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Article: Let's put a smile on that face-A positive facial expression improves aesthetics of portrait photographs.

Valuch, Christian / Pelowski, Matthew / Peltoketo, Veli-Tapani / Hakala, Jussi / Leder, Helmut

2023 Volume 10, Issue 10, Page(s) 230413

Abstract: In today's age of social media and smartphones, portraits-such as selfies or pictures of friends and family-are very frequently produced, shared and viewed images. Despite their prevalence, the psychological factors that characterize a 'good' photo-one ... ...

Abstract	In today's age of social media and smartphones, portraits-such as selfies or pictures of friends and family-are very frequently produced, shared and viewed images. Despite their prevalence, the psychological factors that characterize a 'good' photo-one that people will generally like, keep, and think is especially aesthetically pleasing-are not well understood. Here, we studied how a subtle change in facial expression (smiling) in portraits determines their aesthetic image value (beyond a more positive appearance of the depicted person). We used AI-based image processing tools in a broad set of portrait photographs and generated neutral and slightly smiling versions of the same pictures. Consistent across two experiments, portraits with a subtle smile increased both spontaneous aesthetic preferences in a swiping task as well as improving more explicit aesthetic ratings after prolonged viewing. Participants distinguished between aspects associated with image beauty and the depicted person's attractiveness, resulting in specific interactions between variables related to participant traits, image content, and task. Our study confirms that a subtle-and in this case fully artificial-smile reliably increases the aesthetic quality of portraits, illustrating how current image processing methods can target psychologically important variables and thereby increase the aesthetic value of photographs.
Language	English
Publishing date	2023-10-25
Publishing country	England
Document type	Journal Article
ZDB-ID	2787755-3
ISSN	2054-5703
ISSN	2054-5703
DOI	10.1098/rsos.230413
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Article: Swipes and Saves: A Taxonomy of Factors Influencing Aesthetic Assessments and Perceived Beauty of Mobile Phone Photographs.

Leder, Helmut / Hakala, Jussi / Peltoketo, Veli-Tapani / Valuch, Christian / Pelowski, Matthew

Frontiers in psychology

2022 Volume 13, Page(s) 786977

Abstract: Digital images taken by mobile phones are the most frequent class of images created today. Due to their omnipresence and the many ways they are encountered, they require a specific focus in research. However, to date, there is no systematic compilation ... ...

Abstract	Digital images taken by mobile phones are the most frequent class of images created today. Due to their omnipresence and the many ways they are encountered, they require a specific focus in research. However, to date, there is no systematic compilation of the various factors that may determine our evaluations of such images, and thus no explanation of how users select and identify relatively "better" or "worse" photos. Here, we propose a theoretical taxonomy of factors influencing the aesthetic appeal of mobile phone photographs. Beyond addressing relatively basic/universal image characteristics, perhaps more related to fast (bottom-up) perceptual processing of an image, we also consider factors involved in the slower (top-down) re-appraisal or deepened aesthetic appreciation of an image. We span this taxonomy across specific types of picture genres commonly taken-portraits of other people, selfies, scenes and food. We also discuss the variety of goals, uses, and contextual aspects of users of mobile phone photography. As a working hypothesis, we propose that two main decisions are often made with mobile phone photographs: (1) Users assess images at a first glance-by swiping through a stack of images-focusing on visual aspects that might be decisive to classify them from "low quality" (too dark, out of focus) to "acceptable" to, in rare cases, "an exceptionally beautiful picture." (2) Users make more deliberate decisions regarding one's "favorite" picture or the desire to preserve or share a picture with others, which are presumably tied to aspects such as content, framing, but also culture or personality, which have largely been overlooked in empirical research on perception of photographs. In sum, the present review provides an overview of current focal areas and gaps in research and offers a working foundation for upcoming research on the perception of mobile phone photographs as well as future developments in the fields of image recording and sharing technology.
Language	English
Publishing date	2022-02-28
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2563826-9
ISSN	1664-1078
ISSN	1664-1078
DOI	10.3389/fpsyg.2022.786977
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Article ; Online: PALB2-mutated human mammary cells display a broad spectrum of morphological and functional abnormalities induced by increased TGFβ signaling.

