BACKGROUND: To validate the clinical utility of a previously identified circulating tumor DNA methylation marker (meth-ctDNA) panel for disease detection and survival outcomes, meth-ctDNA markers were compared to PSA levels and PSMA PET/CT findings in men with different stages of prostate cancer (PCa). METHODS: 122 PCa patients who underwent [⁶⁸Ga]Ga-PSMA-11 PET/CT and plasma sampling (03/2019-08/2021) were analyzed. cfDNA was extracted, and a panel of 8 individual meth-ctDNA markers was queried. PET scans were qualitatively and quantitatively assessed. PSA and meth-ctDNA markers were compared to PET findings, and their relative prognostic value was evaluated. RESULTS: PSA discriminated best between negative and tumor-indicative PET scans in all (AUC 0.77) and hormone-sensitive (hsPC) patients (0.737). In castration-resistant PCa (CRPC), the meth-ctDNA marker KLF8 performed best (AUC 0.824). CHST11 differentiated best between non- and metastatic scans (AUC 0.705) overall, KLF8 best in hsPC and CRPC (AUC 0.662, 0.85). Several meth-ctDNA markers correlated low to moderate with the tumor volume in all (5/8) and CRPC patients (6/8), while PSA levels correlated moderately to strongly with the tumor volume in all groups (all p < 0.001). CRPC overall survival was independently associated with LDAH and PSA (p = 0.0168, p < 0.001). CONCLUSION: The studied meth-ctDNA markers are promising for the minimally-invasive detection and prognostication of CRPC but do not allow for clinical characterization of hsPC. Prospective studies are warranted for their use in therapy response and outcome prediction in CRPC and potential incremental value for PCa monitoring in PSA-low settings.

• Klíčová slova
• DNA methylation, Epigenetics, PET/CT, PSMA, Prostate cancer, cfDNA,
• MeSH
• cirkulující nádorová DNA * krev   genetika   MeSH
• izotopy gallia MeSH
• lidé středního věku MeSH
• lidé MeSH
• metylace DNA * MeSH
• nádorové biomarkery * genetika   krev   MeSH
• nádory prostaty * genetika   diagnostické zobrazování   krev   MeSH
• PET/CT * metody   MeSH
• prognóza MeSH
• prostatický specifický antigen krev   MeSH
• průřezové studie MeSH
• radioizotopy galia MeSH
• senioři nad 80 let MeSH
• senioři MeSH
• Check Tag
• lidé středního věku MeSH
• lidé MeSH
• mužské pohlaví MeSH
• senioři nad 80 let MeSH
• senioři MeSH
• Publikační typ
• časopisecké články MeSH
• srovnávací studie MeSH
• Názvy látek
• cirkulující nádorová DNA * MeSH
• gallium 68 PSMA-11 MeSH Prohlížeč
• izotopy gallia MeSH
• nádorové biomarkery * MeSH
• prostatický specifický antigen MeSH
• PSMA-11 MeSH Prohlížeč
• radioizotopy galia MeSH

In advanced prostate cancer (PC), in particular after acquisition of resistance to androgen receptor (AR) signaling inhibitors (ARSI), upregulation of AR splice variants compromises endocrine therapy efficiency. Androgen receptor splice variant-7 (ARV7) is clinically the most relevant and has a distinct 3' untranslated region (3'UTR) compared to the AR full-length variant, suggesting a unique post-transcriptional regulation. Here, we set out to evaluate the applicability of the ARV7 3'UTR as a therapy target. A common single nucleotide polymorphism, rs5918762, was found to affect the splicing rate and thus the expression of ARV7 in cellular models and patient specimens. Serine/arginine-rich splicing factor 9 (SRSF9) was found to bind to and increase the inclusion of the cryptic exon 3 of ARV7 during the splicing process in the alternative C allele of rs5918762. The dual specificity protein kinase CLK2 interferes with the activity of SRSF9 by regulating its expression. Inhibition of the Cdc2-like kinase (CLK) family by the small molecules cirtuvivint or lorecivivint results in the decreased expression of ARV7. Both inhibitors show potent anti-proliferative effects in enzalutamide-treated or -naive PC models. Thus, targeting aberrant alternative splicing at the 3'UTR of ARV7 by disturbing the CLK2/SRSF9 axis might be a valuable therapeutic approach in late stage, ARSI-resistant PC.

