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10,694 results for “carcinoma,”
Dataset Friebus-Kardash et al, A chemerin peptide analog stimulates tumor growth in two xenograft mouse models of human colorectal carcinoma
<p>Dataset Friebus-Kardash et al, A chemerin peptide analog stimulates tumor growth in two xenograft mouse models of human colorectal carcinoma</p> <p> </p>
Tumor-Immune Microenvironment Revealed by Imaging Mass Cytometry in a Metastatic Sarcomatoid Urothelial Carcinoma with a Prolonged Response to Pembrolizumab - IMC data
<blockquote> <p>Sarcomatoid urothelial carcinoma (SUC) is a rare subtype of urothelial carcinoma (UC), that typically presents at an advanced stage compared to more common variants of UC. Locally advanced and metastatic UC have a poor long-term survival following progression on first-line platinum-based chemotherapy. Antibodies directed against the programmed cell death 1 protein (PD-1) or its ligand (PD-L1) are now approved to be used in these scenarios. The need for reliable biomarkers for treatment stratification is still under research. Here we present a novel case report of the first Image Mass Cytometry (IMC) analysis done in SUC to investigate the immune cell repertoire and PD-L1 expression in a patient who presented with metastatic SUC and experienced a prolonged response to the anti-PD1 immune checkpoint inhibitor pembrolizumab after progression on first line chemotherapy. This case report provides an important platform for translating these findings to a larger cohort of UC and UC variants.</p> </blockquote> <p>We make available TIFF files containing imaging mass cytometry data for 4 regions of interest of a sample of metastatic sarcomatoid urothelial carcinoma. The order of the axis in the image stacks is "CYX". The CSV files indicate the identity of the channels.</p>
Molecular Signatures of Tumour and its Microenvironment for Precise Quantitative Diagnosis of Oral Squamous Cell Carcinoma: An Interna-tional Multi-cohort Diagnostic Validation Study
<p><strong>Supplementary Materials: </strong>The following supporting information can be downloaded at: www.mdpi.com/xxx/s1, <strong>Table ST1</strong> – qMIDS<sup>V2 </sup>Gene panel primer sequences; <strong>Figure S1</strong> – qMIDS<sup>V1</sup> vs qMIDS<sup>V2</sup> 384-well assay format and protocols; <strong>Figure S2.</strong> Individual target gene expression pattern in 1761 samples; <strong>Figure S3.</strong> Various statistical methods used for gene selection analysis on 1761 clinical samples; <strong>Figure S4. </strong>Diagnostic performance comparison between qMIDS<sup>V2</sup> vs qMIDS<sup>V2* </sup>(with 4 less effective genes removed from the panel of 14 target genes of qMIDS<sup>V2</sup>); <strong>Figure S5</strong>. Effect of removing individual genes from the 14-target gene panel qMIDS<sup>V2</sup> (qV2) on diagnostic test performance based on the UK patient cohort data.</p>
In vivo screening for functional HIF2A enhancers in renal carcinoma.