Tuppurainen, Hanna / Laurila, Niina / Nätynki, Marjut / Eshraghi, Leila / Tervasmäki, Anna / Erichsen, Louisa / Sørensen, Claus Storgaard / Pylkäs, Katri / Winqvist, Robert / Peltoketo, Hellevi

Cellular and molecular life sciences : CMLS

2024 Volume 81, Issue 1, Page(s) 173

Abstract: Heterozygous mutations in any of three major genes, BRCA1, BRCA2 and PALB2, are associated with high-risk hereditary breast cancer susceptibility frequently seen as familial disease clustering. PALB2 is a key interaction partner and regulator of several ... ...

Abstract	Heterozygous mutations in any of three major genes, BRCA1, BRCA2 and PALB2, are associated with high-risk hereditary breast cancer susceptibility frequently seen as familial disease clustering. PALB2 is a key interaction partner and regulator of several vital cellular activities of BRCA1 and BRCA2, and is thus required for DNA damage repair and alleviation of replicative and oxidative stress. Little is however known about how PALB2-deficiency affects cell function beyond that, especially in the three-dimensional setting, and also about its role during early steps of malignancy development. To answer these questions, we have generated biologically relevant MCF10A mammary epithelial cell lines with mutations that are comparable to certain clinically important PALB2 defects. We show in a non-cancerous background how both mono- and biallelically PALB2-mutated cells exhibit gross spontaneous DNA damage and mitotic aberrations. Furthermore, PALB2-deficiency disturbs three-dimensional spheroid morphology, increases the migrational capacity and invasiveness of the cells, and broadly alters their transcriptome profiles. TGFβ signaling and KRT14 expression are enhanced in PALB2-mutated cells and their inhibition and knock down, respectively, lead to partial restoration of cell functions. KRT14-positive cells are also more abundant with DNA damage than KRT14-negative cells. The obtained results indicate comprehensive cellular changes upon PALB2 mutations, even in the presence of half dosage of wild type PALB2 and demonstrate how PALB2 mutations may predispose their carriers to malignancy.
MeSH term(s)	Humans ; Signal Transduction ; DNA Repair ; Epithelial Cells ; Breast ; Neoplasms ; Fanconi Anemia Complementation Group N Protein/genetics
Chemical Substances	PALB2 protein, human ; Fanconi Anemia Complementation Group N Protein
Language	English
Publishing date	2024-04-10
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	1358415-7
ISSN	1420-9071 ; 1420-682X
ISSN (online)	1420-9071
ISSN	1420-682X
DOI	10.1007/s00018-024-05183-6
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Article ; Online: The Luteinizing Hormone Receptor Knockout Mouse as a Tool to Probe the In Vivo Actions of Gonadotropic Hormones/Receptors in Females.

Jonas, Kim Carol / Rivero Müller, Adolfo / Oduwole, Olayiwola / Peltoketo, Hellevi / Huhtaniemi, Ilpo

Endocrinology

2021 Volume 162, Issue 5

Abstract: Mouse models with altered gonadotropin functions have provided invaluable insight into the functions of these hormones/receptors. Here we describe the repurposing of the infertile and hypogonadal luteinizing hormone receptor (LHR) knockout mouse model ( ... ...

