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1. Torchia EC, Chen Y, Sheng H, Katayama H, Fitzpatrick J, Brinkley WR, Caulin C, Sen S, Roop DR: A genetic variant of Aurora kinase A promotes genomic instability leading to highly malignant skin tumors. Cancer Res; 2009 Sep 15;69(18):7207-15
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  • [Title] A genetic variant of Aurora kinase A promotes genomic instability leading to highly malignant skin tumors.
  • Initially we examined Aurora-A expression levels at different stages of human skin cancer.
  • Nuclear Aurora-A was detected in benign lesions and became more diffused but broadly expressed in well and poorly differentiated squamous cell carcinomas (SCC), indicating that Aurora-A deregulation may contribute to SCC development.
  • To mimic the overexpression of Aurora-A observed in human skin cancers, we established a gene-switch mouse model in which the human variant of Aurora-A (Phe31Ile) was expressed in the epidermis upon topical application of the inducer RU486 (Aurora-AGS).
  • However, Aurora-A overexpression combined with exposure to TPA and the mutagen 7,12-dimethylbenz(a)anthracene accelerated SCC development with greater metastatic activity than control mice, indicating that Aurora-A cannot initiate skin carcinogenesis but rather promotes the malignant conversion of skin papillomas.
  • Our findings strongly implicate Aurora-A overexpression in the malignant progression of skin tumors and suggest that Aurora-A may be an important therapeutic target.

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  • (PMID = 19738056.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA089716-05A1; United States / NCI NIH HHS / CA / U01 CA105491; United States / NIDCR NIH HHS / DE / R01 DE015344-06; United States / NCI NIH HHS / CA / U01 CA105491-06; United States / NCI NIH HHS / CA / CA052607-18; United States / NCI NIH HHS / CA / CA52607; United States / NCI NIH HHS / CA / R01 CA089716; United States / NIDCR NIH HHS / DE / R01 DE015344; United States / NCI NIH HHS / CA / CA089716-05A1; United States / NCI NIH HHS / CA / CA89716; United States / NIDCR NIH HHS / DE / DE015344-06; United States / NCI NIH HHS / CA / CA105491-06; United States / NCI NIH HHS / CA / R01 CA052607-18; United States / NCI NIH HHS / CA / CA105491; United States / NCI NIH HHS / CA / R01 CA052607; United States / NIDCR NIH HHS / DE / DE15344
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 57-97-6 / 9,10-Dimethyl-1,2-benzanthracene; EC 2.7.11.1 / AURKA protein, human; EC 2.7.11.1 / Aurka protein, mouse; EC 2.7.11.1 / Aurora Kinase A; EC 2.7.11.1 / Aurora Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
  • [Other-IDs] NLM/ NIHMS133755; NLM/ PMC2745523
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2. Schaper ID, Marcuzzi GP, Weissenborn SJ, Kasper HU, Dries V, Smyth N, Fuchs P, Pfister H: Development of skin tumors in mice transgenic for early genes of human papillomavirus type 8. Cancer Res; 2005 Feb 15;65(4):1394-400
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  • [Title] Development of skin tumors in mice transgenic for early genes of human papillomavirus type 8.
  • The cutaneous human papillomavirus (HPV) 8 is clearly involved in skin cancer development in epidermodysplasia verruciformis patients and its early genes E2, E6, and E7 have been implicated in cell transformation in vitro.
  • To target their expression to the basal layer of the squamous epithelia the transgenes were put under the control of the keratin-14 promoter.
  • Transgenic mice were back-crossed for up to six generations into both FVB/N and Bl6 mouse strains.
  • Whereas none of the HPV8 transgene-negative littermates developed lesions in the skin or any other organ, 91% of HPV8-transgenic mice developed single or multifocal benign tumors, characterized by papillomatosis, acanthosis, hyperkeratosis, and varying degrees of epidermal dysplasia.
  • Squamous cell carcinomas developed in 6% of the transgenic FVB/N mice.
  • There was no consistent difference in relative viral RNA levels between healthy or dysplastic skin and malignant skin tumors.
  • Whereas UV-induced mutations in the tumor suppressor gene p53 are frequently detected in human skin carcinomas, mutations in p53 were not observed either in the benign or malignant mouse tumors.
  • Nonmelanoma skin cancer developed in HPV8-transgenic mice without any treatment with physical or chemical carcinogens.
  • [MeSH-major] Papillomaviridae / genetics. Skin Neoplasms / genetics. Skin Neoplasms / virology


3. Mordasky Markell L, Pérez-Lorenzo R, Masiuk KE, Kennett MJ, Glick AB: Use of a TGFbeta type I receptor inhibitor in mouse skin carcinogenesis reveals a dual role for TGFbeta signaling in tumor promotion and progression. Carcinogenesis; 2010 Dec;31(12):2127-35
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  • [Title] Use of a TGFbeta type I receptor inhibitor in mouse skin carcinogenesis reveals a dual role for TGFbeta signaling in tumor promotion and progression.
  • To test this, we treated mouse skin with SB431542 (SB), a well-characterized ALK5 inhibitor, during a two-stage skin carcinogenesis assay.
  • In contrast, the frequency of conversion to squamous cell carcinoma (SCC) was 2-fold higher in papillomas treated with SB.
  • Although there was no difference in tumor cell proliferation in early premalignant lesions, those that formed after SB treatment exhibited reduced squamous differentiation and an altered inflammatory microenvironment similar to SCC.
  • In an inducible epidermal RAS transgenic model, treatment with SB enhanced proliferation and cutaneous inflammation in skin but decreased expression of keratin 1 and increased expression of simple epithelial keratin 18, markers of premalignant progression.
  • In contrast to the current paradigm for TGFβ in carcinogenesis, these results demonstrate that cutaneous TGFβ signaling enables promotion of benign tumors but suppresses premalignant progression through context-dependent regulation of epidermal homeostasis and inflammation.

