Recently, an increasing incidence of HPV-induced oropharyngeal squamous cell carcinoma (OPSCC) has been observed. Moreover, locoregionally advanced stages require a combined modal approach, and the prognosis is poor. Therefore, it is essential to find early diagnostic and prognostic biomarkers. DNA methylation changes play a crucial role in the process of carcinogenesis and are often investigated as promising biomarkers in many types of cancer. For analysis of DNA methylation levels of selected tumour suppressor genes in HPV-positive and HPV-negative samples (including primary tumours and corresponding metastases of metastasizing OPSCCs, primary tumours of non-metastasizing OPSCCs, and control samples), methylation-specific MLPA and methylation-specific high-resolution melting analyses were used. A significant difference in methylation between OPSCCs and the control group was observed in WT1, PAX6 (P < 0.01) and CADM1, RARβ (P < 0.05) genes. CADM1 and WT1 hypermethylation was detected mostly in HPV-positive samples; all but one HPV-negative samples were unmethylated. Moreover, hypermethylation of PAX5 gene was observed in metastases compared with control samples and was also associated with shorter overall survival of all patients (P < 0.05). Associations described herein between promoter methylation of selected genes and clinicopathological data could benefit OPSCC patients in the future by improvement in screening, early detection, and prognosis of the disease.

• Klíčová slova
• Biomarker, DNA methylation, epigenetics, head and neck cancer, human papillomavirus, oropharyngeal cancer,
• MeSH
• aktivátorový protein specifický pro B-buňky genetika   MeSH
• Alphapapillomavirus * MeSH
• buněčná adhezní molekula 1 genetika   metabolismus   MeSH
• dlaždicobuněčné karcinomy hlavy a krku genetika   MeSH
• DNA metabolismus   MeSH
• infekce papilomavirem * komplikace   MeSH
• lidé MeSH
• metylace DNA MeSH
• nádory hlavy a krku * genetika   MeSH
• nádory orofaryngu * patologie   MeSH
• Papillomaviridae MeSH
• prognóza MeSH
• proteiny WT1 genetika   metabolismus   MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• aktivátorový protein specifický pro B-buňky MeSH
• buněčná adhezní molekula 1 MeSH
• CADM1 protein, human MeSH Prohlížeč
• DNA MeSH
• PAX5 protein, human MeSH Prohlížeč
• PAX6 protein, human MeSH Prohlížeč
• proteiny WT1 MeSH
• retinoic acid receptor beta MeSH Prohlížeč
• WT1 protein, human MeSH Prohlížeč

Recently, we described B-cell precursor acute lymphoblastic leukemia (BCP-ALL) subtype with early switch to the monocytic lineage and loss of the B-cell immunophenotype, including CD19 expression. Thus far, the genetic background has remained unknown. Among 726 children consecutively diagnosed with BCP-ALL, 8% patients experienced switch detectable by flow cytometry (FC). Using exome and RNA sequencing, switch was found to positively correlate with three different genetic subtypes: PAX5-P80R mutation (5 cases with switch out of 5), rearranged DUX4 (DUX4r; 30 cases of 41) and rearranged ZNF384 (ZNF384r; 4 cases of 10). Expression profiles or phenotypic patterns correlated with genotypes, but within each genotype they could not identify cases who subsequently switched. If switching was not taken into account, the B-cell-oriented FC assessment underestimated the minimal residual disease level. For patients with PAX5-P80R, a discordance between FC-determined and PCR-determined MRD was found on day 15, resulting from a rapid loss of the B-cell phenotype. Discordance on day 33 was observed in all the DUX4r, PAX5-P80R and ZNF384r subtypes. Importantly, despite the substantial phenotypic changes, possibly even challenging the appropriateness of BCP-ALL therapy, the monocytic switch was not associated with a higher incidence of relapse and poorer prognosis in patients undergoing standard ALL treatment.