Abstract	Mouse models with altered gonadotropin functions have provided invaluable insight into the functions of these hormones/receptors. Here we describe the repurposing of the infertile and hypogonadal luteinizing hormone receptor (LHR) knockout mouse model (LuRKO), to address outstanding questions in reproductive physiology. Using crossbreeding strategies and physiological and histological analyses, we first addressed the physiological relevance of forced LHR homomerization in female mice using BAC expression of 2 ligand-binding and signaling deficient mutant LHR, respectively, that have previously shown to undergo functional complementation and rescue the hypogonadal phenotype of male LuRKO mice. In female LuRKO mice, coexpression of signaling and binding deficient LHR mutants failed to rescue the hypogonadal and anovulatory phenotype. This was apparently due to the low-level expression of the 2 mutant LHR and potential lack of luteinizing hormone (LH)/LHR-dependent pleiotropic signaling that has previously been shown at high receptor densities to be essential for ovulation. Next, we utilized a mouse model overexpressing human chorionic gonadotropin (hCG) with increased circulating "LH/hCG"-like bioactivity to ~40 fold higher than WT females, to determine if high circulating hCG in the LuRKO background could reveal putative LHR-independent actions. No effects were found, thus, suggesting that LH/hCG mediate their gonadal and non-gonadal effects solely via LHR. Finally, targeted expression of a constitutively active follicle stimulating hormone receptor (FSHR) progressed antral follicles to preovulatory follicles and displayed phenotypic markers of enhanced estrogenic activity but failed to induce ovulation in LuRKO mice. This study highlights the critical importance and precise control of functional LHR and FSHR for mediating ovarian functions and of the potential repurposing of existing genetically modified mouse models in answering outstanding questions in reproductive physiology.
MeSH term(s)	Animals ; Chorionic Gonadotropin/metabolism ; Female ; Follicle Stimulating Hormone/metabolism ; Gonadotropins/metabolism ; Humans ; Luteinizing Hormone/metabolism ; Male ; Mice ; Mice, Knockout ; Ovarian Follicle/metabolism ; Ovulation ; Phenotype ; Receptors, FSH/genetics ; Receptors, FSH/metabolism ; Receptors, LH/genetics ; Receptors, LH/metabolism ; Signal Transduction
Chemical Substances	Chorionic Gonadotropin ; Gonadotropins ; Receptors, FSH ; Receptors, LH ; Luteinizing Hormone (9002-67-9) ; Follicle Stimulating Hormone (9002-68-0)
Language	English
Publishing date	2021-02-19
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	427856-2
ISSN	1945-7170 ; 0013-7227
ISSN (online)	1945-7170
ISSN	0013-7227
DOI	10.1210/endocr/bqab035
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Article: Role of Follicle-Stimulating Hormone in Spermatogenesis.

Oduwole, Olayiwola O / Peltoketo, Hellevi / Huhtaniemi, Ilpo T

Frontiers in endocrinology

2018 Volume 9, Page(s) 763

Abstract: Spermatogenesis is a concerted sequence of events during maturation of spermatogonia into spermatozoa. The process involves differential gene-expression and cell-cell interplay regulated by the key endocrine stimuli, i.e., follicle-stimulating hormone ( ... ...

Abstract	Spermatogenesis is a concerted sequence of events during maturation of spermatogonia into spermatozoa. The process involves differential gene-expression and cell-cell interplay regulated by the key endocrine stimuli, i.e., follicle-stimulating hormone (FSH) and luteinizing hormone (LH)-stimulated testosterone. FSH affects independently and in concert with testosterone, the proliferation, maturation and function of the supporting Sertoli cells that produce regulatory signals and nutrients for the maintenance of developing germ cells. Rodents are able to complete spermatogenesis without FSH stimulus, but its deficiency significantly decreases sperm quantity. Men carrying loss-of-function mutation in the gene encoding the ligand (
Language	English
Publishing date	2018-12-14
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2592084-4
ISSN	1664-2392
ISSN	1664-2392
DOI	10.3389/fendo.2018.00763
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Article ; Online: ABRAXAS1 orchestrates BRCA1 activities to counter genome destabilizing repair pathways-lessons from breast cancer patients.