<p>High throughput sequencing data and analysis from a CRISPRi-based in vivo functional screen for oncogenic HIF2A-bound transcriptional enhancers in renal cancer. </p>
Mutations in the telomerase reverse transcriptase promoter and PIK3CA gene are common events in penile squamous cell carcinoma of Italian and Ugandan patients
<p>Somatic mutations in the promoter region of TERT (TERTp) gene are highly frequent in penile carcinoma in Italian and Ugandan patients, predominantly in human papillomavirus (HPV) negative cancers (67.6%). TERTp and PIK3CA hotspot changes coexist in 15.8% of cases. The higher mutant allele frequencies (MAFs) of TERT -124A/-146A compared to PIK3CA E545K MAFs suggest an asynchronous mutation timing. The coexistence of TERTp and PIK3CA mutations may represent a novel co-actionable therapeutic target in penile carcinoma patients.</p>
Immune and genetic signature of HER2-driven breast carcinomas triggering anti-Yo paraneoplastic cerebellar degeneration
<ul> <li>Supplementary eTables from: Immune and genetic signature of HER2-driven breast carcinomas triggering anti-Yo paraneoplastic cerebellar degeneration: <ul> <li><strong>eTables 1</strong>: Results of DESeq2 on the differential gene expression analysis between Yo-PCD and control tumours for all genes and for differentially expressed genes.</li> <li><strong>eTables 2</strong>: Results of the Gene Ontology enrichment performed by clusterProfiler on genes over-expressed in Yo-PCD tumours</li> <li><strong>eTables 3</strong>: Results of the Gene Ontology enrichment performed by clusterProfiler on genes under-expressed in Yo-PCD tumours</li> </ul> </li> <li>Gene counts</li> <li>Gene TPMs</li> </ul>
High-resolution AI image dataset for diagnosing oral submucous fibrosis and squamous cell carcinoma
<p>This deposition contains only training dataset of ORCHID database. The validation and test dataset related to the same study can be found at DOI: <strong>10.5281/zenodo.12646943.</strong></p>
Outcome of Childhood Adrenocortical Carcinoma in Developing Countries. Supplementary Table 3: Pathological details
<p>The outcome of Childhood Adrenocortical Carcinoma in Developing Countries; a scene for surgeons or a chance for medicines</p> <p>Supplementary Table 3: Pathological details</p>
The outcome of Childhood Adrenocortical Carcinoma in Developing Countries; Supplementary Table 2: Metastatic sites
<p>The outcome of Childhood Adrenocortical Carcinoma in Developing Countries; a scene for surgeons or a chance for medicines.</p> <p>Supplementary Table 2: Metastatic sites</p>
Outcome of Childhood Adrenocortical Carcinoma in Developing Countries. Supplementary Table 1: Patients' characteristics and endocrinal manifestations
<p>Outcome of Childhood Adrenocortical Carcinoma in Developing Countries. Supplementary Table 1: Patients’ characteristics and endocrinal manifestations</p>
Case report: Adenosquamous carcinoma of the penis
<p><strong>Case history</strong></p> <p>55-year-old patient with a penile tumor located in the perimeatal area of the glans</p> <p> </p> <p><strong>Histologic findings</strong></p> <p>Microphotographs show a biphasic proliferation of tumors cells showing squamous and glandular differentiation, deeply infiltrating penile erectile tissues. Squamous and glandular structures are found either segregated or in the same tumor nests.</p> <p> </p> <p><strong>Discussion</strong></p> <p>Adenosquamous carcinoma is a rare penile SCC variant characterized by the presence of solid squamous tumor nests intermingled with areas of glandular differentiation. Less than 20 cases have been reported. The tumor originates in the glans central/perimeatal region and has a tendency for deep infiltration. Most tumors are of high-grade, with frequent vascular and perineural invasion. Metastatic rate is high but cancer-specific mortality remains low.</p> <p>Histologically, areas with squamous differentiation predominate. The glandular component is positive for mucin stains and CEA.