SMARCB1-deficient sinonasal adenocarcinoma is a rare variant of SWI/SNF-deficient malignancies with SMARCB1 loss and adenocarcinoma features. More than 200 high-grade epithelial sinonasal malignancies were retrieved. A total of 14 cases exhibited complete SMARCB1 (INI1) loss and glandular differentiation. SMARCA2 and SMARCA4 were normal, except for one case with a loss of SMARCA2. Next-generation sequencing (NGS) and/or fluorescence in situ hybridization (FISH) revealed an alteration in the SMARCB1 gene in 9/13 cases, while 2/13 were negative. Two tumors harbored SMARCB1 mutations in c.157C > T p.(Arg53Ter) and c.842G > A p.(Trp281Ter). One harbored ARID1B mutations in c.1469G > A p.(Trp490Ter) and MGA c.3724C > T p.(Arg1242Ter). Seven tumors had a SMARCB1 deletion. One carried an ESR1 mutation in c.644-2A > T, and another carried a POLE mutation in c.352_374del p.(Ser118GlyfsTer78). One case had a PAX3 mutation in c.44del p.(Gly15AlafsTer95). Histomorphology of SMARCB1-deficient adenocarcinoma was oncocytoid/rhabdoid and glandular, solid, or trabecular in 9/14 cases. Two had basaloid/blue cytoplasm and one showed focal signet ring cells. Yolk sac tumor-like differentiation with Schiller-Duval-like bodies was seen in 6/14 cases, with 2 cases showing exclusively reticular-microcystic yolk sac pattern. Follow-up of a maximum of 26 months (median 10 months) was available for 8/14 patients. Distant metastasis to the lung, liver, mediastinum, bone, and/or retroperitoneum was seen in 4/8 cases. Locoregional failure was seen in 75% of patients, with 6/8 local recurrences and 3 cervical lymph node metastases. At the last follow-up, 5 of 8 (62%) patients had died of their disease 2 to 20 months after diagnosis (median 8.2 months), and 3 were alive with the disease. The original diagnosis was usually high-grade non-intestinal-type adenocarcinoma or high-grade myoepithelial carcinoma. A correct diagnosis of these aggressive tumors could lead to improved targeted therapies with potentially better overall disease-specific survival.

• Klíčová slova
• Head and neck, Next-generation sequencing, Rhabdoid, SMARCB1-deficient adenocarcinoma, SWI/SNF complex, Sinonasal, Yolk sac-like,
• MeSH
• adenokarcinom * genetika   patologie   MeSH
• diferenciální diagnóza MeSH
• DNA vazebné proteiny genetika   nedostatek   MeSH
• dospělí MeSH
• gen SMARCB1 * nedostatek   genetika   MeSH
• hybridizace in situ fluorescenční MeSH
• lidé středního věku MeSH
• lidé MeSH
• mutace * MeSH
• myoepiteliální nádor * genetika   patologie   MeSH
• nádorové biomarkery genetika   MeSH
• nádory vedlejších dutin nosních * genetika   patologie   MeSH
• senioři nad 80 let MeSH
• senioři MeSH
• stupeň nádoru MeSH
• transkripční faktory * genetika   nedostatek   MeSH
• vysoce účinné nukleotidové sekvenování MeSH
• Check Tag
• dospělí MeSH
• lidé středního věku MeSH
• lidé MeSH
• mužské pohlaví MeSH
• senioři nad 80 let MeSH
• senioři MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• DNA vazebné proteiny MeSH
• gen SMARCB1 * MeSH
• nádorové biomarkery MeSH
• SMARCB1 protein, human MeSH Prohlížeč
• transkripční faktory * MeSH