Sachsenweger, Juliane / Jansche, Rebecca / Merk, Tatjana / Heitmeir, Benedikt / Deniz, Miriam / Faust, Ulrike / Roggia, Cristiana / Tzschach, Andreas / Schroeder, Christopher / Riess, Angelika / Pospiech, Helmut / Peltoketo, Hellevi / Pylkäs, Katri / Winqvist, Robert / Wiesmüller, Lisa

Cell death & disease

2023 Volume 14, Issue 5, Page(s) 328

Abstract: It has been well-established that mutations in BRCA1 and BRCA2, compromising functions in DNA double-strand break repair (DSBR), confer hereditary breast and ovarian cancer risk. Importantly, mutations in these genes explain only a minor fraction of the ... ...

Abstract	It has been well-established that mutations in BRCA1 and BRCA2, compromising functions in DNA double-strand break repair (DSBR), confer hereditary breast and ovarian cancer risk. Importantly, mutations in these genes explain only a minor fraction of the hereditary risk and of the subset of DSBR deficient tumors. Our screening efforts identified two truncating germline mutations in the gene encoding the BRCA1 complex partner ABRAXAS1 in German early-onset breast cancer patients. To unravel the molecular mechanisms triggering carcinogenesis in these carriers of heterozygous mutations, we examined DSBR functions in patient-derived lymphoblastoid cells (LCLs) and in genetically manipulated mammary epithelial cells. By use of these strategies we were able to demonstrate that these truncating ABRAXAS1 mutations exerted dominant effects on BRCA1 functions. Interestingly, we did not observe haploinsufficiency regarding homologous recombination (HR) proficiency (reporter assay, RAD51-foci, PARP-inhibitor sensitivity) in mutation carriers. However, the balance was shifted to use of mutagenic DSBR-pathways. The dominant effect of truncated ABRAXAS1 devoid of the C-terminal BRCA1 binding site can be explained by retention of the N-terminal interaction sites for other BRCA1-A complex partners like RAP80. In this case BRCA1 was channeled from the BRCA1-A to the BRCA1-C complex, which induced single-strand annealing (SSA). Further truncation, additionally deleting the coiled-coil region of ABRAXAS1, unleashed excessive DNA damage responses (DDRs) de-repressing multiple DSBR-pathways including SSA and non-homologous end-joining (NHEJ). Our data reveal de-repression of low-fidelity repair activities as a common feature of cells from patients with heterozygous mutations in genes encoding BRCA1 and its complex partners.
MeSH term(s)	Female ; Humans ; BRCA1 Protein/genetics ; BRCA1 Protein/metabolism ; BRCA2 Protein/genetics ; BRCA2 Protein/metabolism ; Breast Neoplasms/pathology ; DNA Breaks, Double-Stranded ; DNA Repair/genetics ; Mutagenesis ; Mutation
Chemical Substances	BRCA1 Protein ; BRCA1 protein, human ; BRCA2 Protein ; ABRAXAS1 protein, human
Language	English
Publishing date	2023-05-17
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/s41419-023-05845-6
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Article ; Online: Targeting collagen XVIII improves the efficiency of ErbB inhibitors in breast cancer models.

Devarajan, Raman / Izzi, Valerio / Peltoketo, Hellevi / Rask, Gunilla / Kauppila, Saila / Väisänen, Marja-Riitta / Ruotsalainen, Heli / Martínez-Nieto, Guillermo / Karppinen, Sanna-Maria / Väisänen, Timo / Kaur, Inderjeet / Koivunen, Jussi / Sasaki, Takako / Winqvist, Robert / Manninen, Aki / Wärnberg, Fredrik / Sund, Malin / Pihlajaniemi, Taina / Heljasvaara, Ritva

The Journal of clinical investigation

2023 Volume 133, Issue 18

Abstract: The tumor extracellular matrix (ECM) critically regulates cancer progression and treatment response. Expression of the basement membrane component collagen XVIII (ColXVIII) is induced in solid tumors, but its involvement in tumorigenesis has remained ... ...