• MeSH
• aktivátorový protein specifický pro B-buňky genetika   MeSH
• akutní lymfatická leukemie * MeSH
• B-lymfocyty MeSH
• imunofenotypizace MeSH
• lidé MeSH
• mutace MeSH
• pre-B-buněčná leukemie * diagnóza   genetika   MeSH
• reziduální nádor MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• aktivátorový protein specifický pro B-buňky MeSH
• PAX5 protein, human MeSH Prohlížeč

The widespread use of next generation sequencing for clinical testing is detecting an escalating number of variants in noncoding regions of the genome. The clinical significance of the majority of these variants is currently unknown, which presents a significant clinical challenge. We have screened over 6,000 early-onset and/or familial breast cancer (BC) cases collected by the ENIGMA consortium for sequence variants in the 5' noncoding regions of BC susceptibility genes BRCA1 and BRCA2, and identified 141 rare variants with global minor allele frequency < 0.01, 76 of which have not been reported previously. Bioinformatic analysis identified a set of 21 variants most likely to impact transcriptional regulation, and luciferase reporter assays detected altered promoter activity for four of these variants. Electrophoretic mobility shift assays demonstrated that three of these altered the binding of proteins to the respective BRCA1 or BRCA2 promoter regions, including NFYA binding to BRCA1:c.-287C>T and PAX5 binding to BRCA2:c.-296C>T. Clinical classification of variants affecting promoter activity, using existing prediction models, found no evidence to suggest that these variants confer a high risk of disease. Further studies are required to determine if such variation may be associated with a moderate or low risk of BC.

• Klíčová slova
• BRCA1, BRCA2, breast cancer, promoter, transcription, variants of unknown clinical significance (VUS),
• MeSH
• 5' nepřekládaná oblast MeSH
• aktivátorový protein specifický pro B-buňky metabolismus   MeSH
• faktor vázající CCAAT metabolismus   MeSH
• genetická predispozice k nemoci MeSH
• lidé MeSH
• MFC-7 buňky MeSH
• nádorové buněčné linie MeSH
• nádory prsu genetika   MeSH
• promotorové oblasti (genetika) * MeSH
• protein BRCA1 chemie   genetika   metabolismus   MeSH
• protein BRCA2 chemie   genetika   metabolismus   MeSH
• vazba proteinů MeSH
• věk při počátku nemoci MeSH
• zárodečné mutace * MeSH
• Check Tag
• lidé MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• 5' nepřekládaná oblast MeSH
• aktivátorový protein specifický pro B-buňky MeSH
• BRCA1 protein, human MeSH Prohlížeč
• BRCA2 protein, human MeSH Prohlížeč
• faktor vázající CCAAT MeSH
• NFYA protein, human MeSH Prohlížeč
• PAX5 protein, human MeSH Prohlížeč
• protein BRCA1 MeSH
• protein BRCA2 MeSH

Purpose Somatic deletions that affect the lymphoid transcription factor-coding gene IKZF1 have previously been reported as independently associated with a poor prognosis in pediatric B-cell precursor (BCP) acute lymphoblastic leukemia (ALL). We have now refined the prognostic strength of IKZF1 deletions by analyzing the effect of co-occurring deletions. Patients and Methods The analysis involved 991 patients with BCP ALL treated in the Associazione Italiana Ematologia ed Oncologia Pediatrica-Berlin-Frankfurt-Muenster (AIEOP-BFM) ALL 2000 trial with complete information for copy number alterations of IKZF1, PAX5, ETV6, RB1, BTG1, EBF1, CDKN2A, CDKN2B, Xp22.33/Yp11.31 (PAR1 region; CRLF2, CSF2RA, and IL3RA), and ERG; replication of findings involved 417 patients from the same trial. Results IKZF1 deletions that co-occurred with deletions in CDKN2A, CDKN2B, PAX5, or PAR1 in the absence of ERG deletion conferred the worst outcome and, consequently, were grouped as IKZF1plus. The IKZF1plus group comprised 6% of patients with BCP ALL, with a 5-year event-free survival of 53 ± 6% compared with 79 ± 5% in patients with IKZF1 deletion who did not fulfill the IKZF1plus definition and 87 ± 1% in patients who lacked an IKZF1 deletion ( P ≤ .001). Respective 5-year cumulative relapse incidence rates were 44 ± 6%, 11 ± 4%, and 10 ± 1% ( P ≤ .001). Results were confirmed in the replication cohort, and multivariable analyses demonstrated independence of IKZF1plus. The IKZF1plus prognostic effect differed dramatically in analyses stratified by minimal residual disease (MRD) levels after induction treatment: 5-year event-free survival for MRD standard-risk IKZF1plus patients was 94 ± 5% versus 40 ± 10% in MRD intermediate- and 30 ± 14% in high-risk IKZF1plus patients ( P ≤ .001). Corresponding 5-year cumulative incidence of relapse rates were 6 ± 6%, 60 ± 10%, and 60 ± 17% ( P ≤ .001). Conclusion IKZF1plus describes a new MRD-dependent very-poor prognostic profile in BCP ALL. Because current AIEOP-BFM treatment is largely ineffective for MRD-positive IKZF1plus patients, new experimental treatment approaches will be evaluated in our upcoming trial AIEOP-BFM ALL 2017.