Efforts to address the poor prognosis associated with esophageal adenocarcinoma (EAC) have been hampered by a lack of biomarkers to identify early disease and therapeutic targets. Despite extensive efforts to understand the somatic mutations associated with EAC over the past decade, a gap remains in understanding how the atlas of genomic aberrations in this cancer impacts the proteome and which somatic variants are of importance for the disease phenotype. We performed a quantitative proteomic analysis of 23 EACs and matched adjacent normal esophageal and gastric tissues. We explored the correlation of transcript and protein abundance using tissue-matched RNA-seq and proteomic data from seven patients and further integrated these data with a cohort of EAC RNA-seq data (n = 264 patients), EAC whole-genome sequencing (n = 454 patients), and external published datasets. We quantified protein expression from 5879 genes in EAC and patient-matched normal tissues. Several biomarker candidates with EAC-selective expression were identified, including the transmembrane protein GPA33. We further verified the EAC-enriched expression of GPA33 in an external cohort of 115 patients and confirm this as an attractive diagnostic and therapeutic target. To further extend the insights gained from our proteomic data, an integrated analysis of protein and RNA expression in EAC and normal tissues revealed several genes with poorly correlated protein and RNA abundance, suggesting posttranscriptional regulation of protein expression. These outlier genes, including SLC25A30, TAOK2, and AGMAT, only rarely demonstrated somatic mutation, suggesting post-transcriptional drivers for this EAC-specific phenotype. AGMAT was demonstrated to be overexpressed at the protein level in EAC compared to adjacent normal tissues with an EAC-selective, post-transcriptional mechanism of regulation of protein abundance proposed. Integrated analysis of proteome, transcriptome, and genome in EAC has revealed several genes with tumor-selective, posttranscriptional regulation of protein expression, which may be an exploitable vulnerability.

• Klíčová slova
• biomarker, esophageal adenocarcinoma, multiomics, proteogenomics, proteomics,
• MeSH
• adenokarcinom * genetika   metabolismus   patologie   MeSH
• lidé MeSH
• multiomika MeSH
• nádorové biomarkery * metabolismus   genetika   MeSH
• nádory jícnu * genetika   metabolismus   patologie   MeSH
• posttranskripční úpravy RNA MeSH
• proteom metabolismus   MeSH
• proteomika * metody   MeSH
• regulace genové exprese u nádorů * MeSH
• Check Tag
• lidé MeSH
• mužské pohlaví MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• nádorové biomarkery * MeSH
• proteom MeSH

We report 2 cases of high-grade sinonasal adenocarcinoma with a distinct morphological and immunohistochemical phenotype. Albeit histologically different from secretory carcinoma of the salivary glands, both tumors presented here share an ETV6::NTRK3 fusion. The highly cellular tumors were composed of solid and dense cribriform nests, often with comedo-like necroses in the center, and minor areas with papillary, microcystic, and trabecular formations without secretions, mostly located at the periphery of the lesion. The cells displayed high-grade features, with enlarged, crowded, and often vesicular nuclei with conspicuous nucleoli and brisk mitotic activity. The tumor cells were immunonegative for mammaglobin while showing immunopositivity for p40/p63, S100, SOX10, and GATA3, as well as for cytokeratins 7, 18, and 19. For the first time, we describe 2 cases of primary high-grade non-intestinal type adenocarcinomas of the nasal cavity, distinct from secretory carcinoma by morphology and immunoprofile, harboring the ETV6::NTRK3 fusion.

• Klíčová slova
• ETV6::NTRK3, Nasal cavity, Salivary duct carcinoma, Secretory carcinoma, Sinonasal, non-intestinal-type adenocarcinoma,
• MeSH
• adenokarcinom * genetika   patologie   MeSH
• fúzní onkogenní proteiny genetika   MeSH
• imunohistochemie MeSH
• karcinom * genetika   patologie   MeSH
• lidé MeSH
• nádorové biomarkery genetika   MeSH
• nádory prsu MeSH
• nádory slinných žláz * genetika   patologie   MeSH
• protein ETS, translokační varianta 6 MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• kazuistiky MeSH
• Názvy látek
• fúzní onkogenní proteiny MeSH
• nádorové biomarkery MeSH
• NTRK3 protein, human MeSH Prohlížeč