Abstract	The tumor extracellular matrix (ECM) critically regulates cancer progression and treatment response. Expression of the basement membrane component collagen XVIII (ColXVIII) is induced in solid tumors, but its involvement in tumorigenesis has remained elusive. We show here that ColXVIII was markedly upregulated in human breast cancer (BC) and was closely associated with a poor prognosis in high-grade BCs. We discovered a role for ColXVIII as a modulator of epidermal growth factor receptor tyrosine kinase (ErbB) signaling and show that it forms a complex with ErbB1 and -2 (also known as EGFR and human epidermal growth factor receptor 2 [HER2]) and α6-integrin to promote cancer cell proliferation in a pathway involving its N-terminal portion and the MAPK/ERK1/2 and PI3K/AKT cascades. Studies using Col18a1 mouse models crossed with the mouse mammary tumor virus-polyoma virus middle T antigen (MMTV-PyMT) mammary carcinogenesis model showed that ColXVIII promoted BC growth and metastasis in a tumor cell-autonomous manner. Moreover, the number of mammary cancer stem cells was significantly reduced in the MMTV-PyMT and human cell models upon ColXVIII inhibition. Finally, ablation of ColXVIII substantially improved the efficacy of ErbB-targeting therapies in both preclinical models. In summary, ColXVIII was found to sustain the stemness properties of BC cells and tumor progression and metastasis through ErbB signaling, suggesting that targeting ColXVIII in the tumor milieu may have important therapeutic potential.
MeSH term(s)	Mice ; Animals ; Humans ; Female ; Collagen Type XVIII/metabolism ; Breast Neoplasms/drug therapy ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Receptor, ErbB-2/metabolism ; Cell Transformation, Neoplastic ; Signal Transduction
Chemical Substances	Collagen Type XVIII ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Receptor, ErbB-2 (EC 2.7.10.1)
Language	English
Publishing date	2023-09-15
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI159181
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Article ; Online: Animal models for aberrations of gonadotropin action.

Peltoketo, Hellevi / Zhang, Fu-Ping / Rulli, Susana B

Reviews in endocrine & metabolic disorders

2011 Volume 12, Issue 4, Page(s) 245–258

Abstract: During the last two decades a large number of genetically modified mouse lines with altered gonadotropin action have been generated. These mouse lines fall into three categories: the lack-of-function mice, gain-of-function mice, and the mice generated by ...

Abstract	During the last two decades a large number of genetically modified mouse lines with altered gonadotropin action have been generated. These mouse lines fall into three categories: the lack-of-function mice, gain-of-function mice, and the mice generated by breeding the abovementioned lines with other disease model lines. The mouse strains lacking gonadotropin action have elucidated the necessity of the pituitary hormones in pubertal development and function of gonads, and revealed the processes from the original genetic defect to the pathological phenotype such as hypo- or hypergonadotropic hypogonadism. Conversely, the strains of the second group depict consequences of chronic gonadotropin action. The lines vary from those expressing constitutively active receptors and those secreting follicle-stimulating hormone (FSH) with slowly increasing amounts to those producing human choriogonadotropin (hCG), amount of which corresponds to 2000-fold luteinizing hormone (LH)/hCG biological activity. Accordingly, the phenotypes diverge from mild anomalies and enhanced fertility to disrupted gametogenesis, but eventually chronic, enhanced and non-pulsatile action of both FSH and LH leads to female and male infertility and/or hyper- and neoplasias in most of the gonadotropin gain-of-function mice. Elevated gonadotropin levels also alter the function of several extra-gonadal tissues either directly or indirectly via increased sex steroid production. These effects include promotion of tumorigenesis in tissues such as the pituitary, mammary and adrenal glands. Finally, the crossbreedings of the current mouse strains with other disease models are likely to uncover the contribution of gonadotropins in novel biological systems, as exemplified by the recent crossbreed of LHCG receptor deficient mice with Alzheimer disease mice.
MeSH term(s)	Animals ; Disease Models, Animal ; Endocrine System Diseases/genetics ; Endocrine System Diseases/metabolism ; Endocrine System Diseases/pathology ; Endocrine System Diseases/physiopathology ; Female ; Gonadotropins/deficiency ; Gonadotropins/genetics ; Gonadotropins/metabolism ; Gonadotropins/physiology ; Humans ; Male ; Mice ; Mice, Transgenic ; Ovary/metabolism ; Ovary/pathology ; Ovary/physiology ; Pituitary Gland/metabolism ; Pituitary Gland/pathology ; Pituitary Gland/physiology ; Testis/metabolism ; Testis/pathology ; Testis/physiology
Chemical Substances	Gonadotropins
Language	English
Publishing date	2011-04-13
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2185718-0
ISSN	1573-2606 ; 1389-9155
ISSN (online)	1573-2606
ISSN	1389-9155
DOI	10.1007/s11154-011-9174-4
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Zs.A 6069: Show issues