• Klíčová slova
• 3′ untranslated region, allele‐specific regulation, androgen receptor splice variant 7, dual specificity protein kinase CLK2, serine/arginine‐family of splicing factors, splicing inhibitors,
• MeSH
• 3' nepřekládaná oblast genetika   MeSH
• alternativní sestřih MeSH
• androgenní receptory * genetika   metabolismus   MeSH
• jednonukleotidový polymorfismus genetika   MeSH
• lidé MeSH
• nádorové buněčné linie MeSH
• nádory prostaty * genetika   patologie   metabolismus   MeSH
• protein-serin-threoninkinasy * metabolismus   genetika   antagonisté a inhibitory   MeSH
• regulace genové exprese u nádorů * účinky léků   MeSH
• serin-arginin sestřihové faktory * metabolismus   genetika   MeSH
• sestřih RNA * MeSH
• tyrosinkinasy * metabolismus   genetika   antagonisté a inhibitory   MeSH
• Check Tag
• lidé MeSH
• mužské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• 3' nepřekládaná oblast MeSH
• androgenní receptory * MeSH
• Clk dual-specificity kinases MeSH Prohlížeč
• protein-serin-threoninkinasy * MeSH
• serin-arginin sestřihové faktory * MeSH
• tyrosinkinasy * MeSH

BACKGROUNDS: SWI/SNF complexes represent a family of multi-subunit chromatin remodelers that are affected by alterations in >20% of human tumors. While mutations of SWI/SNF genes are relatively uncommon in prostate cancer (PCa), the literature suggests that deregulation of various subunits plays a role in prostate tumorigenesis. To assess SWI/SNF functions in a clinical context, we studied the mutually exclusive, paralogue accessory subunits SMARCD1, SMARCD2, and SMARCD3 that are included in every known complex and are sought to confer specificity. METHODS: Performing immunohistochemistry (IHC), the protein levels of the SMARCD family members were measured using a tissue microarray (TMA) comprising malignant samples and matching healthy tissue of non-metastatic PCa patients (n = 168). Moreover, IHC was performed in castration-resistant tumors (n = 9) and lymph node metastases (n = 22). To assess their potential role as molecular biomarkers, SMARCD1 and SMARCD3 protein levels were correlated with clinical parameters such as T stage, Gleason score, biochemical recurrence, and progression-free survival. RESULTS: SMARCD1 protein levels in non-metastatic primary tumors, lymph node metastases, and castration-resistant samples were significantly higher than in benign tissues. Likewise, SMARCD3 protein expression was elevated in tumor tissue and especially lymph node metastases compared to benign samples. While SMARCD1 levels in primary tumors did not exhibit significant associations with any of the tested clinical parameters, SMARCD3 exhibited an inverse correlation with pre-operative PSA levels. Moreover, low SMARCD3 expression was associated with progression to metastasis. CONCLUSIONS: In congruence with previous literature, our results implicate that both SMARCD1 and SMARCD3 may exhibit relevant functions in the context of prostate tumorigenesis. Moreover, our approach suggests a potential role of SMARCD3 as a novel prognostic marker in clinically non-metastatic PCa.

• Klíčová slova
• SMARCD1, SMARCD3, SWI/SNF complex, prognostic marker, prostate cancer,
• MeSH
• chromozomální proteiny, nehistonové * genetika   metabolismus   MeSH
• imunohistochemie MeSH
• lidé středního věku MeSH
• lidé MeSH
• lokální recidiva nádoru patologie   metabolismus   genetika   MeSH
• lymfatické metastázy MeSH
• nádorové biomarkery * genetika   metabolismus   MeSH
• nádory prostaty rezistentní na kastraci patologie   genetika   metabolismus   MeSH
• nádory prostaty * patologie   metabolismus   genetika   MeSH
• prognóza MeSH
• senioři MeSH
• stupeň nádoru MeSH
• transkripční faktory genetika   metabolismus   MeSH
• Check Tag
• lidé středního věku MeSH
• lidé MeSH
• mužské pohlaví MeSH
• senioři MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• chromozomální proteiny, nehistonové * MeSH
• nádorové biomarkery * MeSH
• SMARCD1 protein, human MeSH Prohlížeč
• transkripční faktory MeSH