The dysplasia grading of Barrett's esophagus (BE), based on the histomorphological assessment of formalin-fixed, paraffin-embedded (FFPE) tissue, suffers from high interobserver variability leading to an unsatisfactory prediction of cancer risk. Thus, pre-analytic preservation of biological molecules, which could improve risk prediction in BE enabling molecular and genetic analysis, is needed. We aimed to evaluate such a molecular pre-analytic fixation tool, PAXgene-fixed paraffin-embedded (PFPE) biopsies, and their suitability for histomorphological BE diagnostics in comparison to FFPE. In a ring trial, 9 GI pathologists evaluated 116 digital BE slides of non-dysplastic BE (NDBE), low-grade dysplasia (LGD), high-grade dysplasia (HGD), and esophageal adenocarcinomas (EAC) using virtual microscopy. Overall quality, cytological and histomorphological parameters, dysplasia criteria, and diagnosis were analyzed. PFPE showed better preservation of nuclear details as chromatin and nucleoli, whereas overall quality and histomorphologic parameters as visibility of basal lamina, goblet cells, and presence of artifacts were scored as equal to FFPE. The interobserver reproducibility with regard to the diagnosis was best for NDBE and EAC (κF = 0.72-0.75) and poor for LGD and HGD (κF = 0.13-0.3) in both. In conclusion, our data suggest that PFPE allows equally confident histomorphological diagnosis of BE and EAC, introducing a novel tool for molecular analysis and parallel histomorphological evaluation.

• Klíčová slova
• Dysplasia, Esophageal adenocarcinoma, PAXgene-fixed paraffin-embedded,
• MeSH
• adenokarcinom * diagnóza   genetika   patologie   MeSH
• Barrettův syndrom * diagnóza   patologie   MeSH
• fixace tkání MeSH
• hyperplazie MeSH
• lidé MeSH
• nádory jícnu * diagnóza   patologie   MeSH
• prekancerózy * patologie   MeSH
• progrese nemoci MeSH
• reprodukovatelnost výsledků MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• klinická studie MeSH

Colorectal carcinoma (CRC) results from the accumulation of genetic mutations and alterations in signaling pathways. KRAS is mutated in 40% of CRC cases and is involved in increased tumor cells proliferation and survival. Although KRAS mutations are a dominant event in CRC tumorigenesis, increased wild-type KRAS expression has a similar effect on accelerated tumor growth. In this study, we investigated the KRAS status in correlation with clinicopathological features in sporadic CRC and more importantly the role of let-7a-5p and miR-544a-3p in the regulation of wild-type KRAS protein expression in the tumor center (T1) and invasive tumor front (T2). Analysis showed that 39.1% of tumor samples had KRAS mutations. In wild-type KRAS tumors, 62.0% were positive for KRAS protein expression and there was a higher percentage of KRAS-positive tumor cells and a higher intensity of immunohistochemical reaction in T2 than in T1 samples. This could not be attributed to differences in KRAS mRNA levels, suggesting regulation via miR-544a-3p expression which was significantly decreased in T2 samples. Furthermore, we demonstrated that tumor samples carrying the KRAS-LCS6 variant allele had significantly higher protein expression of the wild-type KRAS. Our results suggest the role of the KRAS-LCS6 polymorphism and miR-544a-3p expression in the regulation of wild-type KRAS protein expression in sporadic CRC.

• Klíčová slova
• Colon adenocarcinoma, Immunohistochemistry, KRAS, Let-7a, miR-544a,
• MeSH
• adenokarcinom genetika   patologie   MeSH
• dospělí MeSH
• exprese genu genetika   MeSH
• jednonukleotidový polymorfismus genetika   MeSH
• lidé středního věku MeSH
• lidé MeSH
• mikro RNA genetika   fyziologie   MeSH
• nádory tračníku genetika   patologie   MeSH
• protoonkogenní proteiny p21(ras) genetika   metabolismus   MeSH
• regulace genové exprese u nádorů genetika   MeSH
• senioři nad 80 let MeSH
• senioři MeSH
• Check Tag
• dospělí MeSH
• lidé středního věku MeSH
• lidé MeSH
• mužské pohlaví MeSH
• senioři nad 80 let MeSH
• senioři MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• KRAS protein, human MeSH Prohlížeč
• mikro RNA MeSH
• MIRN544 microRNA, human MeSH Prohlížeč
• protoonkogenní proteiny p21(ras) MeSH