• MeSH
• aktivátorový protein specifický pro B-buňky genetika   MeSH
• delece genu * MeSH
• dítě MeSH
• inhibitor p15 cyklin-dependentní kinasy genetika   MeSH
• inhibitor p16 cyklin-dependentní kinasy genetika   MeSH
• lidé MeSH
• pre-B-buněčná leukemie genetika   patologie   MeSH
• prognóza MeSH
• receptor PAR-1 genetika   MeSH
• reziduální nádor genetika   patologie   MeSH
• transkripční faktor Ikaros genetika   MeSH
• Check Tag
• dítě MeSH
• lidé MeSH
• mužské pohlaví MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• aktivátorový protein specifický pro B-buňky MeSH
• CDKN2A protein, human MeSH Prohlížeč
• CDKN2B protein, human MeSH Prohlížeč
• IKZF1 protein, human MeSH Prohlížeč
• inhibitor p15 cyklin-dependentní kinasy MeSH
• inhibitor p16 cyklin-dependentní kinasy MeSH
• PAX5 protein, human MeSH Prohlížeč
• receptor PAR-1 MeSH
• transkripční faktor Ikaros MeSH

Thyroid transcription factor-1 (TTF-1) is a marker of tumors of pulmonary and thyroid origin, and its expression practically excludes diagnosis of Merkel cell carcinoma (MCC). However, TTF-1 expression in combined MCC was recently reported. PAX5 is a marker of B-cell origin that is also expressed in most classical MCC cases; however, its expression was not described in combined MCC. The authors decided to evaluate the expression of both these markers in a group of 5 combined MCCs (2 with invasive squamous cell carcinoma, 2 with squamous cell carcinoma in situ, and 1 with basal cell carcinoma). Expression of TTF-1 was found in 4 of 5 cases; in 3 cases, the marker was shown in the MCC component (weakly in 2 cases and strongly in 1 case), whereas the non-MCC component presented TTF-1 expression in 2 cases. A weak-to-moderate immunoreactivity for PAX5 was identified in all cases of the MCC component but in none of the non-MCC component. The results show that the expression of TTF-1 is a frequent finding in combined MCC and can be present in the neuroendocrine component, which differs from the conventional MCC. In contrast, PAX5 expression pattern is similar to that of the classical MCC.

• MeSH
• aktivátorový protein specifický pro B-buňky analýza   MeSH
• bazocelulární karcinom chemie   patologie   MeSH
• buněčná diferenciace MeSH
• imunohistochemie MeSH
• jaderné proteiny analýza   MeSH
• karcinom in situ chemie   patologie   MeSH
• lidé MeSH
• Merkelův nádor chemie   patologie   MeSH
• nádorové biomarkery analýza   MeSH
• nádory komplexní a smíšené chemie   patologie   MeSH
• nádory kůže chemie   patologie   MeSH
• prediktivní hodnota testů MeSH
• senioři nad 80 let MeSH
• senioři MeSH
• spinocelulární karcinom chemie   patologie   MeSH
• transkripční faktory analýza   MeSH
• tyreoidální jaderný faktor 1 MeSH
• Check Tag
• lidé MeSH
• mužské pohlaví MeSH
• senioři nad 80 let MeSH
• senioři MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• multicentrická studie MeSH
• Geografické názvy
• Evropa MeSH
• Názvy látek
• aktivátorový protein specifický pro B-buňky MeSH
• jaderné proteiny MeSH
• nádorové biomarkery MeSH
• NKX2-1 protein, human MeSH Prohlížeč
• PAX5 protein, human MeSH Prohlížeč
• transkripční faktory MeSH
• tyreoidální jaderný faktor 1 MeSH