BACKGROUND: Prostate cancer ranks as the second most frequently diagnosed cancer in men worldwide. Recent research highlights the crucial roles IL6ST-mediated signaling pathways play in the development and progression of various cancers, particularly through hyperactivated STAT3 signaling. However, the molecular programs mediated by IL6ST/STAT3 in prostate cancer are poorly understood. METHODS: To investigate the role of IL6ST signaling, we constitutively activated IL6ST signaling in the prostate epithelium of a Pten-deficient prostate cancer mouse model in vivo and examined IL6ST expression in large cohorts of prostate cancer patients. We complemented these data with in-depth transcriptomic and multiplex histopathological analyses. RESULTS: Genetic cell-autonomous activation of the IL6ST receptor in prostate epithelial cells triggers active STAT3 signaling and significantly reduces tumor growth in vivo. Mechanistically, genetic activation of IL6ST signaling mediates senescence via the STAT3/ARF/p53 axis and recruitment of cytotoxic T-cells, ultimately impeding tumor progression. In prostate cancer patients, high IL6ST mRNA expression levels correlate with better recurrence-free survival, increased senescence signals and a transition from an immune-cold to an immune-hot tumor. CONCLUSIONS: Our findings demonstrate a context-dependent role of IL6ST/STAT3 in carcinogenesis and a tumor-suppressive function in prostate cancer development by inducing senescence and immune cell attraction. We challenge the prevailing concept of blocking IL6ST/STAT3 signaling as a functional prostate cancer treatment and instead propose cell-autonomous IL6ST activation as a novel therapeutic strategy.

• Klíčová slova
• Cytotoxic T-cells, IL6ST/STAT3 signaling, Immune cell infiltration, L-gp130, Prostate cancer, Senescence, Senescence-associated secretory phenotype, Tumor microenvironment,
• MeSH
• inhibitor p16 cyklin-dependentní kinasy metabolismus   genetika   MeSH
• lidé MeSH
• modely nemocí na zvířatech MeSH
• myši MeSH
• nádorové buněčné linie MeSH
• nádorové mikroprostředí * MeSH
• nádorový supresorový protein p53 * metabolismus   genetika   MeSH
• nádory prostaty * patologie   metabolismus   genetika   MeSH
• regulace genové exprese u nádorů MeSH
• signální transdukce * MeSH
• stárnutí buněk * MeSH
• transkripční faktor STAT3 * metabolismus   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• mužské pohlaví MeSH
• myši MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• inhibitor p16 cyklin-dependentní kinasy MeSH
• nádorový supresorový protein p53 * MeSH
• STAT3 protein, human MeSH Prohlížeč
• transkripční faktor STAT3 * MeSH

BACKGROUND: The N-myc downstream-regulated gene 1 (NDRG1) has been discovered as a significant gene in the progression of cancers. However, the regulatory mechanism of NDRG1 remained obscure in prostate cancer (PCa). METHODS: The miR-96-5p and NDRG1 expression levels were evaluated in PCa cell lines, and prostate tissues, and validated in public databases by real-time polymerase chain reaction, western blot analysis, and immunohistochemistry. The function of miR-96-5p and NDRG1 were investigated by scratch assay and transwell assays in vitro, and mouse xenograft assay in vivo. The candidate pathway regulated by NDRG1 was conducted by the next-generation gene sequencing technique. Immunofluorescence and luciferase assays were used to detect the relation between miR-96-5p, NDRG1, and NF-kB pathway. RESULTS: Overexpressing NDRG1 suppresses the migration, invasion, and epithelial-mesenchymal transition (EMT) in vitro, and inhibits metastasis in vivo. Moreover, miR-96-5p contributes to NDRG1 deficiency and promotes PCa cell migration and invasion. Furthermore, NDRG1 loss activates the NF-kB pathway, which stimulates p65 and IKBa phosphorylation and induces EMT in PCa. CONCLUSIONS: MiR-96-5p promotes the migration and invasion of PCa by targeting NDRG1 and regulating the NF-kB pathway.

