ATF2 knockout in papillomas
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE9328 | GEO | 2008/09/01
SECONDARY ACCESSION(S): PRJNA103001
REPOSITORIES: GEO
Similar Datasets
Project description:Germline polymorphisms influence gene expression networks in normal mammalian tissues. Analysis of this genetic architecture can identify single genes and whole pathways that influence to complex traits including inflammation and cancer susceptibility. Changes in the genetic architecture during the development of benign and malignant tumours have not been investigated. Here, we document major changes in germline control of gene expression during skin tumour development as a consequence of cell selection, somatic genetic events, and changes in tumour microenvironment. Immune response genes such as Interleukin 18 and Granzyme E are under germline control in tumours but not in normal skin. Gene expression networks linked to tumour susceptibility and hair follicle stem cell markers in normal skin undergo significant reorganization during tumour progression. Our data highlight opposing roles of Interleukin-1 signaling networks in tumour susceptibility and tumour progression and have implications for the development of chemopreventive strategies to reduce cancer incidence. Skin tumors were induced on dorsal back skin from a Mus spretus / Mus musculus backcross ([SPRET/Ei X FVB/N] X FVB/N) mice by treatment of dorsal back skin with dimethyl benzanthracene (DMBA) and tetradecanoyl-phorbol acetate (TPA). This treatment induced multiple benign papillomas as well as malignant squamous cell carcinomas (SCC) and spindle cell carcinomas. Gene expression analysis was performed on mRNA extracted from 68 papillomas: two papillomas from each of 31 FVBBX mice and a single papilloma from six additional FVBBX mice. Papillomas were harvested when mice were sacrificed due to presence of a carcinoma or termination of the experiment.
2010-12-22 | E-GEOD-21263 | biostudies-arrayexpress
Project description:FVB/N mice were subjected to 7,12-Dimethylbenz[a]anthracene (DMBA) two-hit multistage skin carcinogenesis protocol. Mice were topically treated with 200 nmol of DMBA in 0.2 mL acetone then twice weekly for six weeks with 5 nmol PMA (Phorbol 12-myristate 13-acetate). A second hit of DMBA was performed on the eighth week followed by the resumption of PMA treatment for 14 more weeks. Control mice were only topically treated with 0.2 mL acetone vehicle. Healthy skins (acetone-treated), hyperplastic skins, papillomas and tumors were harvested throughout the protocol and biopsies were frozen for RNA extraction.
2014-02-03 | GSE52299 | GEO
Project description:FVB/N mice were subjected to 7,12-Dimethylbenz[a]anthracene (DMBA) two-hit multistage skin carcinogenesis protocol. Mice were topically treated with 200 nmol of DMBA in 0.2 mL acetone then twice weekly for six weeks with 5 nmol PMA (Phorbol 12-myristate 13-acetate). A second hit of DMBA was performed on the eighth week followed by the resumption of PMA treatment for 14 more weeks. Control mice were only topically treated with 0.2 mL acetone vehicle. Healthy skins (acetone-treated), hyperplastic skins, papillomas and tumors were harvested throughout the protocol and biopsies were frozen for RNA extraction. Small RNA libraries were generated from total RNAs of control skins, hyperplastic skins, papillomas and cSCCs biopsies (n=5 in each group) corresponding to a total of 20 samples, and sequenced on the Applied Biosystems SOLiD System.
