Similar Datasets
Project description:We used scRNA-Seq to examine BCC immune cell heterogeneity.
2023-03-29 | GSE204949 | GEO
Project description:We used scATAC-Seq to examine BCC immune cell heterogeneity.
2023-03-29 | GSE204863 | GEO
Project description:Activation of the Sonic hedgehog (Shh) signaling pathway due to Patched 1 (PTCH1) mutation is a key event in sporadic and familial basal cell carcinoma (BCC) development. To find out the specific pathway for therapeutic intervention, we developed a mouse BCC model by skin specific Ptch1 inactivation, and sought to identify novel Shh targets. We used microarrays to identify up-regulated genes in mouse BCC. We used microarrays to identify down-regulated genes in mouse BCC cell line by cyclopamine.
2018-01-15 | GSE20065 | GEO
Project description:In summary, we have validated differential expression of several miRs, namely two that are downregulated in all BCC subtypes compared to control skin (miR.383.5p, miR.145.5p), two that are downregulated in superficial BCC (miR.181c.5p, miR.181b.5p) relative to nodular and infiltrative BCC, and several that are upregulated in infiltrative BCC relative to superficial BCC (miR.22.5p, miR.18a.3p, miR.708.5p, miR.758.3p, miR.30c.5p), and two that are upregulated in infiltrative BCC relative to nodular BCC (miR.22.5p, miR.758.3p). To our knowledge, this study has investigated and validated the largest number of BCC tumors representing the different subtypes.
2024-01-01 | GSE245676 | GEO
Project description:Punch biopsies from patients with BCC (n=3) and non-lesional skin (n=3) were included in the study. Microarray based circRNA expression profiles were acquired using Arraystar circRNA Arrays V. 2.0 screening for 13,617 distinct human circRNA candidates. We identified circRNAs differentially expressed in BCC compared to non-lesional skin (control).
2016-04-21 | GSE74756 | GEO
Project description:A total of 3 patients with basal cell carcinoma (BCC) and 3 healthy individuals (control; non-lesional skin) were enrolled in the study. Punch biopsies (4 mm) were obtained under local anaesthesia and immediately put in RNAlater (Qiagen, Hilden, Germany) and stored at - 80 °C until RNA extraction. The lncRNA and mRNA expression in BCC was compared to lncRNA and mRNA expression in non-lesional skin (control).
2016-03-29 | E-GEOD-74858 | biostudies-arrayexpress
Project description:Imiquimod is a Toll-like receptor (TLR)-7 agonist capable of inducing complete clearance of basal cell carcinoma (BCC) and other cutaneous malignancies. We hypothesized that the characterization of the early transcriptional events induced by imiquimod may provide insights about immunological events preceding acute tissue and/or tumor rejection. We report a paired analysis of adjacent punch biopsies obtained pre- and post-treatment from 36 patients with BCC subjected to local application of imiquimod (N = 22) or vehicle cream (N=14) in a blinded, randomized protocol. Four treatments were assessed (q12 applications for 2 or 4 days, or q24 hrs for 4 or 8 days). RNA was amplified and hybridized to 17.5K cDNA arrays. All treatment schedules similarly affected the transcriptional profile of BCC; however, the q12 X 4days regimen, associated with highest effectiveness, induced the most changes with 637 genes unequivocally stimulated by imiquimod. A minority of transcripts (98 genes) confirmed previous reports of interferon-Â involvement. The remaining 539 genes portrayed additional immunological functions predominantly involving the activation of cellular innate and adaptive immune-effector mechanisms. Importantly, these effector signatures recapitulate previous observations of tissue rejection in the context of cancer immunotherapy, acute allograft rejection and autoimmunity. This study based on a powerful and reproducible model of cancer eradication by innate immune mechanisms provides the first insight in humans of the early transcriptional events associated with immune rejection. This model is likely representative of constant immunological pathways through which innate and adaptive immune responses combine to induce tissue destruction. Keywords: compound treatment design We report a paired analysis of adjacent punch biopsies obtained pre- and post-treatment from 36 patients with BCC subjected to local application of imiquimod (N = 22) or vehicle cream (N=14) in a blinded, randomized protocol. Four treatments were assessed (q12 applications for 2 or 4 days, or q24 hrs for 4 or 8 days). RNA was amplified and hybridized to 17.5K cDNA arrays.