TCF3-HLF-positive acute lymphoblastic leukemia (ALL) is currently incurable. Using an integrated approach, we uncovered distinct mutation, gene expression and drug response profiles in TCF3-HLF-positive and treatment-responsive TCF3-PBX1-positive ALL. We identified recurrent intragenic deletions of PAX5 or VPREB1 in constellation with the fusion of TCF3 and HLF. Moreover somatic mutations in the non-translocated allele of TCF3 and a reduction of PAX5 gene dosage in TCF3-HLF ALL suggest cooperation within a restricted genetic context. The enrichment for stem cell and myeloid features in the TCF3-HLF signature may reflect reprogramming by TCF3-HLF of a lymphoid-committed cell of origin toward a hybrid, drug-resistant hematopoietic state. Drug response profiling of matched patient-derived xenografts revealed a distinct profile for TCF3-HLF ALL with resistance to conventional chemotherapeutics but sensitivity to glucocorticoids, anthracyclines and agents in clinical development. Striking on-target sensitivity was achieved with the BCL2-specific inhibitor venetoclax (ABT-199). This integrated approach thus provides alternative treatment options for this deadly disease.

• MeSH
• aktivátorový protein specifický pro B-buňky genetika   MeSH
• akutní lymfatická leukemie farmakoterapie   genetika   mortalita   MeSH
• chemorezistence MeSH
• exprese genu MeSH
• fúzní onkogenní proteiny genetika   metabolismus   MeSH
• genetické asociační studie MeSH
• genomika MeSH
• inhibiční koncentrace 50 MeSH
• Kaplanův-Meierův odhad MeSH
• kohortové studie MeSH
• kokultivační techniky MeSH
• lidé MeSH
• mutace MeSH
• mutační analýza DNA MeSH
• myši inbrední NOD MeSH
• myši SCID MeSH
• náhradní lehké řetězce imunoglobulinů genetika   MeSH
• protinádorové látky farmakologie   terapeutické užití   MeSH
• sekvenční delece MeSH
• xenogenní modely - testy protinádorové aktivity MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• mužské pohlaví MeSH
• ženské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• aktivátorový protein specifický pro B-buňky MeSH
• fúzní onkogenní proteiny MeSH
• náhradní lehké řetězce imunoglobulinů MeSH
• PAX5 protein, human MeSH Prohlížeč
• protinádorové látky MeSH
• TCF3-HLF fusion protein, human MeSH Prohlížeč
• VPREB1 protein, human MeSH Prohlížeč

Tumor suppressor genes (TSGs) are commonly inactivated by somatic mutation and/or promoter methylation; yet, recent high-throughput genomic studies have not identified key TSGs inactivated by both mechanisms. We pursued an integrated molecular analysis based on methylation binding domain sequencing (MBD-seq), 450K Methylation arrays, whole exome sequencing, and whole genome gene expression arrays in primary head and neck squamous cell carcinoma (HNSCC) tumors and matched uvulopalatopharyngoplasty tissue samples (UPPPs). We uncovered 186 downregulated genes harboring cancer specific promoter methylation including PAX1 and PAX5 and we identified 10 key tumor suppressor genes (GABRB3, HOXC12, PARP15, SLCO4C1, CDKN2A, PAX1, PIK3AP1, HOXC6, PLCB1, and ZIC4) inactivated by both promoter methylation and/or somatic mutation. Among the novel tumor suppressor genes discovered with dual mechanisms of inactivation, we found a high frequency of genomic and epigenomic alterations in the PAX gene family of transcription factors, which selectively impact canonical NOTCH and TP53 pathways to determine cell fate, cell survival, and genome maintenance. Our results highlight the importance of assessing TSGs at the genomic and epigenomic level to identify key pathways in HNSCC, deregulated by simultaneous promoter methylation and somatic mutations.

