary glands. This rapidly growing tumor is known to recur and metastasize to the neck nodes and to distant sites. Given its poor prognosis, researchers have focused on identifying factors and driver genomic alterations that may account for its behavior, ultimately yielding potential therapeutic targets. This review summarizes the growing body of knowledge on SDC since the publication of the latest WHO Classification of Tumors of the Head and Neck. Updates on emerging subtypes, immunohistochemical profiles, molecular alterations, and potential therapeutic targets are succinctly presented. Findings from studies on tumor immune microenvironment (TIME), which may have implications for the treatment and prognosis of SDC, are also discussed in this narrative review.
</description>
<pubDate>Thu, 01 Jan 2026 00:00:00 GMT</pubDate>
<guid isPermaLink="false">https://hdl.handle.net/20.500.14178/3827</guid>
<dc:date>2026-01-01T00:00:00Z</dc:date>
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<item>
<title>Prognostic Role of Serum Neuron-Specific Enolase at Baseline and its Early Dynamics in Metastatic Castration-Resistant Prostate Cancer Treated With Androgen Receptor Signaling Inhibitors</title>
<link>https://hdl.handle.net/20.500.14178/3826</link>
<description>Prognostic Role of Serum Neuron-Specific Enolase at Baseline and its Early Dynamics in Metastatic Castration-Resistant Prostate Cancer Treated With Androgen Receptor Signaling Inhibitors
Fiala, Ondřej; Tkadlecová, Michaela; Váchalová, Zuzana; Hora, Milan; Králíček, Jan; Stránský, Petr; Liška, Václav; Santoni, Matteo; Banna, Giuseppe Luigi; Pivovarčíková, Kristýna; Topolčan, Ondřej; Fínek, Jindřich
BACKGROUND: Outcomes of metastatic castration-resistant prostate cancer (mCRPC) treated with androgen receptor signaling inhibitors (ARSIs) vary widely and may not be fully reflected by PSA and standard clinicopathologic factors. We evaluated the prognostic value of serum neuron-specific enolase (NSE) at baseline and early on-treatment dynamics. METHODS: We retrospectively analyzed ARSI-treated mCRPC patients with available baseline NSE (n = 120). NSE was dichotomized by the upper limit of normal (ULN, 12.5 ng/mL). Radiographic progression-free survival (rPFS) and overall survival (OS) were estimated by Kaplan-Meier methods and compared by log-rank test. Multivariable Cox models adjusted for age, baseline PSA (per 100 ng/mL), line of therapy (2-4 vs 1), Gleason score (&gt; 7 vs &amp;lt;= 7), metastatic timing (synchronous vs metachronous), and visceral metastases (present vs absent). NSE dynamics were evaluated using a 28-day landmark approach among patients alive and at risk at day 28 with available baseline and week-4 NSE (rPFS landmark n = 47; OS landmark n = 48); follow-up was redefined from day 28 and dynamics were modeled as log2(NSE(4w)/NSE(0)) (per doubling). RESULTS: Median follow-up was 44.7 months (95% CI 35.7-48.3). Baseline NSE &gt; ULN was associated with shorter rPFS (9.4 vs 20.8 months) and OS (23.5 vs 38.2 months). In multivariable analyses, baseline NSE &gt; ULN remained independently associated with inferior outcomes (rPFS HR 1.81, 95% CI 1.15-2.85, p = 0.011; OS HR 1.85, 95% CI 1.12-3.05, p = 0.017). In landmark models, higher NSE dynamics were independently associated with worse outcomes (rPFS HR 4.30, 95% CI 1.06-17.39, p = 0.041; OS HR 8.78, 95% CI 2.15-35.77, p = 0.002). CONCLUSIONS: In ARSI-treated mCRPC, baseline NSE above ULN and early 4-week NSE dynamics provide independent prognostic information for rPFS and OS, supporting NSE as a pragmatic adjunct to clinical risk stratification.