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  • (PMID = 20852150.001).
  • [ISSN] 1460-2180
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R0 CA117957; United States / NCI NIH HHS / CA / R0 CA122109
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 4-(5-benzo(1,3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide; 0 / Benzamides; 0 / Dioxoles; 0 / Receptors, Transforming Growth Factor beta; 0 / Smad2 Protein; 0 / Smad2 protein, mouse; 0 / Transforming Growth Factor beta1; EC 2.7.1.11 / TGF-beta type I receptor; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; NI40JAQ945 / Tetradecanoylphorbol Acetate
  • [Other-IDs] NLM/ PMC2994279
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4. Haass NK, Wladykowski E, Kief S, Moll I, Brandner JM: Differential induction of connexins 26 and 30 in skin tumors and their adjacent epidermis. J Histochem Cytochem; 2006 Feb;54(2):171-82
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  • [Title] Differential induction of connexins 26 and 30 in skin tumors and their adjacent epidermis.
  • Gap junctions (GJs) have been shown to play a role in tumor progression including a variety of keratinocyte-derived and non-keratinocyte-derived skin tumors.
  • Here we show that the synthesis of the GJ proteins connexin 26 and connexin 30 (Cx26 and Cx30) is induced in keratinocyte-derived epithelial skin tumors whereas there is either no change or a downregulation of Cx43.
  • Cx26, Cx30, and Cx43 are absent in non-epithelial skin tumors.
  • Further, Cx26 and Cx30 are induced in the epidermis adjacent to malignant melanoma but absent in the epidermis adjacent to benign non-epithelial skin lesions (melanocytic nevi and angioma).
  • The keratinocyte-derived skin tumors are very heterogeneous regarding the Cx26/Cx30 pattern in the epidermis at the periphery of the tumors.
  • [MeSH-major] Connexins / biosynthesis. Epidermis / metabolism. Skin Neoplasms / metabolism
  • [MeSH-minor] Animals. Bowen's Disease / metabolism. Carcinoma, Basal Cell / metabolism. Carcinoma, Squamous Cell / metabolism. Hemangioma / metabolism. Humans. Keratinocytes / metabolism. Keratins / metabolism. Keratosis / metabolism. Liver / metabolism. Melanoma / metabolism. Mice. Mice, Inbred C57BL. Microscopy, Fluorescence. Nevus, Pigmented / metabolism. Warts / metabolism

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  • (PMID = 16046668.001).
  • [ISSN] 0022-1554
  • [Journal-full-title] The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society
  • [ISO-abbreviation] J. Histochem. Cytochem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Connexins; 0 / GJB6 protein, human; 127120-53-0 / connexin 26; 68238-35-7 / Keratins
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5. Ponnamperuma RM, King KE, Elsir T, Glick AB, Wahl GM, Nister M, Weinberg WC: The transcriptional regulatory function of p53 is essential for suppression of mouse skin carcinogenesis and can be dissociated from effects on TGF-beta-mediated growth regulation. J Pathol; 2009 Oct;219(2):263-74
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  • [Title] The transcriptional regulatory function of p53 is essential for suppression of mouse skin carcinogenesis and can be dissociated from effects on TGF-beta-mediated growth regulation.
  • The p53(QS - val135) allele did not confer a dominant-negative phenotype, as p53(+/QS - val135) keratinocytes senesced normally in response to v-ras(Ha) expression and formed benign tumours.
  • These findings support an essential role for p53-mediated transcriptional regulation in suppressing malignancies arising from ras-induced skin tumours, consistent with previous findings in spontaneous carcinogenesis in other organs, and highlight the potential importance of senescence for tumour suppression in vivo.

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  • [Copyright] 2009 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
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  • (PMID = 19718706.001).
  • [ISSN] 1096-9896
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA100845; United States / NCI NIH HHS / CA / R01 CA100845-05; United States / FDA HHS / BO / Z01 BO04006-06
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Transforming Growth Factor beta; 0 / Tumor Suppressor Protein p53
  • [Other-IDs] NLM/ NIHMS146961; NLM/ PMC4208754
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6. Shukla A, Ho Y, Liu X, Ryscavage A, Glick AB: Cripto-1 alters keratinocyte differentiation via blockade of transforming growth factor-beta1 signaling: role in skin carcinogenesis. Mol Cancer Res; 2008 Mar;6(3):509-16
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  • [Title] Cripto-1 alters keratinocyte differentiation via blockade of transforming growth factor-beta1 signaling: role in skin carcinogenesis.
  • Here we report that in the two-stage mouse skin carcinogenesis model, Cripto-1 is highly up-regulated in tumor promoter-treated normal skin and in benign papillomas.
  • Treatment of primary mouse keratinocytes with Cripto-1 stimulated proliferation and induced expression of keratin 8 but blocked induction of the normal epidermal differentiation marker keratin 1, changes that are hallmarks of tumor progression in squamous cancer.
  • We suggest that inhibition of TGF-beta1 by Cripto-1 may play an important role in altering the differentiation state of keratinocytes and promoting outgrowth of squamous tumors in the mouse epidermis.
  • [MeSH-major] Cell Differentiation / physiology. Epidermal Growth Factor / physiology. Membrane Glycoproteins / physiology. Neoplasm Proteins / physiology. Skin Neoplasms / physiopathology. Transforming Growth Factor beta1 / antagonists & inhibitors
  • [MeSH-minor] 9,10-Dimethyl-1,2-benzanthracene. Animals. Carcinoma, Squamous Cell. DNA Replication. Gene Expression Regulation, Neoplastic. Genes, Reporter. Keratinocytes / physiology. Mice. Protein-Serine-Threonine Kinases / physiology. Receptors, Transforming Growth Factor beta / physiology. Signal Transduction