2014-02-03 | E-GEOD-52299 | biostudies-arrayexpress
Project description:Female FVB/N and Tg.Ac (hemizygotes) mice 3-5 weeks of age were purchased from Harlan UK and Taconic UK, respectively. The mice were contained in an isolator and maintained at 19C with 50% relative humidity and a 12-hour light-dark cycle. Following a 1 week acclimatisation period the dorsal skin of the mice was shaved (approximately 8cm2 area) 2 days prior to commencing treatment. FVB/N mice (5 per group) were treated with dimethylbenz[a]anthracene (DMBA) (10ug/200ul in acetone) or vehicle control one week before promotion with TPA. TPA (2.5ug/200ul in acetone) was applied to the back of both FVB/N and Tg.Ac mice (5 per group) twice a week for up to 14 weeks; control mice received acetone. Mice were shaved and examined weekly for the presence of papillomas. At each time point (FVB/N mice 2, 4, 6 and 14 weeks of TPA promotion and Tg.Ac mice 4 days, 1, 2 and 9 weeks of TPA promotion) the mice were killed by cervical dislocation and the dorsal skin removed, a representative portion was fixed in 10% neutral buffered formalin and retained for histological analysis; the remainder was snap frozen in liquid nitrogen.
2005-10-01 | E-MEXP-188 | biostudies-arrayexpress
Project description:Camphor white oil (CWO) application was found to induce regression of papillomas in a mouse chemical carcinogenesis model. In healthy epidermis, CWO induced increased proliferation of basal keratinocytes. RNA-sequencing was performed on epidermal cells 24 hours after CWO or vehicle application (N=3 mice/treatment), and on 4 pooled papillomas harvested after 6 weeks of treatment (N=3 mice/treatment). Sequencing identified transcripts that may alter skin physiology and induce tumor regression.
2019-01-07 | GSE117557 | GEO
Project description:Germline polymorphisms influence gene expression networks in normal mammalian tissues. Analysis of this genetic architecture can identify single genes and whole pathways that influence to complex traits including inflammation and cancer susceptibility. Changes in the genetic architecture during the development of benign and malignant tumours have not been investigated. Here, we document major changes in germline control of gene expression during skin tumour development as a consequence of cell selection, somatic genetic events, and changes in tumour microenvironment. Immune response genes such as Interleukin 18 and Granzyme E are under germline control in tumours but not in normal skin. Gene expression networks linked to tumour susceptibility and hair follicle stem cell markers in normal skin undergo significant reorganization during tumour progression. Our data highlight opposing roles of Interleukin-1 signaling networks in tumour susceptibility and tumour progression and have implications for the development of chemopreventive strategies to reduce cancer incidence. Skin tumors were induced on dorsal back skin from a Mus spretus / Mus musculus backcross ([SPRET/Ei X FVB/N] X FVB/N) mice by treatment of dorsal back skin with dimethyl benzanthracene (DMBA) and tetradecanoyl-phorbol acetate (TPA). This treatment induced multiple benign papillomas as well as malignant squamous cell carcinomas (SCC) and spindle cell carcinomas. 60 carcinomas were harvested from 55 mice; five mice provided two carcinomas each.
2010-12-22 | E-GEOD-21247 | biostudies-arrayexpress
Project description:Papillomaviruses (PVs) are able to induce papillomas, premalignant lesions, and carcinomas in a wide variety of species. PVs are classified first based on their host and tissue tropism and then their genomic diversities. A laboratory mouse papillomavirus, MmuPV1 (formerly MusPV), naturally infects NMRI-Foxn1nu/Foxn1nu (nude; T cell deficient) mice. C57BL/6J wild-type mice were not susceptible to MmuPV1 infection; however, immunocompetent, alopecic, S/RV/Cri-ba/ba (bare) mice developed small papillomas at injection sites that regressed. NMRI-Foxn1nu and B6.Cg-Foxn1nu but not NU/J-Foxn1nu mice were susceptible to MmuPV1 infection. B6 congenic strains, but not other congenic strains carrying the same allelic mutations, that lack B- and T-cells, but not B-cells alone, were susceptible to infection, indicating that mouse strain and T-cell deficiency are critical to tumor formation. Although lesions initially observed were exophytic papillomas around the muzzle, exophytic papillomas on the tail and condylomas of the vaginal lining could be induced by experimental infections. On the dorsal skin, locally invasive, poorly differentiated tumors developed with features similar to human trichoblastomas. Transcriptome analysis revealed significant differences between the normal skin in these anatomic sites and in papillomas versus trichoblastomas. The primarily dysregulated genes involved molecular pathways associated with cancer, cellular development, cellular growth and proliferation, cell morphology, and connective tissue development and function. Surprisingly, few of the genes commonly associated with basal cell carcinoma or squamous cells carcinoma were dramatically dysregulated.