• Klíčová slova
• EMT, NDRG1, NF- kB, miR-96-5p, prostate cancer,
• MeSH
• epitelo-mezenchymální tranzice MeSH
• intracelulární signální peptidy a proteiny * genetika   metabolismus   MeSH
• invazivní růst nádoru * MeSH
• lidé MeSH
• mikro RNA * genetika   MeSH
• myši MeSH
• nádorové buněčné linie MeSH
• nádory prostaty * patologie   genetika   metabolismus   MeSH
• NF-kappa B * metabolismus   MeSH
• pohyb buněk MeSH
• proteiny buněčného cyklu * genetika   metabolismus   MeSH
• regulace genové exprese u nádorů MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• mužské pohlaví MeSH
• myši MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• intracelulární signální peptidy a proteiny * MeSH
• mikro RNA * MeSH
• MIRN96 microRNA, human MeSH Prohlížeč
• N-myc downstream-regulated gene 1 protein MeSH Prohlížeč
• NF-kappa B * MeSH
• proteiny buněčného cyklu * MeSH

Purpose: This study aims to assess whole-mount Gleason grading (GG) in prostate cancer (PCa) accurately using a multiomics machine learning (ML) model and to compare its performance with biopsy-proven GG (bxGG) assessment. Materials and Methods: A total of 146 patients with PCa recruited in a pilot study of a prospective clinical trial (NCT02659527) were retrospectively included in the side study, all of whom underwent 68Ga-PSMA-11 integrated positron emission tomography (PET) / magnetic resonance (MR) before radical prostatectomy (RP) between May 2014 and April 2020. To establish a multiomics ML model, we quantified PET radiomics features, pathway-level genomics features from whole exome sequencing, and pathomics features derived from immunohistochemical staining of 11 biomarkers. Based on the multiomics dataset, five ML models were established and validated using 100-fold Monte Carlo cross-validation. Results: Among five ML models, the random forest (RF) model performed best in terms of the area under the curve (AUC). Compared to bxGG assessment alone, the RF model was superior in terms of AUC (0.87 vs 0.75), specificity (0.72 vs 0.61), positive predictive value (0.79 vs 0.75), and accuracy (0.78 vs 0.77) and showed slightly decreased sensitivity (0.83 vs 0.89) and negative predictive value (0.80 vs 0.81). Among the feature categories, bxGG was identified as the most important feature, followed by pathomics, clinical, radiomics and genomics features. The three important individual features were bxGG, PSA staining and one intensity-related radiomics feature. Conclusion: The findings demonstrate a superior assessment of the developed multiomics-based ML model in whole-mount GG compared to the current clinical baseline of bxGG. This enables personalized patient management by identifying high-risk PCa patients for RP.

• Klíčová slova
• Gleason grading, PSMA, machine learning, multiomics, prostate cancer,
• MeSH
• genomika metody   MeSH
• lidé středního věku MeSH
• lidé MeSH
• magnetická rezonanční tomografie metody   MeSH
• multiomika MeSH
• nádory prostaty * chirurgie   patologie   genetika   diagnostické zobrazování   MeSH
• pilotní projekty MeSH
• pozitronová emisní tomografie metody   MeSH
• prospektivní studie MeSH
• prostatektomie * metody   MeSH
• retrospektivní studie MeSH
• senioři MeSH
• strojové učení * MeSH
• stupeň nádoru * MeSH
• Check Tag
• lidé středního věku MeSH
• lidé MeSH
• mužské pohlaví MeSH
• senioři MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH

Continued exploration of the androgen receptor (AR) is crucial, as it plays pivotal roles in diverse diseases such as prostate cancer (PCa), serving as a significant therapeutic focus. Therefore, the Department of Urology Dresden hosted an international meeting for scientists and clinical oncologists to discuss the newest advances in AR research. The 2nd International Androgen Receptor Symposium was held in Dresden, Saxony, Germany, from 26-27.04.2024, organised by Dr. Holger H.H. Erb. Following the format of the first meeting, more than 35 scientists from 8 countries attended the event to discuss recent developments, research challenges, and identification of venues in AR research. An important new feature was the involvement of PhD students and young investigators, acknowledging the high scientific quality of their work. The symposium included three covers: new advances from clinical research, basic and translational research, and novel strategies to target AR. Moreover, based on its increasing clinical relevance, a PSMA theranostic mini-symposium was added at the end of the AR symposium to allow the audience to discuss the newest advances in PSMA theranostic. This report focuses on the highlights and discussions of the meeting.