The fusion genes containing neuregulin-1 (NRG1) are newly described potentially actionable oncogenic drivers. Initial clinical trials have shown a positive response to targeted treatment in some cases of NRG1 rearranged lung adenocarcinoma, cholangiocarcinoma, and pancreatic carcinoma. The cost-effective large scale identification of NRG1 rearranged tumors is an open question. We have tested a data-drilling approach by performing a retrospective assessment of a de-identified molecular profiling database of 3263 tumors submitted for fusion testing. Gene fusion detection was performed by RNA-based targeted next-generation sequencing using the Archer Fusion Plex kits for Illumina (ArcherDX Inc., Boulder, CO). Novel fusion transcripts were confirmed by a custom-designed RT-PCR. Also, the aberrant expression of CK20 was studied immunohistochemically. The frequency of NRG1 rearranged tumors was 0.2% (7/3263). The most common histologic type was lung adenocarcinoma (n = 5). Also, renal carcinoma (n = 1) and prostatic adenocarcinoma (n = 1) were found. Identified fusion partners were of a wide range (CD74, SDC4, TNC, VAMP2, UNC5D), with CD74, SDC4 being found twice. The UNC5D is a novel fusion partner identified in prostate adenocarcinoma. There was no co-occurrence with the other tested fusions nor KRAS, BRAF, and the other gene mutations specified in the applied gene panels. Immunohistochemically, the focal expression of CK20 was present in 2 lung adenocarcinomas. We believe it should be considered as an incidental finding. In conclusion, the overall frequency of tumors with NRG1 fusion was 0.2%. All tumors were carcinomas. We confirm (invasive mucinous) lung adenocarcinoma as being the most frequent tumor presenting NRG1 fusion. Herein novel putative pathogenic gene fusion UNC5D-NRG1 is described. The potential role of immunohistochemistry in tumor identification should be further addressed.

• Klíčová slova
• EGF-like domain, ERBB, ERBB3, HER, HER 3, MAPK, NRG1, PIK, carcinoma, data drilling, gene fusion, gene rearrangement, genetics, lung, mRNA sequencing, molecular, neuregulin, next-generation sequencing, receptor heterodimerization, receptor tyrosine kinase,
• MeSH
• adenokarcinom genetika   patologie   MeSH
• antigeny diferenciační B-lymfocytární genetika   MeSH
• dospělí MeSH
• fúzní onkogenní proteiny genetika   MeSH
• histokompatibilita - antigeny třídy II genetika   MeSH
• lidé středního věku MeSH
• lidé MeSH
• membránový protein 2 asociovaný s vezikuly genetika   MeSH
• nádory plic genetika   patologie   MeSH
• nádory prostaty genetika   patologie   MeSH
• neuregulin-1 genetika   MeSH
• receptory buněčného povrchu genetika   MeSH
• senioři nad 80 let MeSH
• senioři MeSH
• syndekan-4 genetika   MeSH
• tenascin genetika   MeSH
• Check Tag
• dospělí MeSH
• lidé středního věku MeSH
• lidé MeSH
• mužské pohlaví MeSH
• senioři nad 80 let MeSH
• senioři MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• antigeny diferenciační B-lymfocytární MeSH
• fúzní onkogenní proteiny MeSH
• histokompatibilita - antigeny třídy II MeSH
• invariant chain MeSH Prohlížeč
• membránový protein 2 asociovaný s vezikuly MeSH
• neuregulin-1 MeSH
• NRG1 protein, human MeSH Prohlížeč
• receptory buněčného povrchu MeSH
• SDC4 protein, human MeSH Prohlížeč
• syndekan-4 MeSH
• tenascin MeSH
• TNC protein, human MeSH Prohlížeč
• UNC5D protein, human MeSH Prohlížeč
• VAMP2 protein, human MeSH Prohlížeč

The development of colon cancer, one of the most common malignancies, is accompanied with numerous lipid alterations. However, analyses of whole tumor samples may not always provide an accurate description of specific changes occurring directly in tumor epithelial cells. Here, we analyzed in detail the phospholipid (PL), lysophospholipid (lysoPL), and fatty acid (FA) profiles of purified EpCAM+ cells, isolated from tumor and adjacent non-tumor tissues of colon cancer patients. We found that a number of FAs increased significantly in isolated tumor cells, which also included a number of long polyunsaturated FAs. Higher levels of FAs were associated with increased expression of FA synthesis genes, as well as with altered expression of enzymes involved in FA elongation and desaturation, including particularly fatty acid synthase, stearoyl-CoA desaturase, fatty acid desaturase 2 and ELOVL5 fatty acid elongase 5 We identified significant changes in ratios of specific lysoPLs and corresponding PLs. A number of lysophosphatidylcholine and lysophosphatidylethanolamine species, containing long-chain and very-long chain FAs, often with high numbers of double bonds, were significantly upregulated in tumor cells. Increased de novo synthesis of very long-chain FAs, or, altered uptake or incorporation of these FAs into specific lysoPLs in tumor cells, may thus contribute to reprogramming of cellular phospholipidome and membrane alterations observed in colon cancer.