• Klíčová slova
• DNA methylation, Head and Neck Squamous Cell Carcinoma, Tumor Suppressor Genes, integration analysis, somatic mutations,
• MeSH
• aktivátorový protein specifický pro B-buňky genetika   metabolismus   MeSH
• CpG ostrůvky MeSH
• kohortové studie MeSH
• lidé MeSH
• metylace DNA * MeSH
• mutace MeSH
• nádorové buněčné linie MeSH
• nádorový supresorový protein p53 genetika   metabolismus   MeSH
• nádory hlavy a krku genetika   metabolismus   MeSH
• promotorové oblasti (genetika) * MeSH
• receptor Notch1 genetika   metabolismus   MeSH
• spinocelulární karcinom genetika   metabolismus   MeSH
• transkripční faktory paired box genetika   metabolismus   MeSH
• tumor supresorové geny * MeSH
• umlčování genů * MeSH
• Check Tag
• lidé MeSH
• mužské pohlaví MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• multicentrická studie MeSH
• práce podpořená grantem MeSH
• Research Support, N.I.H., Extramural MeSH
• Názvy látek
• aktivátorový protein specifický pro B-buňky MeSH
• nádorový supresorový protein p53 MeSH
• NOTCH1 protein, human MeSH Prohlížeč
• PAX1 transcription factor MeSH Prohlížeč
• PAX5 protein, human MeSH Prohlížeč
• receptor Notch1 MeSH
• transkripční faktory paired box MeSH

Multiple myeloma (MM) is a haematological malignancy characterized by the accumulation of clonal plasma cells (PCs) in the bone marrow (BM). Although novel therapeutic strategies have prolonged survival of patients, the disease remains difficult to treat with a high risk of relapse. The failure of therapy is thought to be associated with a persistent population of the so-called MM stem cells or myeloma initiating cells (MIC) that exhibit tumour-initiating potential, self-renewal and resistance to chemotherapy. However, the population responsible for the origin and sustainability of tumour mass has not been clearly characterized so far. This review summarizes current myeloma stem cell concepts and suggests that high phenotypic and intra-clonal heterogeneity, together with plasticity potential of MM might be other contributing factors explaining discrepancies among particular concepts and contributing to the treatment failure.

• Klíčová slova
• malignant plasma cells, multiple myeloma, myeloma stem cells, plasticity, precursor B cells,
• MeSH
• aktivátorový protein specifický pro B-buňky nedostatek   genetika   MeSH
• antigeny diferenciační B-lymfocytární analýza   MeSH
• antigeny nádorové analýza   MeSH
• B-lymfocyty patologie   MeSH
• biologické modely MeSH
• buněčné klony patologie   MeSH
• buněčný rodokmen MeSH
• cílená molekulární terapie MeSH
• dediferenciace buněk genetika   MeSH
• genová přestavba B-lymfocytů MeSH
• hypoxie buňky MeSH
• lidé MeSH
• mnohočetný myelom patologie   terapie   MeSH
• myelomové proteiny analýza   genetika   MeSH
• nádorové kmenové buňky patologie   MeSH
• plazmatické buňky patologie   MeSH
• přesmyk imunoglobulinových tříd MeSH
• regulace genové exprese u nádorů MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• přehledy MeSH
• Názvy látek
• aktivátorový protein specifický pro B-buňky MeSH
• antigeny diferenciační B-lymfocytární MeSH
• antigeny nádorové MeSH
• myelomové proteiny MeSH
• PAX5 protein, human MeSH Prohlížeč

OBJECTIVES: To assess the frequency and intensity of PAX5 gene messenger ribonucleic acid (mRNA) expression in TaT1 bladder cancer tissue, as well as its correlation with clinicopathologic variables and patient outcome. METHODS: The RNA expression of PAX5 was evaluated with reverse transcriptase polymerase chain reaction in the tumor tissue of 75 patients with stage TaT1 bladder cancer treated with transurethral resection. Patients were observed with cystoscopy and urinary cytologic evaluation. The association between PAX5 expression and clinicopathologic variables and patient outcome was evaluated. Benign urothelium from 8 patients with benign prostatic hyperplasia was obtained. These patients were used as a control group. RESULTS: PAX5 expression was found in 62 patients with bladder cancer (82.7%) but in no patient from the control group. High PAX5 expression (greater than 0.2) was confirmed in 19 patients (25.3%). No significant relationship was observed between quantity of PAX5 expression and clinicopathologic variables. The 3-year recurrence-free and progression-free survival rates in highly positive patients were 13.2% and 71.6%, compared with 40.6% and 92.8%, respectively, in patients with weak or negative expression (log-rank test, P = 0.0075, P = 0.022). Multivariate Cox proportional hazard model analysis identified PAX5 expression as an independent predictor of tumor recurrence. CONCLUSIONS: PAX5 gene expression is a frequent finding in superficial transitional cell carcinoma of the bladder. High levels of PAX5 are associated with poorer recurrence-free and progression-free survival rates. Moreover, PAX5 expression was found to be an independent prognostic factor for recurrence-free survival by a multivariate analysis.