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  • (PMID = 18337457.001).
  • [ISSN] 1541-7786
  • [Journal-full-title] Molecular cancer research : MCR
  • [ISO-abbreviation] Mol. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA122109; United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Membrane Glycoproteins; 0 / Neoplasm Proteins; 0 / Receptors, Transforming Growth Factor beta; 0 / Tdgf1 protein, mouse; 0 / Transforming Growth Factor beta1; 57-97-6 / 9,10-Dimethyl-1,2-benzanthracene; 62229-50-9 / Epidermal Growth Factor; EC 2.7.1.11 / TGF-beta type I receptor; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
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7. Widyarini S, Husband AJ, Reeve VE: Protective effect of the isoflavonoid equol against hairless mouse skin carcinogenesis induced by UV radiation alone or with a chemical cocarcinogen. Photochem Photobiol; 2005 Jan-Feb;81(1):32-7
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  • [Title] Protective effect of the isoflavonoid equol against hairless mouse skin carcinogenesis induced by UV radiation alone or with a chemical cocarcinogen.
  • In this study, we examined the potential of the isoflavone equol [(S)-4',7-dihydroxyisoflavane] to protect from skin carcinogenesis in the hairless mouse.
  • Daily topical applications of equol lotions significantly protected against skin carcinogenesis induced by chronic exposure to solar-simulated UV radiation (SSUV) or by topical treatment with the chemical carcinogen 7,12-dimethylbenz(a)anthracene (DMBA) or by the combined cocarcinogenic treatment of DMBA followed by chronic SSUV.
  • In mice treated with either SSUV or DMBA + SSUV, equol significantly reduced the proportion of tumors progressing from benign papillomas to malignant squamous cell carcinoma (SCC) by 33-58% and reduced the average diameter of SCC by 71-82%.
  • In a short-term study, equol dose dependently inhibited the SSUV induction of the tumor promotion biomarker enzyme, ornithine decarboxylase, in the skin, suggesting the anticarcinogenic activity of equol may be attributed to its inhibition of the tumor promotion phase of carcinogenesis.
  • [MeSH-major] Carcinogens / toxicity. Flavonoids / pharmacology. Neoplasms, Radiation-Induced / prevention & control. Skin Neoplasms / prevention & control
  • [MeSH-minor] Animals. Cocarcinogenesis. Female. Mice. Mice, Hairless. Ornithine Decarboxylase / metabolism. Skin / enzymology

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  • (PMID = 15323582.001).
  • [ISSN] 0031-8655
  • [Journal-full-title] Photochemistry and photobiology
  • [ISO-abbreviation] Photochem. Photobiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Flavonoids; EC 4.1.1.17 / Ornithine Decarboxylase
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8. Rhiemeier V, Breitenbach U, Richter KH, Gebhardt C, Vogt I, Hartenstein B, Fürstenberger G, Mauch C, Hess J, Angel P: A novel aspartic proteinase-like gene expressed in stratified epithelia and squamous cell carcinoma of the skin. Am J Pathol; 2006 Apr;168(4):1354-64
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  • [Title] A novel aspartic proteinase-like gene expressed in stratified epithelia and squamous cell carcinoma of the skin.
  • Homeostasis of stratified epithelia, such as the epidermis of the skin, is a sophisticated process that represents a tightly controlled balance between proliferation and differentiation.
  • Here, we report the cloning of a novel cDNA sequence, from mouse back skin, that is induced by the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) and codes for a hitherto unknown aspartic proteinase-like protein (Taps).
  • Taps mRNA and protein are restricted to stratified epithelia in mouse embryos and adult tissues, implicating a crucial role for this aspartic proteinase-like gene in differentiation and homeostasis of multilayered epithelia.
  • During chemically induced carcinogenesis, transient elevation of Taps mRNA and protein levels was detected in benign skin tumors.
  • However, its expression is negatively associated with dedifferentiation and malignant progression in squamous cell carcinomas of the skin.
  • Similar expression was observed in squamous skin tumors of patients, suggesting that detection of Taps levels represents a novel strategy to discriminate the progression state of squamous skin cancers.
  • [MeSH-major] Aspartic Acid Endopeptidases / metabolism. Carcinoma, Squamous Cell / metabolism. Skin / metabolism. Skin Neoplasms / metabolism


