Relevant bibliographies by topics / Genes TP53/genetics

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Academic literature on the topic 'Genes TP53/genetics'

Author: Grafiati
Published: 4 June 2021
Last updated: 17 February 2022

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Journal articles on the topic "Genes TP53/genetics"

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Anselmo, N. P., J. A. Rey, L. O. Almeida, et al. "Concurrent sequence variation of TP53 and TP73 genes in anaplastic astrocytoma." Genetics and Molecular Research 8, no. 4 (2009): 1257–63. http://dx.doi.org/10.4238/vol8-4gmr631.

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Vasmatzis, George, Sarah H. Johnson, Ryan A. Knudson, et al. "Genome-wide analysis reveals recurrent structural abnormalities of TP63 and other p53-related genes in peripheral T-cell lymphomas." Blood 120, no. 11 (2012): 2280–89. http://dx.doi.org/10.1182/blood-2012-03-419937.

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Abstract Peripheral T-cell lymphomas (PTCLs) are aggressive malignancies of mature T lymphocytes with 5-year overall survival rates of only ∼ 35%. Improvement in outcomes has been stymied by poor understanding of the genetics and molecular pathogenesis of PTCL, with a resulting paucity of molecular targets for therapy. We developed bioinformatic tools to identify chromosomal rearrangements using genome-wide, next-generation sequencing analysis of mate-pair DNA libraries and applied these tools to 16 PTCL patient tissue samples and 6 PTCL cell lines. Thirteen recurrent abnormalities were identi
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Saffari-Chaleshtori, Javad, Mohammad-Amin Tabatabaiefar, Payam Ghasemi-Dehkordi, Effat Farokhi, Mohammad-Taghi Moradi, and Morteza Hashemzadeh-Chaleshtori. "The lack of correlation between TP53 mutations and gastric cancer: A report from a province of Iran." Genetika 49, no. 1 (2017): 235–46. http://dx.doi.org/10.2298/gensr1701235s.

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Gastric cancer ranks second cause of cancer death worldwide after lung cancer. Its etiology is heterogeneous and genetic factors including protooncogenes and tumor suppressor genes always contribute to the progression of cancer. The TP53 tumor suppressor gene has a broad role in genomic stability and DNA repair. The aim of this study was to determine the TP53 gene mutations in gastric cancer specimens in Chaharmahal Va Bakhtiari province of Iran. In this descriptive-lab based study, we investigated the promoter and exons of TP53 gene mutations in 38 paraffin-embedded gastric cancer specimens.
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Strauss, Bernard S. "Hypermutability in Carcinogenesis." Genetics 148, no. 4 (1998): 1619–26. http://dx.doi.org/10.1093/genetics/148.4.1619.

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Abstract The presence of numerous chromosomal changes and point mutations in tumors is well established. At least some of these changes play a role in the development of the tumors. It has been suggested that the number of these genetic changes requires that tumorigenesis involves an increase in mutation rate. However, the presence of numerous changes can also be accounted for by efficient selection. What is required to settle the issue is some measure of nonselected mutations in tumors. In order to determine whether the tumor suppressor TP53 (coding for the protein p53) is hypermutable at som
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Pouladi, Nasser, Mojtaba Shavali, and Sepehr Abdolahi. "Combined Genotype Effects of TP53 and PAI-1 Polymorphisms in Breast Cancer Susceptibility: Multifactor Dimensionality Reduction and in silico Analysis." Human Heredity 85, no. 2 (2020): 51–60. http://dx.doi.org/10.1159/000514398.

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<b><i>Introduction:</i></b> Breast cancer is a heterogeneous and multifactorial disease. <i>TP53</i> and <i>PAI-1</i> as important tumor suppressor genes are involved in the development, invasion, and metastasis of many cancers. This study’s objective was to demonstrate the combined genotype effects of these 2 genes by investigating their single nucleotide polymorphisms. <b><i>Methods:</i></b> In this case-control study, 200 individuals with breast cancer and 179 healthy individuals were studied. The genotypes were determi
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Wu, Guang, Fei Wang, Kai Li, et al. "Significance of TP53 mutation in bladder cancer disease progression and drug selection." PeerJ 7 (December 16, 2019): e8261. http://dx.doi.org/10.7717/peerj.8261.

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Background The tumor protein p53 (TP53) mutant is one of the most frequent mutant genes in bladder cancer. In this study, we assessed the importance of the TP53 mutation in bladder cancer progression and drug selection, and identified potential pathways and core genes associated with the underlying mechanisms. Methods Gene expression data used in this study were downloaded from The Cancer Genome Atlas and cBioportal databases. Drug sensitivity data were obtained from the Genomics of Drug Sensitivity in Cancer. We did functional enrichment analysis by gene set enrichment analysis (GSEA) and the
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Freudenstein, Donald, Cassandra Litchfield, Franco Caramia, et al. "TP53 Status, Patient Sex, and the Immune Response as Determinants of Lung Cancer Patient Survival." Cancers 12, no. 6 (2020): 1535. http://dx.doi.org/10.3390/cancers12061535.