• MeSH
• aktivátorový protein specifický pro B-buňky genetika   MeSH
• dospělí MeSH
• karcinom z přechodných buněk genetika   patologie   chirurgie   MeSH
• lidé středního věku MeSH
• lidé MeSH
• messenger RNA biosyntéza   MeSH
• nádory močového měchýře genetika   patologie   chirurgie   MeSH
• regulace genové exprese u nádorů * MeSH
• senioři nad 80 let MeSH
• senioři MeSH
• staging nádorů MeSH
• výsledek terapie 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
• práce podpořená grantem MeSH
• Názvy látek
• aktivátorový protein specifický pro B-buňky MeSH
• messenger RNA MeSH
• PAX5 protein, human MeSH Prohlížeč

Pax genes encode transcription factors that control key developmental decisions in various animal phyla. The Pax2/5/8 subfamily plays a key role in specification and/or maintenance of vertebrate mid-hindbrain boundary (MHB) region by directly regulating expression of other genes, most notably En2. In the invertebrate chordate amphioxus, expression of AmphiPax2/5/8 is found in many sites that are homologous to the regions of the vertebrate embryo expressing orthologous genes Pax2, Pax5 or Pax8. However, no co-expression of AmphiPax2/5/8 and AmphiEn is detected in the region of the neural tube that might correspond to the vertebrate MHB. Based on this observation and the absence of AmphiWnt expression in this region it appears that amphioxus does not have a MHB. Here we investigated the possibility that the AmphiPax2/5/8, as a key component of MHB development, has lost some of the properties of its vertebrate counterparts. We have analyzed both the DNA-binding and transactivation properties of AmphiPax2/5/8 as well as its ability to interact with the groucho co-repressor. In all these assays AmphiPax2/5/8 is indistinguishable from the human Pax5. In addition, we found two alternatively spliced AmphiPax2/5/8 isoforms that function similarly to the alternatively spliced isoforms of human Pax8. Analysis of the AmphiEn regulatory region provided no evidence for AmphiPax2/5/8 binding and transactivation. Therefore, in amphioxus, AmphiPax2/5/8, although capable of performing all the necessary functions has not been recruited for a developmental mechanism which usually sets up MHB development in vertebrates.

• MeSH
• aktivátorový protein specifický pro B-buňky MeSH
• alternativní sestřih MeSH
• buněčné linie MeSH
• buňky 3T3 MeSH
• DNA vazebné proteiny genetika   fyziologie   MeSH
• DNA genetika   metabolismus   MeSH
• jaderné proteiny * MeSH
• lidé MeSH
• molekulární sekvence - údaje MeSH
• myši MeSH
• nádorové buňky kultivované MeSH
• nižší strunatci genetika   MeSH
• obratlovci genetika   MeSH
• promotorové oblasti (genetika) genetika   MeSH
• regulace genové exprese MeSH
• regulační oblasti nukleových kyselin genetika   MeSH
• rekombinantní fúzní proteiny genetika   metabolismus   MeSH
• reportérové geny genetika   MeSH
• rombencefalon metabolismus   MeSH
• sekvence aminokyselin MeSH
• sekvence nukleotidů MeSH
• sekvenční homologie aminokyselin MeSH
• trans-aktivátory genetika   fyziologie   MeSH
• transkripční faktor PAX2 MeSH
• transkripční faktor PAX8 MeSH
• transkripční faktory paired box MeSH
• transkripční faktory genetika   fyziologie   MeSH
• vazba proteinů MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• myši MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Research Support, U.S. Gov't, Non-P.H.S. MeSH
• Názvy látek
• aktivátorový protein specifický pro B-buňky MeSH
• DNA vazebné proteiny MeSH
• DNA MeSH
• jaderné proteiny * MeSH
• PAX2 protein, human MeSH Prohlížeč
• Pax2 protein, mouse MeSH Prohlížeč
• PAX5 protein, human MeSH Prohlížeč
• PAX8 protein, human MeSH Prohlížeč
• Pax8 protein, mouse MeSH Prohlížeč
• rekombinantní fúzní proteiny MeSH
• trans-aktivátory MeSH
• transkripční faktor PAX2 MeSH
• transkripční faktor PAX8 MeSH
• transkripční faktory paired box MeSH
• transkripční faktory MeSH