9. Kwei KA, Finch JS, Ranger-Moore J, Bowden GT: The role of Rac1 in maintaining malignant phenotype of mouse skin tumor cells. Cancer Lett; 2006 Jan 18;231(2):326-38
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  • [Title] The role of Rac1 in maintaining malignant phenotype of mouse skin tumor cells.
  • We have previously developed an in vitro tumor progression model with mouse skin keratinocytes to study the molecular targets that mediate the tumor cell's progression from a benign to a malignant phenotype.
  • The malignantly transformed cells were found to have elevated MAP kinase signaling and increases in AP-1, NFkappaB and cAMP response element (CRE) transcription factors activities compared to their benign counter-part.
  • We used a doxycycline inducible system to express dominant negative Rac1 (N17 Rac1) in the squamous cell carcinomas producing 6M90 cell line.
  • These observations led us to conclude that Rac1 signaling is required for the malignant phenotypes of the squamous cell carcinoma cells.


10. Darwiche N, Ryscavage A, Perez-Lorenzo R, Wright L, Bae DS, Hennings H, Yuspa SH, Glick AB: Expression profile of skin papillomas with high cancer risk displays a unique genetic signature that clusters with squamous cell carcinomas and predicts risk for malignant conversion. Oncogene; 2007 Oct 18;26(48):6885-95
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  • [Title] Expression profile of skin papillomas with high cancer risk displays a unique genetic signature that clusters with squamous cell carcinomas and predicts risk for malignant conversion.
  • Chemical induction of squamous tumors in the mouse skin induces multiple benign papillomas: high-frequency terminally benign low-risk papillomas and low-frequency high-risk papillomas, the putative precursor lesions to squamous cell carcinoma (SCC).
  • We have compared the gene expression profile of twenty different early low- and high-risk papillomas with normal skin and SCC.
  • Additional classifier algorithms generated a gene list that correctly classified unknown benign tumors as low- or high-risk concordant with promotion protocol and keratin profiling.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Carcinoma, Squamous Cell / metabolism. Cell Transformation, Neoplastic / pathology. Gene Expression Profiling. Papilloma / metabolism. Skin Neoplasms / metabolism
  • [MeSH-minor] 9,10-Dimethyl-1,2-benzanthracene / toxicity. Animals. Carcinogens / toxicity. Female. Immunity, Cellular. Immunophenotyping. Mice. Mice, Inbred SENCAR. Oligonucleotide Array Sequence Analysis. Predictive Value of Tests. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Risk Factors. Skin / metabolism. Skin / pathology. Tetradecanoylphorbol Acetate / toxicity

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  • (PMID = 17525749.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA117957; United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Carcinogens; 0 / RNA, Messenger; 57-97-6 / 9,10-Dimethyl-1,2-benzanthracene; NI40JAQ945 / Tetradecanoylphorbol Acetate
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11. Shoji Y, Takahashi M, Takasuka N, Niho N, Kitamura T, Sato H, Maruyama T, Sugimoto Y, Narumiya S, Sugimura T, Wakabayashi K: Prostaglandin E receptor EP3 deficiency modifies tumor outcome in mouse two-stage skin carcinogenesis. Carcinogenesis; 2005 Dec;26(12):2116-22
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  • [Title] Prostaglandin E receptor EP3 deficiency modifies tumor outcome in mouse two-stage skin carcinogenesis.
  • Here we examined the effects of EP(3)-deficiency on two-stage skin carcinogenesis.
  • 7,12-Dimethylbenz[a]anthracene (50 microg/200 microl of acetone) was thus applied to the back skin of female EP(3)-knockout and wild-type mice at 8 weeks of age, followed by treatment with 12-O-tetradecanoylphorbol-13-acetate (5 microg/200 microl of acetone) twice a week for 25 weeks.
  • Interestingly, there were no squamous cell carcinomas (SCCs) in the EP(3)-knockout mice, while SCCs were observed in 3 out of 24 wild-type mice.
  • Furthermore, benign keratoacanthomas only developed in EP(3)-knockout mice (6/19 versus 0/24, P < 0.01).
  • The results suggest that PGE(2) receptor EP(3) signaling might contribute to development of SCCs in the skin.
  • [MeSH-major] Receptors, Prostaglandin E / physiology. Skin Neoplasms / metabolism. Skin Neoplasms / pathology
  • [MeSH-minor] 9,10-Dimethyl-1,2-benzanthracene / toxicity. Animals. Cadherins / metabolism. Carcinoma, Squamous Cell / chemically induced. Carcinoma, Squamous Cell / metabolism. Carcinoma, Squamous Cell / pathology. Female. Incidence. Keratoacanthoma / chemically induced. Keratoacanthoma / metabolism. Keratoacanthoma / pathology. Mice. Mice, Inbred C57BL. Mice, Knockout. RNA, Messenger / genetics. RNA, Messenger / metabolism. Receptors, Prostaglandin E, EP3 Subtype. Reverse Transcriptase Polymerase Chain Reaction. Tetradecanoylphorbol Acetate / toxicity. Treatment Outcome