• Klíčová slova
• AR, Androgen deprivation therapy, NR3C4, PCa, PSMA,
• MeSH
• androgenní receptory * metabolismus   genetika   MeSH
• lidé MeSH
• nádory prostaty * metabolismus   terapie   genetika   MeSH
• Check Tag
• lidé MeSH
• mužské pohlaví MeSH
• Publikační typ
• kongresy MeSH
• Názvy látek
• androgenní receptory * MeSH
• AR protein, human MeSH Prohlížeč

BACKGROUND: Circulating-tumor DNA (ctDNA) and prostate-specific membrane antigen (PSMA) ligand positron-emission tomography (PET) enable minimal-invasive prostate cancer (PCa) detection and survival prognostication. The present study aims to compare their tumor discovery abilities and prognostic values. METHODS: One hundred thirty men with confirmed PCa (70.5 ± 8.0 years) who underwent [68Ga]Ga-PSMA-11 PET/CT (184.8 ± 19.7 MBq) imaging and plasma sample collection (March 2019-August 2021) were included. Plasma-extracted cell-free DNA was subjected to whole-genome-based ctDNA analysis. PSMA-positive tumor lesions were delineated and their quantitative parameters extracted. ctDNA and PSMA PET/CT discovery rates were compared, and the prognostic value for overall survival (OS) was evaluated. RESULTS: PSMA PET discovery rates according to castration status and PSA ranges did differ significantly (P = 0.013, P < 0.001), while ctDNA discovery rates did not (P = 0.311, P = 0.123). ctDNA discovery rates differed between localized and metastatic disease (P = 0.013). Correlations between ctDNA concentrations and PSMA-positive tumor volume (PSMA-TV) were significant in all (r = 0.42, P < 0.001) and castration-resistant (r = 0.65, P < 0.001), however not in hormone-sensitive patients (r = 0.15, P = 0.249). PSMA-TV and ctDNA levels were associated with survival outcomes in the Logrank (P < 0.0001, P < 0.0001) and multivariate Cox regression analysis (P = 0.0023, P < 0.0001). CONCLUSION: These findings suggest that PSMA PET imaging outperforms ctDNA analysis in detecting prostate cancer across the whole spectrum of disease, while both modalities are independently highly prognostic for survival outcomes.

• Klíčová slova
• Liquid biopsy, PET/CT, PSMA, Prostate cancer, ctDNA,
• MeSH
• cirkulující nádorová DNA * krev   genetika   MeSH
• EDTA * analogy a deriváty   MeSH
• izotopy gallia * MeSH
• lidé středního věku MeSH
• lidé MeSH
• nádory prostaty * diagnostické zobrazování   genetika   krev   MeSH
• oligopeptidy MeSH
• PET/CT * MeSH
• prognóza MeSH
• průřezové studie MeSH
• radioizotopy galia * MeSH
• senioři MeSH
• Check Tag
• lidé středního věku MeSH
• lidé MeSH
• mužské pohlaví MeSH
• senioři MeSH
• Publikační typ
• časopisecké články MeSH
• srovnávací studie MeSH
• Názvy látek
• cirkulující nádorová DNA * MeSH
• EDTA * MeSH
• gallium 68 PSMA-11 MeSH Prohlížeč
• izotopy gallia * MeSH
• oligopeptidy MeSH
• PSMA-11 MeSH Prohlížeč
• radioizotopy galia * MeSH