</p> <p>The main differential diagnosis is with penile tumors with glandular features, including mucoepidermoid, pseudoglandular, urothelial carcinomas of distal urethra with glandular differentiation and true adenocarcinomas of Littré glands. Mucoepidermoid carcinoma of penis is an exceedingly rare tumor which is histologically similar to its cervical counterpart. Neoplastic population is composed of cell with squamous differentiation and cells showing evidence of glandular differentiation (pale, granular and ample cytoplasm with positivity for mucin stains and CEA) without well-defined glandular or ductal structures. Although more data are needed, it seems that mucoepidermoid carcinoma is more aggressive than conventional adenosquamous carcinoma.</p> <p>In pseudoglandular carcinoma the extensive acantholysis can simulate glands lumina but there is no true epithelial lining. Urothelial carcinomas originating in the penile distal urethra or extending from prostate, bladder or even ureter/renal pelvis, can depict glandular features. However, a previous history of urothelial carcinoma elsewhere and the frequent finding of in situ urothelial carcinoma (which is absent in adenosquamous carcinoma) aid in the differential diagnosis.</p> <p>In adenocarcinomas originating in Littré glands there is no true squamous differentiation and tumors tend to be ventrally located with only secondary extension to the perimeatal glans area. Finally, entrapment of Littré’s glans by an otherwise usual SCC can simulate the aspect of an adenosquamous carcinoma. However, the morphology of the glandular component remains bland and admixtures are limited to the periurethral area.</p> <p> </p> <p><strong>Selected references</strong></p> <p><a href="https://www.ncbi.nlm.nih.gov/pubmed/22641956">Chaux & Cubilla. Semin Diagn Pathol. 2012 29(2): 72-82</a></p> <p><a href="https://www.ncbi.nlm.nih.gov/pubmed/8554104">Cubilla et al. Am J Surg Pathol. 1996 20(2): 156-60</a></p> <p><a href="https://www.ncbi.nlm.nih.gov/pubmed/16924331">Romero et al. Clinics (Sao Paulo). 2006 61(4): 363-4</a></p>
Supplementary data for: Transposon mutagenesis identifies cooperating genetic drivers during keratinocyte transformation and cutaneous squamous cell carcinoma progression
<p><strong>Supplementary Note 1:</strong></p> <ul> <li>S1 Text: Oncogenomic comparisons between SB candidate Trunk driver genes and their direct orthologs in human Cancer Gene Census; Pyrosequencing analysis of SB-driven keratinocyte cancer models; References.</li> </ul> <p><strong>Supplementary Figures 1-11:</strong></p> <ul> <li>S1 Fig: Overview of genetic crosses to generate SB|Trp53|Onc3 mouse model.</li> <li>S2 Fig: SB insertion patterns in activated and inactivated drivers.</li> <li>S3 Fig: Evaluating the reproducibility of SBCapSeq results from bulk cuSCC and normal skin specimens.</li> <li>S4 Fig. Hierarchical two-dimensional clustering of recurrent events in cuKA and cuSCC.</li> <li>S5 Fig. Curated biological pathways and processes enriched within SB-induced cuSCC.</li> <li>S7 Fig: ZMIZ1 metagene within the TCGA Head & Neck Squamous Cell Carcinoma (hnSCC) RNA-seq dataset.</li> <li>S8 Fig: Clonally selected SB insertions affect trunk driver proto-oncogene expression in SB-cuSCC genomes.</li> <li>S9 Fig: Clonally selected SB insertions affect trunk driver genes by inactivating expression in SB-cuSCC genomes.</li> <li>S10 Fig: CREBBP knockdown does not alter proliferation rate in cuSCC cell lines.</li> <li>S11 Fig: Gross photographs of cuSCC xenograft masses collected at necropsy showing robust TurboGFP expression.</li> <li>S12 Fig: SB T2/Onc3 TG.12740 allele donor position mapping and exclusion for SB Driver Analysis.</li> </ul> <p><strong>Supplementary Tables 1-20:</strong></p> <ul> <li>S1 Table: Tumor incidence and subgroup classifications by cohort.