• Klíčová slova
• EpCAM, colorectal carcinoma, desaturation, epithelial cells, fatty acid synthesis, lipidomics, lysophospholipids, phospholipids,
• MeSH
• adenokarcinom enzymologie   genetika   metabolismus   MeSH
• desaturasy mastných kyselin genetika   metabolismus   MeSH
• elongasy mastných kyselin genetika   metabolismus   MeSH
• epitelové buňky enzymologie   metabolismus   MeSH
• fosfolipidy metabolismus   MeSH
• lidé MeSH
• lipidomika MeSH
• lipogeneze MeSH
• mastné kyseliny metabolismus   MeSH
• metabolismus lipidů * MeSH
• nádory tračníku enzymologie   genetika   metabolismus   MeSH
• regulace genové exprese u nádorů * MeSH
• senioři MeSH
• stearyl-CoA-desaturasa genetika   metabolismus   MeSH
• syntázy mastných kyselin genetika   metabolismus   MeSH
• Check Tag
• lidé MeSH
• mužské pohlaví MeSH
• senioři MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• desaturasy mastných kyselin MeSH
• elongasy mastných kyselin MeSH
• ELOVL5 protein, human MeSH Prohlížeč
• FADS2 protein, human MeSH Prohlížeč
• fosfolipidy MeSH
• mastné kyseliny MeSH
• stearyl-CoA-desaturasa MeSH
• syntázy mastných kyselin MeSH

Primary urethral adenocarcinomas are very rare neoplasms accounting for <10% of all urethral carcinomas. Site of their origin is unclear, but they seem to arise from Skene's paraurethral glands, which is the female homologue of the male prostate. The aim of this article is to report the first case of Skene's gland adenocarcinoma in which a molecular genetic profiling was performed. The patient was a 73-year-old woman with a polypoid lesion sized 3 × 2 cm located at the interface between the bladder neck and the proximal urethra. Transurethral resection was performed and small tissue fragments with positive margins were obtained. Histology revealed an epithelial neoplasm consisting of cribriform structures located in the subepithelial connective tissue of the bladder wall and proximal urethra. The lesion showed positive immunohistochemical staining with prostate specific antigen, prostatic acid phosphatase, NKX3.1, and alpha-methylacyl-CoA racemase. Using the Illumina TruSight Tumor 170 next-generation sequencing assay, a mutation and loss of heterozygosity of the phosphatase and tensin homologue (PTEN) gene was detected. No fusion in any of the examined genes was found using this assay as well as FusionPlex Solid Tumor Kit and FusionPlex Sarcoma kit assays from ArcherDX. Given the rarity of Skene's gland adenocarcinoma, it is uncertain whether the same grading and prognostic criteria that are currently used for prostatic cancer apply here as well. It is also unclear what treatment strategy should be applied, but according to the available literature, it seems that local excision or wide surgical resection could represent sufficient therapeutic modalities.

• Klíčová slova
• PTEN gene, Skene’s gland adenocarcinoma, molecular genetics, next-generation sequencing, paraurethral glands,
• MeSH
• adenokarcinom diagnóza   genetika   patologie   MeSH
• fosfohydroláza PTEN genetika   MeSH
• lidé MeSH
• mutace MeSH
• nádorové biomarkery genetika   MeSH
• nádory močové trubice diagnóza   genetika   patologie   MeSH
• senioři MeSH
• uretra patologie   MeSH
• ztráta heterozygozity MeSH
• Check Tag
• lidé MeSH
• senioři MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• kazuistiky MeSH
• Názvy látek
• fosfohydroláza PTEN MeSH
• nádorové biomarkery MeSH
• PTEN protein, human MeSH Prohlížeč

A hallmark of cancer, including pancreatic ductal adenocarcinoma (PDA), is a massive stromal and inflammatory reaction. Many efforts have been made to identify the anti- or protumoral role of cytokines and immune subpopulations within the stroma. Here, we investigated the role of interleukin-17A (IL17A) and its effect on tumor fibroblasts and the tumor microenvironment. We used a spontaneous PDA mouse model (KPC) crossed to IL17A knockout mice to show an extensive desmoplastic reaction, without impaired immune infiltration. Macrophages, especially CD80+ and T cells, were more abundant at the earlier time point. In T cells, a decrease in FoxP3+ cells and an increase in CD8+ T cells were observed in KPC/IL17A-/- mice. Fibroblasts isolated from IL17A+/+ and IL17A-/- KPC mice revealed very different messenger RNA (mRNA) and protein profiles. IL17A-/- fibroblasts displayed the ability to restrain tumor cell invasion by producing factors involved in extracellular matrix remodeling, increasing T cell recruitment, and producing higher levels of cytokines and chemokines favoring T helper 1 cell recruitment and activation and lower levels of those recruiting myeloid/granulocytic immune cells. Single-cell quantitative PCR on isolated fibroblasts confirmed a very divergent profile of IL17A-proficient and -deficient cells. All these features can be ascribed to increased levels of IL17F observed in the sera of IL17A-/- mice, and to the higher expression of its cognate receptor (IL17RC) specifically in IL17A-/- cancer-associated fibroblasts (CAFs). In addition to the known effects on neoplastic cell transformation, the IL17 cytokine family uniquely affects fibroblasts, representing a suitable candidate target for combinatorial immune-based therapies in PDA.

• Klíčová slova
• IL17A, cancer-associated fibroblast, extracellular matrix, fibrosis, pancreatic cancer,
• MeSH
• adenokarcinom genetika   patologie   MeSH
• CD8-pozitivní T-lymfocyty metabolismus   patologie   MeSH
• duktální karcinom pankreatu genetika   patologie   MeSH
• fibroblasty asociované s nádorem metabolismus   patologie   MeSH
• forkhead transkripční faktory genetika   MeSH
• interleukin-17 genetika   MeSH
• karcinogeneze genetika   MeSH
• lidé MeSH
• modely nemocí na zvířatech MeSH
• myši knockoutované MeSH
• myši MeSH
• nádorové mikroprostředí genetika   MeSH
• receptory interleukinů genetika   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• myši MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• forkhead transkripční faktory MeSH
• Foxp3 protein, mouse MeSH Prohlížeč
• Il17a protein, mouse MeSH Prohlížeč
• Il17rc protein, mouse MeSH Prohlížeč
• interleukin-17 MeSH
• receptory interleukinů MeSH

Mutation spectra of 250 cancer driver, druggable, and actionable genes were analyzed in surgically resected pancreatic ductal adenocarcinoma (PDAC) patients who developed metachronous pulmonary metastases. Targeted sequencing was performed in DNA from blood and archival samples of 15 primary tumors and three paired metastases. Results were complemented with the determination of G12V mutation in KRAS by droplet digital PCR. The median number of protein-changing mutations was 52 per patient. KRAS and TP53 were significantly enriched in fractions of mutations in hotspots. Individual gene mutation frequencies or mutational loads accounting separately for drivers, druggable, or clinically actionable genes, did not significantly associate with patients' survival. LRP1B was markedly mutated in primaries of patients who generalized (71%) compared to those developing solitary pulmonary metastases (0%). FLG2 was mutated exclusively in primary tumors compared to paired metastases. In conclusion, signatures of prognostically differing subgroups of PDAC patients were generated for further utilization in precision medicine.

• Klíčová slova
• adenocarcinoma, metastases, next-generation sequencing, pancreas, pulmonary, survival,
• MeSH
• adenokarcinom genetika   patologie   MeSH
• filagriny MeSH
• frekvence genu genetika   MeSH
• lidé středního věku MeSH
• lidé MeSH
• mutace genetika   MeSH
• nádorový supresorový protein p53 genetika   MeSH
• nádory plic genetika   patologie   MeSH
• nádory slinivky břišní genetika   patologie   MeSH
• proteiny S100 genetika   MeSH
• protoonkogenní proteiny p21(ras) genetika   MeSH
• Check Tag
• lidé středního věku MeSH
• lidé MeSH
• mužské pohlaví MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• filagriny MeSH
• FLG2 protein, human MeSH Prohlížeč
• nádorový supresorový protein p53 MeSH
• proteiny S100 MeSH
• protoonkogenní proteiny p21(ras) MeSH