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Lung cancer poses the greatest cancer-related death risk and males have poorer outcomes than females, for unknown reasons. Patient sex is not a biological variable considered in lung cancer standard of care. Correlating patient genetics with outcomes is predicted to open avenues for improved management. Using a bioinformatics approach across non-small cell lung cancer (NSCLC) subtypes, we identified where patient sex, mutation of the major tumor suppressor gene, Tumour protein P53 (TP53), and immune signatures stratified outcomes in lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (
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Cerrato, Aniello, Valentina De Falco, and Massimo Santoro. "Molecular genetics of medullary thyroid carcinoma: the quest for novel therapeutic targets." Journal of Molecular Endocrinology 43, no. 4 (2009): 143–55. http://dx.doi.org/10.1677/jme-09-0024.

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Medullary thyroid carcinoma (MTC) is a rare tumour arising from neural crest-derived parafollicular C-cells. Metastatic MTC patients are incurable because the cancer does not respond to radiotherapy or chemotherapy. The REarranged during Transfection (RET) proto-oncogene plays a key role in the development of MTC. However, one-half of the sporadic MTC do not carry RET mutations. Mice models and early evidence obtained in human samples suggest that other genes, including those encoding components of the RB1 (retinoblastoma) and TP53 tumour-suppressor pathways, may be involved in MTC formation.
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Mirgayazova, Regina, Raniya Khadiullina, Vitaly Chasov, et al. "Therapeutic Editing of the TP53 Gene: Is CRISPR/Cas9 an Option?" Genes 11, no. 6 (2020): 704. http://dx.doi.org/10.3390/genes11060704.

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The TP53 gene encodes the transcription factor and oncosuppressor p53 protein that regulates a multitude of intracellular metabolic pathways involved in DNA damage repair, cell cycle arrest, apoptosis, and senescence. In many cases, alterations (e.g., mutations of the TP53 gene) negatively affect these pathways resulting in tumor development. Recent advances in genome manipulation technologies, CRISPR/Cas9, in particular, brought us closer to therapeutic gene editing for the treatment of cancer and hereditary diseases. Genome-editing therapies for blood disorders, blindness, and cancer are cur
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Chiereghin, Chiara, Erica Travaglino, Matteo Zampini, et al. "The Genetics of Myelodysplastic Syndromes: Clinical Relevance." Genes 12, no. 8 (2021): 1144. http://dx.doi.org/10.3390/genes12081144.

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Myelodysplastic syndromes (MDS) are a clonal disease arising from hematopoietic stem cells, that are characterized by ineffective hematopoiesis (leading to peripheral blood cytopenia) and by an increased risk of evolution into acute myeloid leukemia. MDS are driven by a complex combination of genetic mutations that results in heterogeneous clinical phenotype and outcome. Genetic studies have enabled the identification of a set of recurrently mutated genes which are central to the pathogenesis of MDS and can be organized into a limited number of cellular pathways, including RNA splicing (SF3B1,
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Dissertations / Theses on the topic "Genes TP53/genetics"

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Galatro, Thais Fernanda de Almeida. "Estudo das associações moleculares de ID4 em astrocitomas difusamente infiltrativos." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/5/5138/tde-25092013-161402/.

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O inibidor da ligação do DNA 4 (ID4) é membro da família hélice-alça-hélice de fatores de transcrição, presente durante o desenvolvimento embrionário Sistema Nervoso Central, e que tem sido associado à mutações no gene TP53 e a ativação de SOX2. Juntamente com outros fatores de transcrição, ID4 está envolvido no processo de tumorigênese dos astrocitomas, contribuindo para a de-diferenciação celular, a proliferação e a quimiorresistência. Nesse estudo, nosso objetivo foi caracterizar o padrão de expressão de ID4 em astrocitomas humanos difusamente infiltrativos de graus II a IV de malignidade,
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Eeles, Rosalind Anne. "Germline and somatic studies in the TP53 gene in breast and other cancers." Thesis, Institute of Cancer Research (University Of London), 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.322381.

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Silva, Ana Manoela Maria da. "ANÁLISE DO POLIMORFISMO DOS GENES TP53 E CYP1A1m1 EM BIÓPSIA DE ENDOMÉTRIO DE PACIENTES COM ENDOMETRIOSE." Pontifícia Universidade Católica de Goiás, 2012. http://localhost:8080/tede/handle/tede/2343.