</description>
<pubDate>Thu, 01 Jan 2026 00:00:00 GMT</pubDate>
<guid isPermaLink="false">https://hdl.handle.net/20.500.14178/3826</guid>
<dc:date>2026-01-01T00:00:00Z</dc:date>
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<item>
<title>O čem také přemýšlejí naši medici. Sborník studentských prací (2026)</title>
<link>https://hdl.handle.net/20.500.14178/3814</link>
<description>O čem také přemýšlejí naši medici. Sborník studentských prací (2026)
Fiala, Luděk; Krejčová, Karolína; Krejčová, Kristýna; Batrakouli, Fani; Muliere, Pierluigi; Pulina, Francesca; Fraňková, Natálie; Pospíšil, Ondřej; Vavřina, Vojtěch; Jiráková, Natálie; Rybáková, Linda; Amin, Nisha Yara; Pfister, Nisha; Boudová, Nela; Fulnečková, Anna; Busse, Konrad; Čiháková, Tereza; Kulovaná, Tereza; Dagdeleni, Eirini; Kaza, Kristabel; Chan, Tiffany Chi Jing; Cordoba Rodriguez, Anna; Keřková, Sylvie; Parkánová, Michaela; Kešeláková, Markéta; Leupoldová, Miriam; Kocourková, Tereza; Neradová, Lucie; Spilková, Klára; Košek, Jindřich; Langová, Nela; Seichert, Metoděj; Krystlová, Yvona; Marková, Marie; Bryndačová, Leona; Kunftová, Karin; Štuksová, Carolina; Lust, Elina; Mecová, Martina; Němejcová, Viktorie; Morelli, Martina; Möbes, Lilli Sophie; Novák, Lukáš; Bláha, Jan; Novotná, Anna; Matějková, Anděla; Rezková, Vendula; Petrovičová, Andrea; Tausch, Jakub; Semiginovská, Klára Sofie; Pečenková, Michaela; Bauerová, Martina; Shafiei, Liyousa; Naderi Koupaei, Negin; Akhtari, Mohammadali; Nedela, Timo Joachim; Schneider, Simon; Školoudíková, Hana; Horský, Marek; Nekuda, Pavel; Plešmíd, Vojtěch; Šavlová, Eliška; Miller, Robert Joseph; Tenglerová, Nikola; Vobrubová, Julie; Vísnerová, Klára; Jankovcová, Klára-Marie; Broďániová, Barbora; Komínek, Adam; Hložková, Julie; Srkal, Jiří; Vršková, Lucie; Kaňková, Tereza; Miletín, Marek; Holub, Vojtěch; Šandová, Terezie; Šťavíčková, Nikola; Háčková, Anna; Hagenhoferová, Kateřina; Neuvirt, Maxim; Bubnenkov, Dmitrii; Drokin, Myron; Lee, Denis
Výběr nejlepších esejí napsaných studenty Lékařské fakulty v Plzni Univerzity Karlovy pro předmět Lékařská psychologie a etika v akademickém roce 2025/2026.; A collection of the best essays written by students of the Faculty of Medicine in Pilsen, Charles University as part of the course Medical Psychology and Ethics in the academic year 2025/2026.
</description>
<pubDate>Thu, 01 Jan 2026 00:00:00 GMT</pubDate>
<guid isPermaLink="false">https://hdl.handle.net/20.500.14178/3814</guid>
<dc:date>2026-01-01T00:00:00Z</dc:date>
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<title>Familial risks in prostate cancer between brothers and half-brothers as clues to germline genetic and environmental causes</title>
<link>https://hdl.handle.net/20.500.14178/3813</link>
<description>Familial risks in prostate cancer between brothers and half-brothers as clues to germline genetic and environmental causes
Hemminki, Kari Jussi; Zitrický, František; Sundquist, Kristina; Sundquist, Jan; Försti, Asta; Hemminki, Akseli; Hemminki, Oto
Swedish family and cancer data constitute the largest source on familial cancer in the world. We analyze here familial risks in prostate cancer (PC) with focus on multiple affected brothers and comparation of full-brothers to maternal and paternal half-brothers. Age-specific incidence and standardized incidence ratios (SIRs) were calculated for PC in brothers. Curves for relative risk (RR) by diagnostic age were plotted for risk distributions. A total of 115,066 PCs were diagnosed in 1.2 million men. Familial SIR for full brothers was 2.23, for maternal half-brothers it was 1.92 and paternal half-brothers was 1.34. Considering SIRs with least possible detection bias (7+ years after first brother's diagnosis) the above SIRs were 2.06, 1.66 and 1.41. SIRs in full brothers increased stepwise by the number of affected brothers reaching 21.33 when 6 brothers were affected. Age-RR curves for two affected brothers declined evenly from RR 2.8 at age 45 to below 2.0 at age 80. When four or more brothers were affected, a discrete high-risk peak (RR 4 to 7) was detected between ages 60 and 69. Data on full-brothers and half-brothers indicate that familial risk in PC is largely genetic which is also supported by discrete RR peaks in high-risk families at ages matching preferential penetrance age for known predisposition genes of PC. Familial risk increased already when two brothers were affected calling for clinical vigilance concerning family history. Family history should deserve a place as an inclusion criterium in schemes for PC screening.
</description>
<pubDate>Thu, 01 Jan 2026 00:00:00 GMT</pubDate>
<guid isPermaLink="false">https://hdl.handle.net/20.500.14178/3813</guid>
<dc:date>2026-01-01T00:00:00Z</dc:date>
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