2014-10-28 | GSE58094 | GEO
Project description:Papillomaviruses (PVs) are able to induce papillomas, premalignant lesions, and carcinomas in a wide variety of species. PVs are classified first based on their host and tissue tropism and then their genomic diversities. A laboratory mouse papillomavirus, MmuPV1 (formerly MusPV), naturally infects NMRI-Foxn1nu/Foxn1nu (nude; T cell deficient) mice. C57BL/6J wild-type mice were not susceptible to MmuPV1 infection; however, immunocompetent, alopecic, S/RV/Cri-ba/ba (bare) mice developed small papillomas at injection sites that regressed. NMRI-Foxn1nu and B6.Cg-Foxn1nu but not NU/J-Foxn1nu mice were susceptible to MmuPV1 infection. B6 congenic strains, but not other congenic strains carrying the same allelic mutations, that lack B- and T-cells, but not B-cells alone, were susceptible to infection, indicating that mouse strain and T-cell deficiency are critical to tumor formation. Although lesions initially observed were exophytic papillomas around the muzzle, exophytic papillomas on the tail and condylomas of the vaginal lining could be induced by experimental infections. On the dorsal skin, locally invasive, poorly differentiated tumors developed with features similar to human trichoblastomas. Transcriptome analysis revealed significant differences between the normal skin in these anatomic sites and in papillomas versus trichoblastomas. The primarily dysregulated genes involved molecular pathways associated with cancer, cellular development, cellular growth and proliferation, cell morphology, and connective tissue development and function. Surprisingly, few of the genes commonly associated with basal cell carcinoma or squamous cells carcinoma were dramatically dysregulated. To determine if there were transcriptome differences between papillomas on the tail skin compared to invasive trichoblastomas on the dorsal skin, tumors from the tail and dorsal skin from 3 B6.Cg-Foxn1nu/Foxn1nu mice and unaffected skin from the tail or contra-lateral (dorsal skin) were compared using the Affymetrix GeneChip Mouse Genome 1.0 ST Array. Concurrently, a matched study was done at the University of Louisville comparing facial (muzzle) papillomas and dorsal skin trichoblastomas to respective unaffected contralateral skin.
2014-10-28 | E-GEOD-58094 | biostudies-arrayexpress
Project description:We report that P2ry6-deficient mice exhibit marked resistance to 7,12-dimethylbenzanthracene (DMBA)/12-O-tetradecanoylphorbol-13-acetate (TPA)-induced two-stage skin papilloma formation compared with wild-type mice. Consistent with these findings, epidermal hyperplasia in response to TPA stimulation was suppressed in the P2ry6 knockout or MRS2578 (P2RY6 antagonist)-treated mice. The dramatic decrease in hyperplasia and tumorigenesis due to P2ry6 disruption was associated with the suppression of TPA-induced keratinocyte proliferation and inflammatory reactions.We have employed whole genome microarray expression profiling as a discovery platform to identify genes with the potential to distinguish differentially expressed genes induced by TPA stimulation between the P2ry6+/+ and P2ry6-/- mice. Notably, P2ry6 deletion prevented the TPA-induced increase in YAP nuclear accumulation and hence its downstream gene expression in an MST/LATS1-dependent manner.
2021-11-26 | GSE189478 | GEO
Project description:WT or Cd226-/- mice were treated with DMBA and TPA. Three weeks later, cells were isolated from mice back skin, and divided CD45+ and CD45- cells by cell sorter. CD45+ and CD45- cells were mixed in 1:1 ratio, and we performed scRNA sequencing of skin cells.
2021-10-26 | GSE174776 | GEO