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Made available in DSpace on 2016-08-10T10:38:32Z (GMT). No. of bitstreams: 1 ANA MANOELA MARIA DA SILVA.pdf: 819143 bytes, checksum: e4c543c7bf8fe8063cf665a20af885e5 (MD5) Previous issue date: 2012-06-25<br>Endometriosis is a benign gynecological disease estrogen dependent that affects women at reproductive age. It is characterized by the presence of endometrial tissue outside the uterine cavity designated as ectopic endometrium, involving chronic inflammation in the pelvic cavity. The four stages of endometriosis are classified as: minimal (stage I), mild (stage II), moderat
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Ng, Ho-yin, and 吳灝賢. "Promoter methylation of tumor suppressor genes and microRNAs engaged in TP53 network in acute promyelocytic leukemia." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/196025.

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Acute promyelocytic leukemia (APL) is one of the subtypes of acute myeloid leukemia carrying t(15;17), and constitutes 10 to 15% of adult AMLs. One of the mechanisms of gene inactivation is hypermethylation of promoter-associated CpG islands. Cancers are characterized by global hypomethylation with locus-specific hypermethylation and hence silencing of tumor suppressor genes. Apart from tumor suppressor genes, microRNA, a class of non-coding RNA measuring 19-25 nucleotides, with tumor suppressive function is also found to be inactivated by DNA methylation in hematological malignancies. microRN
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LOPES, Cleiton Mendes. "Análises dos genes TP53, PTEN, IDH1 e IDH2 em tumores não gliais do sistema nervoso humano." Universidade Federal do Pará, 2016. http://repositorio.ufpa.br/jspui/handle/2011/8059.

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Submitted by Cássio da Cruz Nogueira (cassionogueirakk@gmail.com) on 2017-03-27T13:33:17Z No. of bitstreams: 2 license_rdf: 0 bytes, checksum: d41d8cd98f00b204e9800998ecf8427e (MD5) Dissertacao_AnaliseGenesTP53.pdf: 906769 bytes, checksum: 868736765e91f437e42d5aca6b356441 (MD5)<br>Approved for entry into archive by Edisangela Bastos (edisangela@ufpa.br) on 2017-03-30T12:15:36Z (GMT) No. of bitstreams: 2 license_rdf: 0 bytes, checksum: d41d8cd98f00b204e9800998ecf8427e (MD5) Dissertacao_AnaliseGenesTP53.pdf: 906769 bytes, checksum: 868736765e91f437e42d5aca6b356441 (MD5)<br>Made available in DSpa
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Sandrini, Fabiano. "Tumor adrenocortical em crianças : avaliação da relação com cancer em familiares e com alterações no gene TP53." reponame:Repositório Institucional da UFPR, 1999. http://hdl.handle.net/1884/50029.

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Orientador: Romolo Sandrini<br>Dissertação (mestrado) - Universidade Federal do Paraná, Setor de Ciências da Saúde, Programa de Pós graduação em Pediatria<br>Resumo:O tumor de córtex de supra-renal é raro em crianças. Contudo, sua incidência está aumentada na Região Sul do Brasil e no Estado de São Paulo. O tumor adrenocortical é freqüentemente associado ao síndrome de Li-Fraumeni. Foram avaliados 51 pacientes com diagnóstico de tumor de córtex adrenocortical. Obteve-se a história de câncer em familiares de 48 pacientes, provenientes de 46 famílias. Utilizouse o índice relativo de grau de pare
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Borges, Joao Lino Franco. "Relação dos polimorfismos dos genes TP53 e ATM em pacientes com câncer de mama e efeitos colaterais à radioterapia." Pontifícia Universidade Católica de Goiás, 2014. http://localhost:8080/tede/handle/tede/2377.

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Made available in DSpace on 2016-08-10T10:38:48Z (GMT). No. of bitstreams: 1 JOAO LINO FRANCO BORGES.pdf: 1554450 bytes, checksum: 2c0f4d5c22814fcc52394573bf4f06f6 (MD5) Previous issue date: 2014-03-28<br>The purpose of this study wasto evaluate the association of single nucleotide polymorphisms of ATM and TP53 genes in breast cancer patients with skin and subcutaneous systems morbidity after radiotherapy. These two genes encode important proteins of the DNA repair pathways. It is believed that their polymorphisms are likely to modify the response of normal tissues to radiation. A group of 7
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Achatz, Maria Isabel Alves de Souza Waddington. "Modificadores de penetrância de mutações germinativas no gene TP53 em famílias brasileiras com diagnóstico clínico da síndrome de Li-Fraumeni e Li-Fraumeni like: impacto dos polimorfismos intragênicos do TP53 e de genes." Universidade de São Paulo, 2008. http://www.teses.usp.br/teses/disponiveis/5/5155/tde-29012009-172419/.

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A síndrome de Li-Fraumeni (LFS) e sua variante like (LFL) são associadas a mutações germinativas no gene TP53 e predispõe ao alto risco para múltiplos tumores em idade jovem. Analisamos 91 famílias LFS/LFL do sul/sudeste do Brasil para mutações germinativas e haplótipos de TP53 (PIN2, PIN3 e PEX4) e MDM2 (309T-G). A mutação R337H ocorreu em 44,4% das famílias avaliadas. Em 750 controles da região a freqüência populacional da mutação foi 0,3%. A genotipagem de oito indivíduos não relacionados R337H-positivos para 29 TAG SNPs intragênicos demonstrou o mesmo haplótipo raro estabelecendo efeito fu
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Rodrigues, Marina Silva. "Análise de polimorfismos genéticos de TP53 e XRCC1 e sua associação com as características de casos de câncer de mama." Universidade do Estado do Rio de Janeiro, 2009. http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=1124.

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Fundação de Amparo à Pesquisa do Estado do Rio de Janeiro<br>O câncer de mama é o tipo de câncer mais comum em mulheres brasileiras e o principal responsável pelos óbitos neste grupo. Segundo dados do Instituto Nacional do Câncer, em 2008, na região Sudeste do Brasil, o câncer de mama foi o mais incidente, com um risco estimado de 68,12 casos novos por 100 mil. No Estado do Rio de Janeiro a estimativa foi de 7.680 casos, sendo 4.160 na capital. O presente estudo teve como objetivo determinar, através da metodologia de PCRRFLP, as freqüências alélicas e genotípicas dos polimorfismos PIN3 Ins 16
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Luciano, Cristiana da Costa. "RADIOINJÚRIA ASSOCIADA AOS POLIMORFISMOS DE BASE ÚNICA DOS GENES ATM E TP53 EM PACIENTES COM CÂNCER DE CABEÇA E PESCOÇO." Pontifícia Universidade Católica de Goiás, 2012. http://localhost:8080/tede/handle/tede/2370.

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Made available in DSpace on 2016-08-10T10:38:45Z (GMT). No. of bitstreams: 1 Cristiana da Costa Luciano.pdf: 1987242 bytes, checksum: 2f3402c7b9c457e5f89de59897be59ea (MD5) Previous issue date: 2012-11-14<br>The head and neck cancer is the fifth most common in Brazil, being the most predominant histology type the squamous cell carcinoma. Radiation therapy is a procedure for treatment with the efficacy variable, and may play an important role in controlling tumor growth. Faced with this therapy, the patient is exposed to ionizing radiation that can cause adverse effects resulting cessation of
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Book chapters on the topic "Genes TP53/genetics"

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Koleckova, Marketa, Katherine Vomackova, and Zdenek Kolar. "Molecular Prognostic and Predictive Markers in Triple - Negative Breast Cancer." In Breast Cancer [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.97282.

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Triple-negative breast cancer (TNBC) is defined as a molecular subtype of breast cancer that lacks expression of hormone receptors (oestrogen and progesterone receptor) and HER2/neu/ErbB2 protein. It accounts for 15–20% of all invasive breast cancers. The occurrence of TNBC is often associated with younger age at the time of diagnosis and pre-menopausal status, early onset of menarche, higher body mass index (BMI) in the pre-menopausal period, race and ethnicity (African, Hispanic) and the presence of germline mutation in the BRCA1/2 genes or somatic mutation in the TP53 or PTEN genes. TNBCs are specific in its aggressive biological behaviour, shorter interval to disease progression and more frequent relapse within five years (19 to 40 months). The most of TNBCs are represented by high-grade invasive carcinomas of no special type (NST) with high proliferation index measured by Ki-67 nuclear expression, followed by metaplastic carcinomas, secretory carcinomas, and adenoid cystic carcinomas. Genetical and morphological heterogeneity inside TNBC is responsible for the higher frequency of primary and secondary resistance to systemic therapy. The scope of this chapter is to summarise the potential therapeutic agents involved in regulation of cell proliferation, migration, angiogenesis, apoptosis, gene expression and DNA damage or immune response. The insight into this issue is essential for the setting of the optimal chemotherapy regimen and targeted therapeutic strategy.
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Favero Salvadori, Daisy Maria, and Glenda Nicioli da Silv. "Genetic Instability in Normal-Appearing and Tumor Urothelium Cells and the Role of the TP53 Gene in the Toxicogenomic Effects of Antineoplastic Drugs." In Advances in the Scientific Evaluation of Bladder Cancer and Molecular Basis for Diagnosis and Treatment. InTech, 2013. http://dx.doi.org/10.5772/53502.

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