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  • (PMID = 16051640.001).
  • [ISSN] 0143-3334
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cadherins; 0 / Ptger3 protein, mouse; 0 / RNA, Messenger; 0 / Receptors, Prostaglandin E; 0 / Receptors, Prostaglandin E, EP3 Subtype; 57-97-6 / 9,10-Dimethyl-1,2-benzanthracene; NI40JAQ945 / Tetradecanoylphorbol Acetate
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12. Liu Y, Lagowski J, Sundholm A, Sundberg A, Kulesz-Martin M: Microtubule disruption and tumor suppression by mitogen-activated protein kinase phosphatase 4. Cancer Res; 2007 Nov 15;67(22):10711-9
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  • The loss of MKP4 was associated with squamous cell carcinoma (SCC) but not benign papilloma clonal lineages and with independently induced SCC relative to benign tumors in mouse skin.
  • [MeSH-major] Dual-Specificity Phosphatases / physiology. Gene Expression Regulation, Neoplastic. Microtubules / metabolism. Mitogen-Activated Protein Kinase Phosphatases / physiology. Neoplasms / pathology
  • [MeSH-minor] Animals. Carcinoma, Squamous Cell / metabolism. Cell Line, Tumor. Cytosol / metabolism. Gene Expression Regulation, Enzymologic. Humans. Mice. Mice, Inbred BALB C. Papilloma / metabolism. p38 Mitogen-Activated Protein Kinases / metabolism

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  • (PMID = 18006813.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA69533; United States / NCI NIH HHS / CA / CA98893
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; EC 3.1.3.- / DUSP9 protein, human; EC 3.1.3.- / Mitogen-Activated Protein Kinase Phosphatases; EC 3.1.3.48 / Dual-Specificity Phosphatases; EC 3.1.3.48 / Dusp9 protein, mouse
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13. Ferreira M, Fujiwara H, Morita K, Watt FM: An activating beta1 integrin mutation increases the conversion of benign to malignant skin tumors. Cancer Res; 2009 Feb 15;69(4):1334-42
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  • [Title] An activating beta1 integrin mutation increases the conversion of benign to malignant skin tumors.
  • One of these, T188Ibeta1, was identified as a heterozygous mutation in a poorly differentiated squamous cell carcinoma (SCC) and shown to activate extracellular matrix adhesion and inhibit keratinocyte differentiation in vitro.
  • To study its contribution to tumor development, we overexpressed the mutant or wild-type (WT) human beta1 subunit in the basal layer of mouse epidermis using the keratin 14 promoter.
  • [MeSH-major] Antigens, CD29 / genetics. Mutation. Skin Neoplasms / genetics
  • [MeSH-minor] Animals. Carcinoma, Squamous Cell / genetics. Carcinoma, Squamous Cell / pathology. Cell Adhesion. Cell Differentiation. Cell Division. Female. Flow Cytometry. Heterozygote Detection. Humans. In Situ Hybridization. Keratinocytes / cytology. Keratinocytes / physiology. Mice. Mice, Transgenic. Polymerase Chain Reaction. Polymorphism, Genetic. Skin / cytology


14. Mancuso M, Gallo D, Leonardi S, Pierdomenico M, Pasquali E, De Stefano I, Rebessi S, Tanori M, Scambia G, Di Majo V, Covelli V, Pazzaglia S, Saran A: Modulation of basal and squamous cell carcinoma by endogenous estrogen in mouse models of skin cancer. Carcinogenesis; 2009 Feb;30(2):340-7
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  • [Title] Modulation of basal and squamous cell carcinoma by endogenous estrogen in mouse models of skin cancer.
  • Analogously, skin carcinogenesis-susceptible (Car-S) mice are elective for studies of papilloma and squamous cell carcinoma (SCC) induction.
  • We previously reported a striking effect of gender on BCC induction in Ptch1(+/-) mice, with total resistance of females; likewise, Car-S females show increased skin tumor resistance relative to males.
  • Here, we investigated the protective role of endogenous estrogen in skin keratinocyte tumorigenesis.
  • Remarkably, progression of initially benign papillomas to malignant SCC occurred only in ovariectomized Car-S females.
  • Thus, an imbalanced ERalpha/ERbeta expression may be associated with estrogen-mediated modulation of non-melanoma skin carcinogenesis, with a key role played by cyclin D1.
  • Our findings underscore a highly protective role of endogenous estrogen against skin tumorigenesis by diverse agents in two independent mouse models of skin cancer.
  • [MeSH-major] Carcinoma, Basal Cell / metabolism. Carcinoma, Squamous Cell / metabolism. Estrogens / physiology. Skin Neoplasms / metabolism
  • [MeSH-minor] Animals. Cell Transformation, Neoplastic / metabolism. Cell Transformation, Neoplastic / pathology. Cyclin D1 / metabolism. Disease Models, Animal. Estrogen Receptor alpha / metabolism. Estrogen Receptor beta / metabolism. Female. Male. Mice. Neoplasms, Radiation-Induced / metabolism. Neoplasms, Radiation-Induced / pathology. Ovariectomy. Papilloma / metabolism. Papilloma / pathology. Receptors, Cell Surface / genetics. Receptors, Cell Surface / metabolism. Ultraviolet Rays