</li> <li>S2 Table: Specimen metafile data for projects sequenced using SBCapSeq protocol with Ion Torrent Proton sequencer.</li> <li>S3 Table: Discovery and progression SB Driver Analysis for cuSCC60_SBC.</li> <li>S4 Table: Trunk SB Driver Analysis for cuSCC60_SBC.</li> <li>S5 Table: Discovery and progression SB Driver Analysis for cuKA11_SBC.</li> <li>S6 Table: Trunk SB Driver Analysis for cuKA11_SBC.</li> <li>S7 Table: Discovery and progression SB Driver Analysis for cuSK32_SBC.</li> <li>S8 Table: SBCapSeq read depth and analysis for 4 cuSCC genomes selected for multi-region resequencing because they had intermixing of cuSCC and cuKA histologies.</li> <li>S9 Table: Enrichr gene set pathway enrichment analysis of cuSCC drivers.</li> <li>S10 Table: Summary of 7 cuSCC transcriptomes selected for whole transcriptome RNAseq analysis.</li> <li>S11 Table: BED file of SBfusion insertions in 7 cuSCC genomes by whole transcriptome RNAseq analysis.</li> <li>S12 Table: Venn diagram for overlap of genes with SBfusion reads detected by whole transcriptome RNAseq analysis and cuSCC60_SBC discovery driver.</li> <li>S13 Table: Venn diagram for overlap of genes with SBfusion reads detected by whole transcriptome RNAseq analysis and all cuSCC drivers.</li> <li>S14 Table: Transcripts per million (TPM) normalized whole transcriptome RNAseq values per gene from RNA isolated from cuSCC genomes with and without Zmiz1 insertions.</li> <li>S15 Table: Fragments Per Kilobase of Transcripts per Million (FPKM) normalized whole transcriptome RNAseq values per gene transcript from RNA isolated from cuSCC genomes with and without Zmiz1 insertions.</li> <li>S16 Table: Normalized microarray values per gene from RNA isolated from cuSCC genomes with and without <em>Zmiz1</em> insertions.</li> <li>S17 Table: Normalized microarray values per probe from RNA isolated from cuSCC genomes with and without <em>Zmiz1</em> insertions.</li> <li>S18 Table: All 289 genes with differential expression analysis from microarray data from RNA isolated from cuSCC genomes with and without Zmiz1 insertions with P<0.0001 and q<0.05.</li> <li>S19 Table: Lentiviral vectors containing shRNAs used in this study.</li> <li>S20 Table: TaqMan probes used in this study.</li> </ul> <p><strong>Supplementary Datasets 1-5:</strong></p> <ul> <li>S1 Data: BED file of SB insertions for cuSCC60_SBC.</li> <li>S2 Data: BED file of SB insertions for cuKA11_SBC.</li> <li>S3 Data: BED file of SB insertions for cuSK32_SBC</li> <li>S4 Data: BED file of SB insertions for 4 cuSCC genomes selected for multi-region resequencing because they had intermixing of cuSCC and cuKA histologies.</li> <li>S5 Data: Numerical data for graphs pertaining to Figure Panels Fig1A; Fig5A–E; Fig6A–B,D; Fig7C–G; Fig8A–B,D–F; Fig9A–I in the paper on the publicly availble <em>PLOS Genetics</em> Web site.</li> </ul>
"PROGNOSTIC ROLE OF TUMOR BUDDING IN ORAL SQUAMOUS CELL CARCINOMA"
<p>Master Data Sheet</p>
Basaloid Squamous Cell Carcinoma: A Case Report
<p><strong>Background:</strong> The upper aerodigestive tract is where BSCC (basaloid squamous cell carcinoma), a rare variation of conventional SCC, is most frequently found. The hypopharynx, tonsil, supraglottic larynx, tongue (base), and head-neck regions are particularly susceptible to BSCC. Clinically, the presentation of BSCC is similar to that of conventional SCC, but it has a poor prognosis than traditional SCC. BSCC is distinguished histopathologically by a dimorphic-pattern, a distinctive basal cell component paired with a squamous component, and a squamous component. Compared to traditional SCC, the prognosis for BSCC is worse. However, clinically it shows similar features like conventional SCC which makes it difficult to diagnose. Therefore, histopathology and immunohistochemistry have a crucial role in diagnosing such tumors. We here present a case of a seventy-year male diagnosed with BSCC involving the tongue.</p> <p><strong>Keywords</strong>: Basaloid squamous cell carcinoma, dimorphic pattern, basaloid cells, comedo necrosis.</p>