2006-10-04 | E-GEOD-5121 | biostudies-arrayexpress
Project description:The mammalian Hippo signaling pathway, through its effectors YAP and TAZ, coerces epithelial progenitor cell expansion for appropriate tissue development or regeneration upon damage. Its ability to drive rapid tissue growth explains why many oncogenic events frequently exploit this pathway to promote cancer phenotypes. Indeed, several tumor types including basal cell carcinoma (BCC) show genetic aberrations in the Hippo (or YAP/TAZ) regulators. Here, we uncover that while YAP is dispensable for homeostatic epidermal regeneration, it is required for BCC development. Our clonal analyses further demonstrate that few emerging Yap-null dysplasia have lower fitness and thus are diminished as they progress to invasive BCC. Mechanistically, YAP depletion in BCC tumors leads to effective impairment of the JNK-JUN signaling, a well-established tumor driving cascade. Importantly, in this context, YAP does not influence canonical Wnt or Hedgehog signaling. Overall, we reveal the Hippo signaling as an independent promoter of BCC pathogenesis and thereby a viable target for drug-resistant BCC.
2018-09-04 | GSE115222 | GEO
Project description:The mammalian Hippo signaling pathway, through its effectors YAP and TAZ, coerces epithelial progenitor cell expansion for appropriate tissue development or regeneration upon damage. Its ability to drive rapid tissue growth explains why many oncogenic events frequently exploit this pathway to promote cancer phenotypes. Indeed, several tumor types including basal cell carcinoma (BCC) show genetic aberrations in the Hippo (or YAP/TAZ) regulators. Here, we uncover that while YAP is dispensable for homeostatic epidermal regeneration, it is required for BCC development. Our clonal analyses further demonstrate that few emerging Yap-null dysplasia have lower fitness and thus are diminished as they progress to invasive BCC. Mechanistically, YAP depletion in BCC tumors leads to effective impairment of the JNK-JUN signaling, a well-established tumor driving cascade. Importantly, in this context, YAP does not influence canonical Wnt or Hedgehog signaling. Overall, we reveal the Hippo signaling as an independent promoter of BCC pathogenesis and thereby a viable target for drug-resistant BCC.
2018-09-04 | GSE115147 | GEO
Project description:BACKGROUND: Basal cell carcinoma (BCC) is the most common form of human cancer. Though the genetic mutation and subsequent aberrant signaling role of the Hedgehog pathway in BCC development is understood, little is known about the downstream genetic mechanisms underlying BCC growth. The characterization of molecular events would improve our understanding of carcinogenesis and may define new therapeutic intervention opportunities. OBJECTIVE: To identify differential gene expression associated with tumorigenesis promotion and to define common signaling pathways significant in BCC survival and growth. METHODS: Microarray analysis, using a 21K expanded sequence verified cDNA set was performed on tissues obtained from previously untreated patients undergoing Mohs surgical resection (8 superficial BCC, 8 nodular BCC, 7 morphea form, 8 normal skin). Significantly differentially expressed genes were identified by analysis of microarray results in various data sets and subsequently screened for signaling pathway involvement. Selected genes were validated using real-time PCR analysis using an expanded set of 31 BCC samples. RESULTS: The global gene expression profiles in BCCs and normal skin were distinguishable by unpaired T test. 2429 genes were at least 1.5 fold differentially expressed between BCC (all morphological types) and normal skin (p < 0.01). Multiple singaling pathways were activated, but the hedgehog, WNT, MAPK and calcium signal transduction pathways predominated. CONCLUSION: Our findings may have important implications for understanding the pathogenesis of BCC and suggest targeting of the WNT and MAPK pathways with therapeutic intervention. Keywords: disease state analysis
2006-12-15 | GSE6520 | GEO