15. Glick A, Ryscavage A, Perez-Lorenzo R, Hennings H, Yuspa S, Darwiche N: The high-risk benign tumor: evidence from the two-stage skin cancer model and relevance for human cancer. Mol Carcinog; 2007 Aug;46(8):605-10
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  • [Title] The high-risk benign tumor: evidence from the two-stage skin cancer model and relevance for human cancer.
  • Benign tumors that form following chemical initiation and promotion in the mouse skin can be grouped into two classes.
  • The majority of papillomas do not progress to squamous cell carcinoma (SCC), and these are designated as low-risk or terminally benign papillomas.
  • [MeSH-major] Carcinoma, Squamous Cell / etiology. Disease Models, Animal. Papilloma / etiology. Skin Neoplasms / etiology

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  • (PMID = 17538943.001).
  • [ISSN] 0899-1987
  • [Journal-full-title] Molecular carcinogenesis
  • [ISO-abbreviation] Mol. Carcinog.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA117957; United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Review
  • [Publication-country] United States
  • [Number-of-references] 27
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16. Michel A, Kopp-Schneider A, Zentgraf H, Gruber AD, de Villiers EM: E6/E7 expression of human papillomavirus type 20 (HPV-20) and HPV-27 influences proliferation and differentiation of the skin in UV-irradiated SKH-hr1 transgenic mice. J Virol; 2006 Nov;80(22):11153-64
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  • [Title] E6/E7 expression of human papillomavirus type 20 (HPV-20) and HPV-27 influences proliferation and differentiation of the skin in UV-irradiated SKH-hr1 transgenic mice.
  • The functional role of UV irradiation, in combination with the E6 and E7 proteins of the cutaneous human papillomavirus (HPV) types in the malignant conversion of benign papillomatous lesions, has not been elucidated.
  • Histological and immunohistochemical examination of skin samples revealed enhanced proliferation of the epidermal layers and papilloma formation in both transgenic strains in comparison to what was observed with nontransgenic mice.
  • Squamous cell carcinoma developed in the HPV-20 E6/E7 transgenic line as well as in the HPV-27 E6/E7 transgenic line.
  • Several weeks after cessation of UV-B exposure, enhanced proliferation, as measured by BrdU incorporation, was maintained only in HPV-20 transgenic skin.
  • Expression of the differentiation markers involucrin and loricrin was reduced and disturbed. p63alpha expression was differentially regulated with high levels of cytoplasmic expression in clusters of cells in the granular layer of the skin in the transgenic lines 20 weeks after cessation of UV-B exposure, in contrast to uninterrupted staining in the nontransgenic lines. p53 was expressed in clusters of cells in nontransgenic and HPV-27 transgenic mice, in contrast to an even distribution in a higher number of cells in HPV-20 transgenic animals.
  • [MeSH-major] Alphapapillomavirus / metabolism. Betapapillomavirus / metabolism. Cell Differentiation. Cell Proliferation. Oncogene Proteins, Viral / biosynthesis. Skin / radiation effects. Skin / virology
  • [MeSH-minor] Animals. Bromodeoxyuridine / metabolism. Epidermis / metabolism. Epidermis / radiation effects. Epidermis / virology. Female. Histocytochemistry. Immunohistochemistry. Keratin-6 / biosynthesis. Male. Membrane Proteins / biosynthesis. Mice. Mice, Transgenic. Papilloma / pathology. Papilloma / virology. Papillomavirus Infections / virology. Phosphoproteins / biosynthesis. Protein Precursors / biosynthesis. Skin Neoplasms / pathology. Skin Neoplasms / virology. Trans-Activators / biosynthesis. Tumor Suppressor Protein p53 / biosynthesis

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  • (PMID = 16971438.001).
  • [ISSN] 0022-538X
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Keratin-6; 0 / Membrane Proteins; 0 / Oncogene Proteins, Viral; 0 / Phosphoproteins; 0 / Protein Precursors; 0 / Trans-Activators; 0 / Trp63 protein, mouse; 0 / Tumor Suppressor Protein p53; 0 / loricrin; 60108-77-2 / involucrin; G34N38R2N1 / Bromodeoxyuridine
  • [Other-IDs] NLM/ PMC1642157
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17. Gurumurthy S, Hezel AF, Sahin E, Berger JH, Bosenberg MW, Bardeesy N: LKB1 deficiency sensitizes mice to carcinogen-induced tumorigenesis. Cancer Res; 2008 Jan 1;68(1):55-63
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  • Germ line-inactivating mutation of Lkb1 leads to Peutz-Jeghers syndrome, which is characterized by benign hamartomas and a susceptibility to malignant epithelial tumors.
  • Lkb1(+/-) mice are highly prone to DMBA-induced squamous cell carcinoma (SCC) of the skin and lung.
  • Our data indicate that Lkb1 is a potent suppressor of carcinogen-induced skin and lung cancers and that downstream targets beyond the AMPK-mTOR pathway are likely mediators of Lkb1-dependent tumor suppression.


18. Machida K, Urano K, Yoshimura M, Tsutsumi H, Nomura T, Usui T: Carcinogenic comparative study on rasH2 mice produced by two breeding facilities. J Toxicol Sci; 2008 Oct;33(4):493-501
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  • CByB6F1-Tg(HRAS)2Jic mice (brand name: rasH2 mouse) are produced by two breeding facilities, CLEA Japan, Inc. (Fuji, Shizuoka, Japan) and Taconic (Germantown, NY, USA), and supplied world wide.
  • In the pathological examination, only benign tumors of lungs, spleen, forestomach and skin were observed in a few mice in the vehicle group of both facilities.
  • In the MNU group, the incidence of forestomach papilloma/squamous cell carcinoma in mice from both facilities was 100%.
  • Although lung adenoma and skin papilloma/keratoacanthoma, which are major MNU induced tumors in this strain, were observed in several mice from both facilities, no significant differences were found.
  • [MeSH-minor] Animals. Breeding. Carcinogens / toxicity. Disease Models, Animal. Female. Genes, ras. Male. Mice. Mice, Inbred Strains. Neoplasms, Experimental / chemically induced

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  • (PMID = 18827450.001).
  • [ISSN] 1880-3989
  • [Journal-full-title] The Journal of toxicological sciences
  • [ISO-abbreviation] J Toxicol Sci
  • [Language] eng
  • [Publication-type] Comparative Study; Letter
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Carcinogens; 684-93-5 / Methylnitrosourea
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19. Ruddell A, Kelly-Spratt KS, Furuya M, Parghi SS, Kemp CJ: p19/Arf and p53 suppress sentinel lymph node lymphangiogenesis and carcinoma metastasis. Oncogene; 2008 May 15;27(22):3145-55
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  • Deletion of the p19/Arf or p53 tumor suppressor genes accelerates malignant progression and metastatic spread of 7,12-dimethylbenz(a)anthracene (DMBA)/12-O-tetradecanoyl-phorbol-13-acetate (TPA)-induced squamous cell carcinomas, providing a model system to address mechanisms of metastasis.
  • Here, we show that benign pre-metastatic papillomas from wild-type mice trigger lymphangiogenesis within draining lymph nodes, whereas there is no growth of primary tumor lymphatic vessels.
  • [MeSH-major] Carcinoma, Squamous Cell / pathology. Cyclin-Dependent Kinase Inhibitor p16 / physiology. Lymph Nodes / physiology. Lymphangiogenesis / genetics. Lymphatic Metastasis. Skin Neoplasms / pathology. Tumor Suppressor Protein p53 / physiology

  • MedlinePlus Health Information. consumer health - Skin Cancer.
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  • Hazardous Substances Data Bank. 12-O-TETRADECANOYLPHORBOL-13-ACETATE .
  • Hazardous Substances Data Bank. 7,12-DIMETHYLBENZ(A)ANTHRACENE .
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
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  • (PMID = 18059331.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01-CA68328; United States / NCI NIH HHS / CA / R01-CA99517
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cdkn2a protein, mouse; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Tumor Suppressor Protein p53; 0 / Vascular Endothelial Growth Factor A; 0 / vascular endothelial growth factor A, mouse; 57-97-6 / 9,10-Dimethyl-1,2-benzanthracene; NI40JAQ945 / Tetradecanoylphorbol Acetate
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20. Grosse-Wilde A, Voloshanenko O, Bailey SL, Longton GM, Schaefer U, Csernok AI, Schütz G, Greiner EF, Kemp CJ, Walczak H: TRAIL-R deficiency in mice enhances lymph node metastasis without affecting primary tumor development. J Clin Invest; 2008 Jan;118(1):100-10
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  • Although mouse models employing tumor transplantation have shown that TRAIL can reduce tumor growth, autochthonous tumor models have generated conflicting results with respect to the physiological role of the TRAIL system during tumorigenesis.
  • We used a multistage model of squamous cell carcinoma to examine the role of TRAIL-R throughout all steps of tumor development.
  • DMBA/TPA-treated TRAIL-R-deficient mice showed neither an increase in number or growth rate of benign papillomas nor an increase in the rate of progression to squamous cell carcinoma.
  • We also found that adherent TRAIL-R-expressing skin carcinoma cells were TRAIL resistant in vitro but were sensitized to TRAIL upon detachment by inactivation of the ERK signaling pathway.

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  • (PMID = 18079967.001).
  • [ISSN] 0021-9738
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA070414; United States / NCI NIH HHS / CA / R01 CA099517; United States / NCI NIH HHS / CA / R01 CA099817
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / Tnfrsf10b protein, mouse; 0 / Tnfsf10 protein, mouse
  • [Other-IDs] NLM/ PMC2129237
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21. Gebhardt C, Breitenbach U, Richter KH, Fürstenberger G, Mauch C, Angel P, Hess J: c-Fos-dependent induction of the small ras-related GTPase Rab11a in skin carcinogenesis. Am J Pathol; 2005 Jul;167(1):243-53
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  • [Title] c-Fos-dependent induction of the small ras-related GTPase Rab11a in skin carcinogenesis.
  • Malignant transformation of mouse skin by tumor promoters and chemical carcinogens, such as the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA), is a multistage process leading to the formation of squamous cell carcinomas.
  • It has been shown that mice lacking the AP-1 family member c-Fos exhibit an impaired transition from benign to malignant skin tumors.
  • Here, we demonstrate enhanced expression of the small Ras-related GTPase Rab11a after short-term TPA treatment of mouse back skin.
  • Expression of Rab11a in vivo and in vitro critically depended on c-Fos, because TPA application to the back skin of c-Fos-deficient mice and to mouse embryonic fibroblasts did not induce Rab11a mRNA or protein expression.
  • Enhanced expression was not restricted to chemically induced mouse skin tumors but was also found in tumor specimens derived from patients with epithelial skin tumors.
  • These data identify Rab11a as a novel, tumor-associated c-Fos/AP-1 target and may point to an as yet unrecognized function of Rab11a in the development of skin cancer.
  • [MeSH-major] Cell Transformation, Neoplastic / metabolism. Proto-Oncogene Proteins c-fos / metabolism. Skin Neoplasms / metabolism. rab GTP-Binding Proteins / metabolism