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Article ; Online: Tumor suppressor MCPH1 regulates gene expression profiles related to malignant conversion and chromosomal assembly.

Tervasmäki, Anna / Mantere, Tuomo / Eshraghi, Leila / Laurila, Niina / Tuppurainen, Hanna / Ronkainen, Veli-Pekka / Koivuluoma, Susanna / Devarajan, Raman / Peltoketo, Hellevi / Pylkäs, Katri

International journal of cancer

2019 Volume 145, Issue 8, Page(s) 2070–2081

Abstract: Strong inherited predisposition to breast cancer is estimated to cause about 5-10% of all breast cancer cases. As the known susceptibility genes, such as BRCA1 and BRCA2, explain only a fraction of this, additional predisposing genes and related ... ...

Abstract	Strong inherited predisposition to breast cancer is estimated to cause about 5-10% of all breast cancer cases. As the known susceptibility genes, such as BRCA1 and BRCA2, explain only a fraction of this, additional predisposing genes and related biological mechanisms are actively being searched for. We have recently identified a recurrent MCPH1 germline mutation, p.Arg304ValfsTer3, as a breast cancer susceptibility allele. MCPH1 encodes a multifunctional protein involved in maintenance of genomic integrity and it is also somatically altered in various cancer types, including breast cancer. Additionally, biallelic MCPH1 mutations are causative for microcephaly and at cellular level premature chromosome condensation. To study the molecular mechanisms leading to cancer predisposition and malignant conversion, here we have modeled the effect of MCPH1 p.Arg304ValfsTer3 mutation using gene-edited MCF10A breast epithelial cells. As a complementary approach, we also sought for additional potential cancer driver mutations in MCPH1 p.Arg304ValfsTer3 carrier breast tumors. We show that mutated MCPH1 de-regulates transcriptional programs related to invasion and metastasis and leads to downregulation of histone genes. These global transcriptional changes are mirrored by significantly increased migration and invasion potential of the cells as well as abnormal chromosomal condensation both before and after mitosis. These findings provide novel molecular insights to MCPH1 tumor suppressor functions and establish a role in regulation of transcriptional programs related to malignant conversion and chromosomal assembly. The MCPH1 p.Arg304ValfsTer3 carrier breast tumors showed recurrent tumor suppressor gene TP53 mutations, which were also significantly over-represented in breast tumors with somatically inactivated MCPH1.
MeSH term(s)	Breast Neoplasms/genetics ; Cell Cycle Proteins/genetics ; Cell Line ; Cell Transformation, Neoplastic/genetics ; Chromosome Aberrations ; Class I Phosphatidylinositol 3-Kinases/genetics ; Cytoskeletal Proteins/genetics ; Genes, Tumor Suppressor ; Genetic Predisposition to Disease/genetics ; Humans ; Mutation ; Transcriptome ; Tumor Suppressor Protein p53/genetics
Chemical Substances	Cell Cycle Proteins ; Cytoskeletal Proteins ; MCPH1 protein, human ; TP53 protein, human ; Tumor Suppressor Protein p53 ; Class I Phosphatidylinositol 3-Kinases (EC 2.7.1.137) ; PIK3CA protein, human (EC 2.7.1.137)
Language	English
Publishing date	2019-03-21
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	218257-9
ISSN	1097-0215 ; 0020-7136
ISSN (online)	1097-0215
ISSN	0020-7136
DOI	10.1002/ijc.32234
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Zs.A 478: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article: Adrenal hyperplasia and tumours in mice in connection with aberrant pituitary-gonadal function.