BACKGROUND: Prostate cancer develops through malignant transformation of the prostate epithelium in a stepwise, mutation-driven process. Although activator protein-1 transcription factors such as JUN have been implicated as potential oncogenic drivers, the molecular programs contributing to prostate cancer progression are not fully understood. METHODS: We analyzed JUN expression in clinical prostate cancer samples across different stages and investigated its functional role in a Pten-deficient mouse model. We performed histopathological examinations, transcriptomic analyses and explored the senescence-associated secretory phenotype in the tumor microenvironment. RESULTS: Elevated JUN levels characterized early-stage prostate cancer and predicted improved survival in human and murine samples. Immune-phenotyping of Pten-deficient prostates revealed high accumulation of tumor-infiltrating leukocytes, particularly innate immune cells, neutrophils and macrophages as well as high levels of STAT3 activation and IL-1β production. Jun depletion in a Pten-deficient background prevented immune cell attraction which was accompanied by significant reduction of active STAT3 and IL-1β and accelerated prostate tumor growth. Comparative transcriptome profiling of prostate epithelial cells revealed a senescence-associated gene signature, upregulation of pro-inflammatory processes involved in immune cell attraction and of chemokines such as IL-1β, TNF-α, CCL3 and CCL8 in Pten-deficient prostates. Strikingly, JUN depletion reversed both the senescence-associated secretory phenotype and senescence-associated immune cell infiltration but had no impact on cell cycle arrest. As a result, JUN depletion in Pten-deficient prostates interfered with the senescence-associated immune clearance and accelerated tumor growth. CONCLUSIONS: Our results suggest that JUN acts as tumor-suppressor and decelerates the progression of prostate cancer by transcriptional regulation of senescence- and inflammation-associated genes. This study opens avenues for novel treatment strategies that could impede disease progression and improve patient outcomes.

• Klíčová slova
• AP-1 transcription factors, Immune infiltration, JUN, Prostate cancer, SASP, Senescence,
• MeSH
• fosfohydroláza PTEN * genetika   metabolismus   MeSH
• lidé MeSH
• modely nemocí na zvířatech MeSH
• myši MeSH
• nádorové buněčné linie MeSH
• nádorové mikroprostředí * imunologie   MeSH
• nádory prostaty * patologie   genetika   metabolismus   MeSH
• progrese nemoci * MeSH
• protoonkogenní proteiny c-jun metabolismus   MeSH
• regulace genové exprese u nádorů MeSH
• sekreční fenotyp asociovaný se senescencí MeSH
• stanovení celkové genové exprese MeSH
• stárnutí buněk genetika   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• mužské pohlaví MeSH
• myši MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• fosfohydroláza PTEN * MeSH
• protoonkogenní proteiny c-jun MeSH

The Guidelines for Clinical Practice for carriers of pathogenic variants in clinically relevant cancer predisposition genes define the steps of primary and secondary prevention that should be provided to these individuals at high risk of developing hereditary cancer in the Czech Republic. The drafting of the guidelines was organized by the Oncogenetics Working Group of the Society for Medical Genetics and Genomics of J. E. Purkyně Czech Medical Society (SLG ČLS JEP) in cooperation with the representatives of oncology and oncogynecology. The guidelines are based on the current recommendations of the National Comprehensive Cancer Network (NCCN), European Society of Medical Oncology (ESMO) and take into account the capacity of the Czech healthcare system.

• Klíčová slova
• ATM, BRCA1, BRCA2, CHEK2, PALB2, consensus, germline mutation carriers, guidelines for clinical practice,
• MeSH
• ATM protein * genetika   MeSH
• checkpoint kinasa 2 * genetika   MeSH
• genetická predispozice k nemoci * MeSH
• lidé MeSH
• nádory prostaty genetika   MeSH
• nádory prsu genetika   MeSH
• nádory slinivky břišní genetika   MeSH
• nádory vaječníků genetika   MeSH
• protein BRCA1 genetika   MeSH
• protein BRCA2 * genetika   MeSH
• protein FANCN * genetika   MeSH
• směrnice pro lékařskou praxi jako téma MeSH
• zárodečné mutace * MeSH
• Check Tag
• lidé MeSH
• mužské pohlaví MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• Geografické názvy
• Česká republika MeSH
• Názvy látek
• ATM protein, human MeSH Prohlížeč
• ATM protein * MeSH
• BRCA1 protein, human MeSH Prohlížeč
• BRCA2 protein, human MeSH Prohlížeč
• checkpoint kinasa 2 * MeSH
• CHEK2 protein, human MeSH Prohlížeč
• PALB2 protein, human MeSH Prohlížeč
• protein BRCA1 MeSH
• protein BRCA2 * MeSH
• protein FANCN * MeSH