22. Jansen AP, Camalier CE, Colburn NH: Epidermal expression of the translation inhibitor programmed cell death 4 suppresses tumorigenesis. Cancer Res; 2005 Jul 15;65(14):6034-41
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  • In response to the 7,12-dimethylbenz(a)anthracene (DMBA)/12-O-tetradecanoylphorbol-13-acetate (TPA) mouse skin carcinogenesis protocol, K14-Pdcd4 mice showed significant reductions in papilloma formation, carcinoma incidence, and papilloma-to-carcinoma conversion frequency compared with wild-type mice.
  • These results extend to an in vivo model the observations that Pdcd4 inhibits both translation initiation and AP-1 activation while decreasing benign tumor development and malignant progression.
  • [MeSH-major] Carcinoma, Squamous Cell / prevention & control. Papilloma / prevention & control. RNA-Binding Proteins / physiology. Skin Neoplasms / prevention & control


23. National Toxicology Program: Toxicology and carcinogenesis studies of isoeugenol (CAS No. 97-54-1) in F344/N rats and B6C3F1 mice (gavage studies). Natl Toxicol Program Tech Rep Ser; 2010 Sep;(551):1-178
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  • Genetic toxicity tests were conducted in Salmonella typhimurium, Escherichia coli, cultured Chinese hamster ovary cells, and mouse peripheral blood erythrocytes.
  • Two male rats in the 300 mg/kg group had rare benign or malignant thymomas, while two other males in this group had rare mammary gland carcinomas.
  • Incidences of keratoacanthoma of the skin were decreased in 150 and 300 mg/kg males.
  • Incidences of forestomach squamous hyperplasia, inflammation, and ulceration (males only) increased with exposure and were significant in the 300 mg/kg groups.
  • [MeSH-major] Eugenol / analogs & derivatives. Neoplasms, Experimental / chemically induced

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  • (PMID = 21372857.001).
  • [ISSN] 0888-8051
  • [Journal-full-title] National Toxicology Program technical report series
  • [ISO-abbreviation] Natl Toxicol Program Tech Rep Ser
  • [Language] eng
  • [Publication-type] Journal Article; Technical Report
  • [Publication-country] United States
  • [Chemical-registry-number] 3T8H1794QW / Eugenol; 97-54-1 / isoeugenol
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24. Okunade GW, Miller ML, Azhar M, Andringa A, Sanford LP, Doetschman T, Prasad V, Shull GE: Loss of the Atp2c1 secretory pathway Ca(2+)-ATPase (SPCA1) in mice causes Golgi stress, apoptosis, and midgestational death in homozygous embryos and squamous cell tumors in adult heterozygotes. J Biol Chem; 2007 Sep 7;282(36):26517-27
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  • [Title] Loss of the Atp2c1 secretory pathway Ca(2+)-ATPase (SPCA1) in mice causes Golgi stress, apoptosis, and midgestational death in homozygous embryos and squamous cell tumors in adult heterozygotes.
  • Loss of one copy of the human ATP2C1 gene, encoding SPCA1 (secretory pathway Ca(2+)-ATPase isoform 1), causes Hailey-Hailey disease, a skin disorder.
  • Adult heterozygous mice appeared normal and exhibited no evidence of Hailey-Hailey disease; however, aged heterozygotes had an increased incidence of squamous cell tumors of keratinized epithelial cells of the skin and esophagus.
  • [MeSH-major] Calcium-Transporting ATPases / deficiency. Carcinoma, Squamous Cell / metabolism. Embryo Loss / metabolism. Esophageal Neoplasms / metabolism. Golgi Apparatus / metabolism. Loss of Heterozygosity. Skin Neoplasms / metabolism
  • [MeSH-minor] Aging / genetics. Aging / metabolism. Aging / pathology. Animals. Apoptosis / genetics. Basement Membrane / metabolism. Basement Membrane / ultrastructure. Cardiovascular System / embryology. Coated Pits, Cell-Membrane / genetics. Coated Pits, Cell-Membrane / metabolism. Coated Pits, Cell-Membrane / ultrastructure. Desmosomes / genetics. Desmosomes / metabolism. Desmosomes / ultrastructure. Endoplasmic Reticulum, Rough / genetics. Endoplasmic Reticulum, Rough / metabolism. Endoplasmic Reticulum, Rough / ultrastructure. Female. Genetic Predisposition to Disease. Hematopoiesis / genetics. Heterozygote. Homozygote. Humans. Inbreeding. Male. Mice. Mice, Knockout. Neural Tube Defects / embryology. Neural Tube Defects / metabolism. Neural Tube Defects / pathology. Pemphigus, Benign Familial / genetics. Pemphigus, Benign Familial / metabolism. Pemphigus, Benign Familial / pathology. Pregnancy. Protein Transport / genetics. Ribosomes / metabolism. Secretory Vesicles / genetics. Secretory Vesicles / metabolism. Secretory Vesicles / ultrastructure. Water-Electrolyte Balance / genetics






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