Supplementary Tables - Re-analysis of hepatitis B virus integration sites reveals potential new loci associated with oncogenesis in hepatocellular carcinoma
<p>------------------------------------------------------------</p> <p><strong>Supplementary Tables</strong></p> <p>supplementary_table.xlsx</p> <ul> <li>T2T-CHM13_human</li> <li>T2T-CHM13_hbv</li> <li>GRCh38_human</li> <li>GRCh38_hbv</li> <li>GRCh_human_annotation</li> <li>meta</li> </ul> <p>------------------------------------------------------------</p> <p><strong>Re-analysis of hepatitis B virus integration sites reveals potential new loci associated with oncogenesis in hepatocellular carcinoma</strong><br> <a href="https://doi.org/10.5501/wjv.v12.i3.209">https://doi.org/10.5501/wjv.v12.i3.209</a></p><br> <p><strong>BACKGROUND</strong></p> <p>Hepatitis B virus (HBV) is a major cause of hepatocellular carcinoma (HCC). HBV DNA can get integrated into the hepatocyte genome to promote carcinogenesis. However, the precise mechanism by which the integrated HBV genome promotes HCC has not been elucidated.</p> <p><strong>AIM</strong></p> <p>To analyze the features of HBV integration in HCC using a new reference database and integration detection method.</p> <p><strong>METHODS</strong></p> <p>Published data, consisting of 426 Liver tumor samples and 426 paired adjacent non-tumor samples, were re-analyzed to identify the integration sites. Genome Reference Consortium Human Build 38 (GRCh38) and Telomere-to-Telomere Consortium CHM13 (T2T-CHM13 (v2.0)) were used as the human reference genomes. In contrast, human genome 19 (hg19) was used in the original study. In addition, GRIDSS VIRUSBreakend was used to detect HBV integration sites, whereas high-throughput viral integration detection (HIVID) was applied in the original study (HIVID-hg19).</p> <p><strong>RESULTS</strong></p> <p>A total of 5361 integration sites were detected using T2T-CHM13. In the tumor samples, integration hotspots in the cancer driver genes, such as TERT and KMT2B, were consistent with those in the original study. GRIDSS VIRUSBreakend detected integrations in more samples than by HIVID-hg19. Enrichment of integration was observed at chromosome 11q13.3, including the CCND1 pro-moter, in tumor samples. Recurrent integration sites were observed in mitochondrial genes.</p> <p><strong>CONCLUSION</strong></p> <p>GRIDSS VIRUSBreakend using T2T-CHM13 is accurate and sensitive in detecting HBV integration. Re-analysis provides new insights into the regions of HBV integration and their potential roles in HCC development.</p>
Pazopanib Versus Sunitinib in the Treatment of Locally Advanced and/or Metastatic Renal Cell Carcinoma
ClinicalTrials.gov study NCT00720941. IPD Sharing: YES. Countries: 14. Publications: 10.
Study Efficacy and Safety of INC280 in Patients With Advanced Hepatocellular Carcinoma.
ClinicalTrials.gov study NCT01737827. IPD Sharing: YES. Countries: 4. Publications: 1.
Patritumab With Cetuximab and a Platinum Agent for Squamous Cell Carcinoma (Cancer) of the Head and Neck (SCCHN )
ClinicalTrials.gov study NCT02633800. IPD Sharing: YES. Countries: 7. Publications: 2.
A Study to Investigate Tislelizumab (BGB-A317) Versus Placebo in Combination With Concurrent Chemoradiotherapy in Participants With Localized Esophageal Squamous Cell Carcinoma
ClinicalTrials.gov study NCT03957590. IPD Sharing: YES. Countries: 1. Publications: 1.
A Study to Evaluate Pazopanib as an Adjuvant Treatment for Localized Renal Cell Carcinoma (RCC)
ClinicalTrials.gov study NCT01235962. IPD Sharing: YES. Countries: 26. Publications: 2.
ScienceDex guides
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These curated guides explain access requirements, typical timelines, costs, and reuse considerations for widely used research datasets.
Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.