Bernichtein, Sophie / Peltoketo, Hellevi / Huhtaniemi, Ilpo

Molecular and cellular endocrinology

2009 Volume 300, Issue 1-2, Page(s) 164–168

Abstract: Gonadectomy induces in certain inbred stains of mice adrenal hyperplasia and tumorigenesis, originating from the putative subcapsular stem/progenitor cell layer. This response is apparently triggered by the elevated post-gonadectomy levels of luteinising ...

Abstract	Gonadectomy induces in certain inbred stains of mice adrenal hyperplasia and tumorigenesis, originating from the putative subcapsular stem/progenitor cell layer. This response is apparently triggered by the elevated post-gonadectomy levels of luteinising hormone (LH), followed by ectopic upregulation of adrenal LH/chorionic gonadotrophin (CG) receptors (Lhcgr). The clear strain dependence of this adrenal response to gonadectomy prompted us to study its genetic basis. Tumorigenic DBA/2J and non-tumorigenic C57BL/6J mice, as well as their F2 and backcrosses, were studied by whole genome linkage analysis. Gonadectomy induced similar upregulation of adrenal Lhcgr in both parental strains and their crosses, irrespective of the tumour status, indicating that ectopic expression of this receptor is not the immediate cause of tumours. Linkage analysis revealed one major significant quantitative trait locus (QTL) for the tumorigenesis on chromosome 8, modulated by epistasis with another QTL on chromosome 18. Hence, post-gonadectomy adrenal tumorigenesis in DBA/2J mice is a dominant trait, not a direct consequence of adrenal Lhcgr expression, and is driven by a complex genetic architecture. A promising candidate gene in the tumorigenesis linkage region is Sfrp1 (secreted frizzled-related protein 1), a tumour suppressor gene, which was down-regulated in the neoplastic tissue. Our findings may have relevance to the human pathogenesis of macronodular adrenal hyperplasia and postmenopausal adrenocortical tumours. A distinctly different adrenal response was observed in TG mice overexpressing LH or CG, or a constitutively activated form of the follicle-stimulating hormone receptor (Fshr). These mice developed perimedullary hyperlasia of foamy multinucleated cells, reminding of macrophages and filled with lipofuscin. Similar response was observed in TG mice overexpressing aromatase (CYP19). The cause of this response is not related to direct LH/CG action, but merely to adrenal response to chronically elevated oestrogen levels. This phenotype is reminiscent of the rare 'black adenomas' of the human adrenal cortex.
MeSH term(s)	Adrenal Cortex Neoplasms/pathology ; Adrenal Cortex Neoplasms/physiopathology ; Animals ; Estrogens/metabolism ; Gonads/physiopathology ; Humans ; Hyperplasia/pathology ; Hyperplasia/physiopathology ; Mice ; Mice, Inbred C57BL ; Mice, Inbred DBA ; Mice, Transgenic ; Orchiectomy ; Ovariectomy ; Pituitary Gland/physiopathology
Chemical Substances	Estrogens
Language	English
Publishing date	2009-03-05
Publishing country	Ireland
Document type	Journal Article ; Review
ZDB-ID	187438-x
ISSN	1872-8057 ; 0303-7207
ISSN (online)	1872-8057
ISSN	0303-7207
DOI	10.1016/j.mce.2008.10.005
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In stock of ZB MED Cologne/Königswinter

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More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito