Log in

Relevant bibliographies by topics / P53 Alterations / Journal articles

To see the other types of publications on this topic, follow the link: P53 Alterations.

Journal articles on the topic 'P53 Alterations'

Author: Grafiati

Published: 3 June 2025

Last updated: 31 July 2025

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 journal articles for your research on the topic 'P53 Alterations.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.

1

SAFFARI, B., L. BERNSTEIN, D. C. HONG, et al. "Association of p53 mutations and a codon 72 single nucleotide polymorphism with lower overall survival and responsiveness to adjuvant radiotherapy in endometrioid endometrial carcinomas." International Journal of Gynecologic Cancer 15, no. 5 (2005): 952–63. http://dx.doi.org/10.1136/ijgc-00009577-200509000-00038.

Full text

Abstract:

p53 genetic alterations are associated with advanced stage and aggressive tumors in a variety of human malignancies. The aim of this study was to examine p53 for genetic alterations and to evaluate the association of these alterations with clinical outcome and response to adjuvant radiotherapy in endometrioid endometrial carcinomas. p53 mutations in exons 2–11 were assessed in 59 endometrioid carcinomas by polymerase chain reaction–single-strand conformational polymorphism and sequence analysis. Twelve mutations (20.3%) and nine polymorphisms were identified. Seven of the nine polymorphisms we

APA, Harvard, Vancouver, ISO, and other styles

2

Chapuy, Bjoern, Stefano Monti, Kunihiko Takeyama, et al. "Integrative Analysis Reveals Multiple Alterations of p53 Signaling Pathway Components In Primary Diffuse Large B-Cell Lymphomas." Blood 116, no. 21 (2010): 635. http://dx.doi.org/10.1182/blood.v116.21.635.635.

Full text

Abstract:

Abstract Abstract 635 Diffuse large B-cell lymphoma (DLBCL) is a genetically heterogeneous disease with infrequent alterations of multiple apoptotic, developmental and signaling pathways. Inactivating somatic mutations of the p53 tumor suppressor are uncommon in DLBCL, prompting speculation regarding alternative mechanisms of modulating p53 activity in this disease. As part of a comprehensive analysis of genetic alterations in DLBCL, we recently integrated high-resolution copy number data and transcription profiles in a series of 81 newly diagnosed previously untreated DLBCLs. Copy number (CN)

APA, Harvard, Vancouver, ISO, and other styles

3

Arranz-Salas, Isabel, Andres Sanz-Trelles, and Dolores Bautista Ojeda. "p53 alterations in porokeratosis." Journal of Cutaneous Pathology 30, no. 7 (2003): 455–58. http://dx.doi.org/10.1034/j.1600-0560.2003.00097.x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

4

Muto, T., S. Wakui, H. Takahashi, et al. "p53 Gene Mutations Occurring in Spontaneous Benign and Malignant Mammary Tumors of the Dog." Veterinary Pathology 37, no. 3 (2000): 248–53. http://dx.doi.org/10.1354/vp.37-3-248.

Full text

Abstract:

Sixty-three cases of benign and malignant canine mammary tumors were analyzed to define the alteration of exons 5–8 for the p53 tumor suppressor gene using polymerase chain reaction direct sequence analysis with paraffin-embedded tissues. Four missense mutations were found in 38 benign mammary tumors (11%), and five missense (one tumor had two missense mutations) and one nonsense mutations were found in 25 mammary carcinomas (20%). These data suggest that the p53 gene alterations might be initiated at an early stage of canine mammary carcinogenesis and p53 mutations might be associated with ma

APA, Harvard, Vancouver, ISO, and other styles

5

Huang, Hsuan-Ying, Peter B. Illei, Zhiquan Zhao, et al. "Ewing Sarcomas Withp53Mutation orp16/p14ARFHomozygous Deletion: A Highly Lethal Subset Associated With Poor Chemoresponse." Journal of Clinical Oncology 23, no. 3 (2005): 548–58. http://dx.doi.org/10.1200/jco.2005.02.081.

Full text

Abstract:

PurposeEWS-FLI1 fusion type, p53 mutation, and homozygous deletion of p16/p14ARF have each been shown to be prognostically significant in Ewing sarcoma (ES). We provide the first combined prognostic analysis of these three molecular parameters in ES.Patients and MethodsWe studied 60 patients with ES (stage: localized in 54, metastatic in six). All cases were confirmed to contain the EWS-FLI1 (29 type 1, 12 type 2, 14 other types) or EWS-ERG fusions (five cases). Homozygous deletion of p16/p14ARF, and p53 mutations were determined by fluorescent in situ hybridization and Affymetrix (Santa Clara

APA, Harvard, Vancouver, ISO, and other styles

6

Yoshimoto, T., M. Naruse, Z. Zeng, et al. "The relatively high frequency of p53 gene mutations in multiple and malignant phaeochromocytomas." Journal of Endocrinology 159, no. 2 (1998): 247–55. http://dx.doi.org/10.1677/joe.0.1590247.

Full text

Abstract:

To explore the clinical significance of p53 in the pathogenesis of adrenal neoplasms, we investigated the incidence of p53 gene mutations in functioning human adrenal tumours using the polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) technique to screen p53 exons 4 to 9. We examined 29 adrenocortical adenomas (primary aldosteronism, n=17; Cushing's syndrome, n=12, all benign), and 33 phaeochromocytomas (benign solitary, n=18; benign multiple, n=5; malignant, n=10) in Japanese and Chinese patients. PCR-SSCP did not show any abnormal band-shifts in any of the adrenoco

APA, Harvard, Vancouver, ISO, and other styles

7

Curtin, Karen, Martha L. Slattery, Richard Holubkov, Sandra Edwards, Joseph A. Holden, and Wade S. Samowitz. "p53 Alterations in Colon Tumors." Applied Immunohistochemistry & Molecular Morphology 12, no. 4 (2004): 380–86. http://dx.doi.org/10.1097/00129039-200412000-00017.

Full text

APA, Harvard, Vancouver, ISO, and other styles

8

Boyapati, Anita, Eiki Kanbe, and Dong-Er Zhang. "p53 Alterations in Myeloid Leukemia." Acta Haematologica 111, no. 1-2 (2003): 100–106. http://dx.doi.org/10.1159/000074489.

Full text

APA, Harvard, Vancouver, ISO, and other styles

9

Seruca, Raquel, Leonor David, Sérgio Castedo, Isabel Veiga, Anne-Lise Børresen, and Manuel Sobrinho-Simões. "p53 alterations in gastric carcinoma:." Cancer Genetics and Cytogenetics 75, no. 1 (1994): 45–50. http://dx.doi.org/10.1016/0165-4608(94)90214-3.

Full text

APA, Harvard, Vancouver, ISO, and other styles

10

Ichikawa, A., T. Hotta, N. Takagi, et al. "Mutations of p53 gene and their relation to disease progression in B- cell lymphoma." Blood 79, no. 10 (1992): 2701–7. http://dx.doi.org/10.1182/blood.v79.10.2701.2701.

Full text

Abstract:

Abstract The alteration of p53 tumor suppressor gene was studied in 48 patients with B-cell lymphoma. A sequential combined technique of polymerase chain reaction-mediated single-strand conformational polymorphism (PCR- SSCP) or reverse transcription (RT)-PCR-SSCP and direct sequencing were used as a simple and sensitive approach to analyze nucleotide changes. By these methods, we identified 8 missense point mutations and 2 codon deletions in 9 of the 48 patients. These mutations were located in or close to the evolutionally highly conserved regions of the p53 gene. Eight of nine patients havi

APA, Harvard, Vancouver, ISO, and other styles

11

Ichikawa, A., T. Hotta, N. Takagi, et al. "Mutations of p53 gene and their relation to disease progression in B- cell lymphoma." Blood 79, no. 10 (1992): 2701–7. http://dx.doi.org/10.1182/blood.v79.10.2701.bloodjournal79102701.

Full text

Abstract:

The alteration of p53 tumor suppressor gene was studied in 48 patients with B-cell lymphoma. A sequential combined technique of polymerase chain reaction-mediated single-strand conformational polymorphism (PCR- SSCP) or reverse transcription (RT)-PCR-SSCP and direct sequencing were used as a simple and sensitive approach to analyze nucleotide changes. By these methods, we identified 8 missense point mutations and 2 codon deletions in 9 of the 48 patients. These mutations were located in or close to the evolutionally highly conserved regions of the p53 gene. Eight of nine patients having p53 ge

APA, Harvard, Vancouver, ISO, and other styles

12

Lang, Frederick F., Douglas C. Miller, Maxim Koslow, and Elizabeth W. Newcomb. "Pathways leading to glioblastoma multiforme: a molecular analysis of genetic alterations in 65 astrocytic tumors." Journal of Neurosurgery 81, no. 3 (1994): 427–36. http://dx.doi.org/10.3171/jns.1994.81.3.0427.

Full text

Abstract:

✓ To characterize some of the genetic events underlying the development of glioblastoma multiforme, the authors analyzed 65 astrocytic tumors (seven pilocytic astrocytomas, eight astrocytomas, 16 anaplastic astrocytomas, and 34 glioblastomas multiforme) for loss of heterozygosity for chromosome 17p, loss of heterozygosity for chromosomes 10p and 10q, amplification of the epidermal growth factor receptor (EGFR) gene, and amplification of the oncogenes N-myc, c-myc, and N-ras using Southern blot analysis. Alterations of the p53 gene (positive immunostaining for p53 protein in tumors with or with

APA, Harvard, Vancouver, ISO, and other styles

13

Mattar, Rejane, Suely Nonogaki, Cleonice Silva, Venancio Alves, and Joaquim J. Gama-Rodrigues. "P53 and Rb tumor suppressor gene alterations in gastric cancer." Revista do Hospital das Clínicas 59, no. 4 (2004): 172–80. http://dx.doi.org/10.1590/s0041-87812004000400004.

Full text

Abstract:

Inactivation of tumor suppressor genes has been frequently observed in gastric carcinogenesis. Our purpose was to study the involvement of p53, APC, DCC, and Rb genes in gastric carcinoma. METHOD: Loss of heterozygosity of the p53, APC, DCC and Rb genes was studied in 22 gastric cancer tissues using polymerase chain reaction; single-strand conformation polymorphism of the p53 gene exons 5-6 and exons 7-8 was studied using 35S-dATP, and p53 expression was detected using a histological immunoperoxidase method with an anti-p53 clone. RESULTS AND DISCUSSION: No loss of heterozygosity was observed

APA, Harvard, Vancouver, ISO, and other styles

14

Moller, Michael B., Ole Nielsen, Bjarne E. Christensen, and Niels T. Pedersen. "Molecular and Clinical Features of Diffuse Large B-Cell Lymphoma with MYC Alterations: Inverse Correlation with p53 Pathway Disruption." Blood 106, no. 11 (2005): 1912. http://dx.doi.org/10.1182/blood.v106.11.1912.1912.

Full text

Abstract:

Abstract Diffuse large B-cell lymphoma (DLBCL) is a clinically and genetically heterogeneous disease. Frequent genetic lesions include alterations of BCL2 and BCL6, as well as aberrations of the RB pathway and the p53 pathway resulting in deregulation of cell cycle progression and apoptosis. MYC translocations and amplifications have been detected in a subset of cases. Recently, MYC was shown to control a major regulatory network in B-cells (Nature Genet. 37; 382–90: 2005). We thus hypothesized that DLBCLs with constitutively active MYC are associated with distinctive genetic and clinical feat

APA, Harvard, Vancouver, ISO, and other styles

15

Sugimoto, K., N. Hirano, H. Toyoshima, et al. "Mutations of the p53 gene in myelodysplastic syndrome (MDS) and MDS- derived leukemia." Blood 81, no. 11 (1993): 3022–26. http://dx.doi.org/10.1182/blood.v81.11.3022.3022.

Full text

Abstract:

Abstract The p53 gene is currently thought to be a tumor suppressor gene, and its alterations have been suggested to be involved in the pathogenesis of several human malignancies, including some leukemias and lymphomas. We present here evidence for the possible involvement of p53 gene mutations in the myelodysplastic syndrome (MDS), although the incidence is relatively low. Forty-four patients with MDS and six patients with overt leukemias that developed from MDS were studied for p53 gene alterations using reverse transcriptase-polymerase chain reaction, single-strand conformation polymorphism

APA, Harvard, Vancouver, ISO, and other styles

16

Sugimoto, K., N. Hirano, H. Toyoshima, et al. "Mutations of the p53 gene in myelodysplastic syndrome (MDS) and MDS- derived leukemia." Blood 81, no. 11 (1993): 3022–26. http://dx.doi.org/10.1182/blood.v81.11.3022.bloodjournal81113022.

Full text

Abstract:

The p53 gene is currently thought to be a tumor suppressor gene, and its alterations have been suggested to be involved in the pathogenesis of several human malignancies, including some leukemias and lymphomas. We present here evidence for the possible involvement of p53 gene mutations in the myelodysplastic syndrome (MDS), although the incidence is relatively low. Forty-four patients with MDS and six patients with overt leukemias that developed from MDS were studied for p53 gene alterations using reverse transcriptase-polymerase chain reaction, single-strand conformation polymorphism analysis

APA, Harvard, Vancouver, ISO, and other styles

17

Farrugia, MM, LJ Duan, MD Reis, BY Ngan, and NL Berinstein. "Alterations of the p53 tumor suppressor gene in diffuse large cell lymphomas with translocations of the c-MYC and BCL-2 proto-oncogenes." Blood 83, no. 1 (1994): 191–98. http://dx.doi.org/10.1182/blood.v83.1.191.191.

Full text

Abstract:

Abstract Diffuse large cell lymphomas are aggressive tumors of B-cell origin. In some cases they arise from low-grade follicular lymphomas carrying the t(14;18) translocation, an event that leads to the overexpression of the BCL-2 gene product. More frequently, however, they lack the t(14;18) translocation. Rearrangements of the c-MYC proto-oncogene and mutations of the p53 tumor suppressor gene have also been documented in these lymphomas. This study examines the extent to which alterations in the BCL-2, c-MYC, and p53 genes co-exist within individual lymphomas. Eight diffuse large cell lymph

APA, Harvard, Vancouver, ISO, and other styles

18

Farrugia, MM, LJ Duan, MD Reis, BY Ngan, and NL Berinstein. "Alterations of the p53 tumor suppressor gene in diffuse large cell lymphomas with translocations of the c-MYC and BCL-2 proto-oncogenes." Blood 83, no. 1 (1994): 191–98. http://dx.doi.org/10.1182/blood.v83.1.191.bloodjournal831191.

Full text

Abstract:

Diffuse large cell lymphomas are aggressive tumors of B-cell origin. In some cases they arise from low-grade follicular lymphomas carrying the t(14;18) translocation, an event that leads to the overexpression of the BCL-2 gene product. More frequently, however, they lack the t(14;18) translocation. Rearrangements of the c-MYC proto-oncogene and mutations of the p53 tumor suppressor gene have also been documented in these lymphomas. This study examines the extent to which alterations in the BCL-2, c-MYC, and p53 genes co-exist within individual lymphomas. Eight diffuse large cell lymphoma cell

APA, Harvard, Vancouver, ISO, and other styles

19

Weirich, G., P. Schneider, C. Fellbaum, et al. "p53 Alterations in thymic epithelial tumours." Virchows Archiv 431, no. 1 (1997): 17–23. http://dx.doi.org/10.1007/s004280050064.

Full text

APA, Harvard, Vancouver, ISO, and other styles

20

Lonardo, Fulvio, Takafumi Ueda, Andrew G. Huvos, John Healey, and Marc Ladanyi. "p53 and MDM2 alterations in osteosarcomas." Cancer 79, no. 8 (1997): 1541–47. http://dx.doi.org/10.1002/(sici)1097-0142(19970415)79:8<1541::aid-cncr15>3.0.co;2-y.

Full text

APA, Harvard, Vancouver, ISO, and other styles

21

Kabat, Geoffrey C., Rita A. Kandel, Andrew G. Glass, et al. "A Cohort Study of p53 Mutations and Protein Accumulation in Benign Breast Tissue and Subsequent Breast Cancer Risk." Journal of Oncology 2011 (2011): 1–9. http://dx.doi.org/10.1155/2011/970804.

Full text

Abstract:

Mutations in the p53 tumor suppressor gene and accumulation of its protein in breast tissue are thought to play a role in breast carcinogenesis. However, few studies have prospectively investigated the association of p53 immunopositivity and/or p53 alterations in women with benign breast disease in relation to the subsequent risk of invasive breast cancer. We carried out a case-control study nested within a large cohort of women biopsied for benign breast disease in order to address this question. After exclusions, 491 breast cancer cases and 471 controls were available for analysis. Unconditi

APA, Harvard, Vancouver, ISO, and other styles

22

Nigam, Pallavi, Upama Misra, T. S. Negi, Balraj Mittal, and Gourdas Choudhuri. "Alterations of p53 gene in gallbladder cancer patients of North India." Tropical Gastroenterology 31, no. 2 (2010): 96–100. https://doi.org/10.4103/trog_20103102_96.

Full text

Abstract:

Background: Mutations in p53 gene are found in a majority of human malignancies and usually occur in the exons 5, 6, 7 and 8. Mutated p53 protein is more stable and gets accumulated in the cells that induce the host to develop anti-p53 antibodies in sera of cancer patients. Aim: This study is aimed to observe the frequency and nature of mutations in exons 5-8 of p53 gene and to evaluate its correlation with prevalence of serum p53 antibodies in Indian patients with gallbladder cancer (GBC). Methods: Mutation studies were done in cancer tissues obtained from 62 patients with proven GBC (40 cyto

APA, Harvard, Vancouver, ISO, and other styles

23

Patel, K. R., B. N. Vajaria, R. D. Singh, R. Begum, and P. S. Patel. "CLINICAL IMPLICATIONS OF p53 ALTERATIONS IN ORAL CANCER PROGRESSION: A REVIEW FROM INDIA." Experimental Oncology 40, no. 1 (2018): 10–18. http://dx.doi.org/10.31768/2312-8852.2018.40(1):10-18.

Full text

Abstract:

p53 plays a central role in prevention of normal cell from the development of the malignant phenotype. Somatic alterations (mutations, loss of heterozygosity, deletions) in p53 are a hallmark of most human cancers and cause defects in normal p53 function. However, in the tumors harboring wild-type p53, there are alterations in the regulation of the p53. Thus, understanding why p53 is unable to perform its role as a tumor suppressor in these wild-type tumors is very crucial. Germ-line polymorphisms in p53 are also anticipated to cause measurable disturbance in p53 function. Over-expression as w

APA, Harvard, Vancouver, ISO, and other styles

24

Tomicic, Maja T., Mona Dawood, and Thomas Efferth. "Epigenetic Alterations Upstream and Downstream of p53 Signaling in Colorectal Carcinoma." Cancers 13, no. 16 (2021): 4072. http://dx.doi.org/10.3390/cancers13164072.

Full text

Abstract:

Colorectal cancer (CRC) belongs to the most common tumor types, and half of all CRC harbor missense mutations in the TP53 tumor suppressor gene. In addition to genetically caused loss of function of p53, epigenetic alterations (DNA methylation, histone modifications, micro-RNAs) contribute to CRC development. In this review, we focused on epigenetic alterations related to the entire p53 signaling pathway upstream and downstream of p53. Methylation of genes which activate p53 function has been reported, and methylation of APC and MGMT was associated with increased mutation rates of TP53. The mi

APA, Harvard, Vancouver, ISO, and other styles

25

Ahuja, H., M. Bar-Eli, S. H. Advani, S. Benchimol, and M. J. Cline. "Alterations in the p53 gene and the clonal evolution of the blast crisis of chronic myelocytic leukemia." Proceedings of the National Academy of Sciences 86, no. 17 (1989): 6783–87. http://dx.doi.org/10.1073/pnas.86.17.6783.

Full text

Abstract:

Molecular mechanisms responsible for the clinical progression of chronic myelocytic leukemia to its accelerated phase or to blast crisis have not been defined. We found alterations of the p53 gene (p53 is a 53-kDa nuclear protein) including deletions and rearrangements in 8 of 34 patients in blast crisis and 1 of 4 patients in the accelerated phase, but in only 1 of 38 patients in the chronic phase of chronic myelocytic leukemia. Only two other examples of p53 gene alterations were found among 203 patients with hematologic malignancies and solid tumors. Transcripts of the p53 gene were uniform

APA, Harvard, Vancouver, ISO, and other styles

26

Sugimoto, K., H. Toyoshima, R. Sakai, et al. "Frequent mutations in the p53 gene in human myeloid leukemia cell lines." Blood 79, no. 9 (1992): 2378–83. http://dx.doi.org/10.1182/blood.v79.9.2378.2378.

Full text

Abstract:

Abstract The p53 gene is currently considered to function as a tumor-suppressor gene in various human malignancies. In hematologic malignancies, alterations in the p53 gene have been shown in some human leukemias and lymphomas. Although mutations in the p53 gene are infrequent in acute myelogenous leukemia (AML) patients, we show in this report that alterations in the p53 gene are frequent in myeloid leukemia cell lines. We studied alterations of the p53 gene in nine human myeloid leukemia cell lines by reverse transcriptase-polymerase chain reaction (RT-PCR), single-strand conformation polymo

APA, Harvard, Vancouver, ISO, and other styles

27

Sugimoto, K., H. Toyoshima, R. Sakai, et al. "Frequent mutations in the p53 gene in human myeloid leukemia cell lines." Blood 79, no. 9 (1992): 2378–83. http://dx.doi.org/10.1182/blood.v79.9.2378.bloodjournal7992378.

Full text

Abstract:

The p53 gene is currently considered to function as a tumor-suppressor gene in various human malignancies. In hematologic malignancies, alterations in the p53 gene have been shown in some human leukemias and lymphomas. Although mutations in the p53 gene are infrequent in acute myelogenous leukemia (AML) patients, we show in this report that alterations in the p53 gene are frequent in myeloid leukemia cell lines. We studied alterations of the p53 gene in nine human myeloid leukemia cell lines by reverse transcriptase-polymerase chain reaction (RT-PCR), single-strand conformation polymorphism (S

APA, Harvard, Vancouver, ISO, and other styles

28

Rashid, A., M. Zahurak, S. N. Goodman, and S. R. Hamilton. "Genetic epidemiology of mutated K-rasproto-oncogene, altered suppressor genes, and microsatellite instability in colorectal adenomas." Gut 44, no. 6 (1999): 826–33. http://dx.doi.org/10.1136/gut.44.6.826.

Full text

Abstract:

BACKGROUNDThe genetic epidemiology of colorectal adenomas has not been studied prospectively in colonoscopy patients without cancer.AIMSTo study genetic alterations in colorectal adenomas and correlate these with patient demographics and adenoma characteristics.METHODSMutations and allelic deletions in 201 adenomas from 60 patients were compared with demographic features, adenoma characteristics, and family history.RESULTSThe most common alteration was K-ras proto-oncogene mutation, present in 35% of adenomas and 65% of patients. Patients 65 years of age and older had a decreased probability o

APA, Harvard, Vancouver, ISO, and other styles

29

Gené, Míriam, Míriam Cuatrecasas, Irene Amat, et al. "Alterations in p53, Microsatellite Stability and Lack of MUC5AC Expression as Molecular Features of Colorectal Carcinoma Associated with Inflammatory Bowel Disease." International Journal of Molecular Sciences 24, no. 10 (2023): 8655. http://dx.doi.org/10.3390/ijms24108655.

Full text

Abstract:

Colitis-associated colorectal carcinoma (CAC) occurs in inflammatory bowel disease (IBD) because of the “chronic inflammation-dysplasia-cancer” carcinogenesis pathway characterized by p53 alterations in the early stages. Recently, gastric metaplasia (GM) has been described as the initial event of the serrated colorectal cancer (CRC) process, resulting from chronic stress on the colon mucosa. The aim of the study is to characterize CAC analyzing p53 alterations and microsatellite instability (MSI) to explore their relationship with GM using a series of CRC and the adjacent intestinal mucosa. Im

APA, Harvard, Vancouver, ISO, and other styles

30

Lu, X., and A. Feki. "Phenotypic features with p53 alterations related to human papillomavirus and prognostic evaluation in cervical cancer." International Journal of Gynecologic Cancer 16, no. 2 (2006): 708–17. http://dx.doi.org/10.1136/ijgc-00009577-200603000-00040.

Full text

Abstract:

Cervical cancer is one of the most common tumor affecting women worldwide. Human papillomavirus (HPV) was found to have a causal relationship with cervical cancer and its precursors. The interaction between HPV E6 protein and p53 was identified inin vitrostudies. The aim of the study was to evaluate the prevalence of p53 alterations related to HPV infection and the prognostic significance of p53 alterations in cervical cancer. Studies were identified by a MEDLINE search, and all relevant articles were retrieved from 1991 to March 2004. The prevalence of p53 mutations is a rare event in cervica

APA, Harvard, Vancouver, ISO, and other styles

31

Chang, H., S. Benchimol, MD Minden, and HA Messner. "Alterations of p53 and c-myc in the clonal evolution of malignant lymphoma." Blood 83, no. 2 (1994): 452–59. http://dx.doi.org/10.1182/blood.v83.2.452.452.

Full text

Abstract:

Abstract We derived the lymphoma cell lines OCI-Ly 13.1 and OCI-Ly 13.2 from a patient with non-Hodgkin's lymphoma at the time of presentation and during chemotherapy-resistant relapse. These lines were of T-cell phenotype and contained the identical T-cell receptor beta-chain rearrangement, indicating that both lines were members of the same malignant clone. The lines differed in their growth characteristics; OCI-Ly 13.1 grew slowly and required growth factors for colony formation, whereas OCI-Ly 13.2 grew rapidly and formed colonies without addition of growth factors. To test whether or not

APA, Harvard, Vancouver, ISO, and other styles

32

Chang, H., S. Benchimol, MD Minden, and HA Messner. "Alterations of p53 and c-myc in the clonal evolution of malignant lymphoma." Blood 83, no. 2 (1994): 452–59. http://dx.doi.org/10.1182/blood.v83.2.452.bloodjournal832452.

Full text

Abstract:

We derived the lymphoma cell lines OCI-Ly 13.1 and OCI-Ly 13.2 from a patient with non-Hodgkin's lymphoma at the time of presentation and during chemotherapy-resistant relapse. These lines were of T-cell phenotype and contained the identical T-cell receptor beta-chain rearrangement, indicating that both lines were members of the same malignant clone. The lines differed in their growth characteristics; OCI-Ly 13.1 grew slowly and required growth factors for colony formation, whereas OCI-Ly 13.2 grew rapidly and formed colonies without addition of growth factors. To test whether or not these bio

APA, Harvard, Vancouver, ISO, and other styles

33

Ho, Park Jong, Baek Hee Jong, Zo Joe Ill, Lee Choon Tack, Kim Chang Min, and Shim Young Mog. "High Prevalence of p53 Gene Mutation in Esophageal Cancer." Asian Cardiovascular and Thoracic Annals 5, no. 4 (1997): 213–19. http://dx.doi.org/10.1177/021849239700500407.

Full text

Abstract:

Tissue samples from 24 patients with esophageal cancer were studied to determine the incidence and clinical implications of alterations of the p53 gene. Allelic deletion of chromosome 17p and mutation of the p53 gene were determined by Southern blot analysis and polymerase chain reaction single-stranded conformation polymorphism. Nucleotide sequence analysis was performed using the direct sequencing method when abnormalities were detected. Eighteen of the 24 cases of esophageal cancer showed either gene deletions or mutations of the p53 gene. Among 15 tumors with p53 gene deletion or mutation,

APA, Harvard, Vancouver, ISO, and other styles

34

Nelson, W. G., and M. B. Kastan. "DNA strand breaks: the DNA template alterations that trigger p53-dependent DNA damage response pathways." Molecular and Cellular Biology 14, no. 3 (1994): 1815–23. http://dx.doi.org/10.1128/mcb.14.3.1815-1823.1994.

Full text

Abstract:

The tumor suppressor protein p53 serves as a critical regulator of a G1 cell cycle checkpoint and of apoptosis following exposure of cells to DNA-damaging agents. The mechanism by which DNA-damaging agents elevate p53 protein levels to trigger G1/S arrest or cell death remains to be elucidated. In fact, whether damage to the DNA template itself participates in transducing the signal leading to p53 induction has not yet been demonstrated. We exposed human cell lines containing wild-type p53 alleles to several different DNA-damaging agents and found that agents which rapidly induce DNA strand br

APA, Harvard, Vancouver, ISO, and other styles

35

Nelson, W. G., and M. B. Kastan. "DNA strand breaks: the DNA template alterations that trigger p53-dependent DNA damage response pathways." Molecular and Cellular Biology 14, no. 3 (1994): 1815–23. http://dx.doi.org/10.1128/mcb.14.3.1815.

Full text

Abstract:

The tumor suppressor protein p53 serves as a critical regulator of a G1 cell cycle checkpoint and of apoptosis following exposure of cells to DNA-damaging agents. The mechanism by which DNA-damaging agents elevate p53 protein levels to trigger G1/S arrest or cell death remains to be elucidated. In fact, whether damage to the DNA template itself participates in transducing the signal leading to p53 induction has not yet been demonstrated. We exposed human cell lines containing wild-type p53 alleles to several different DNA-damaging agents and found that agents which rapidly induce DNA strand br

APA, Harvard, Vancouver, ISO, and other styles

36

Alduaij, Ahmad, Katrine Hansen, Tahreem A. Karim, et al. "Clear Cell Carcinomas of the Mullerian System: Does the Pathogenesis Vary Depending on Their Nuclear Grade and Their Association with Endometriosis? An Immunohistochemical Analysis." Pathology Research International 2012 (November 1, 2012): 1–6. http://dx.doi.org/10.1155/2012/674748.

Full text

Abstract:

Clear cell carcinomas (CCC) of the mullerian system are considered high grade tumors, but morphologically, the cells of CCC show both low and high grade features. The aims of the current study were to categorize CCC into low and high nuclear grade types, correlate their association with endometriosis, and then observe possible variations in pathogenesis based on their expression of p53 and Ki-67. We studied 41 pure mullerian CCCs and designated each as either a high (HNG) or low (LNG) nuclear grade tumor. Morphologically, 17 (41%) CCCs were LNG and 24 (59%) were HNG. Nine (38%) HNG and 2 (12%)

APA, Harvard, Vancouver, ISO, and other styles

37

Cabelguenne, Arnauld, Hélène Blons, Isabelle de Waziers, et al. "p53 Alterations Predict Tumor Response to Neoadjuvant Chemotherapy in Head and Neck Squamous Cell Carcinoma: A Prospective Series." Journal of Clinical Oncology 18, no. 7 (2000): 1465–73. http://dx.doi.org/10.1200/jco.2000.18.7.1465.

Full text

Abstract:

PURPOSE: The tumor suppressor gene p53 plays a crucial role in cell cycle control and apoptosis in response to DNA damages. p53 gene mutations and allelic losses at 17p are one of the most common genetic alterations in primary head and neck squamous cell carcinoma (HNSCC). Alterations of the p53 gene have been shown to contribute to carcinogenesis and drug resistance. PATIENTS AND METHODS: In this prospective series, patients with HNSCC were treated with cisplatin-fluorouracil neoadjuvant chemotherapy. p53 status was characterized in 106 patients with HNSCC (p53 mutations, allelic losses at p5

APA, Harvard, Vancouver, ISO, and other styles

38

Mattar, R., A. M. Alexandrino, and A. A. Laudanna. "Infrequent p53 gene alterations in ulcerative colitis." Brazilian Journal of Medical and Biological Research 32, no. 9 (1999): 1083–88. http://dx.doi.org/10.1590/s0100-879x1999000900005.

Full text

APA, Harvard, Vancouver, ISO, and other styles

39

Effert, Peter J., Rachael H. McCoy, Philip J. Walther, and Edison T. Liu. "P53 Gene Alterations in Human Prostate Carcinoma." Journal of Urology 150, no. 1 (1993): 257–61. http://dx.doi.org/10.1016/s0022-5347(17)35458-7.

Full text

APA, Harvard, Vancouver, ISO, and other styles

40

de Vos, Sven, Sharon P. Wilczynski, Michael Fleischhacker, and Phillip Koeffler. "p53 Alterations in Uterine Leiomyosarcomas versus Leiomyomas." Gynecologic Oncology 54, no. 2 (1994): 205–8. http://dx.doi.org/10.1006/gyno.1994.1194.

Full text

APA, Harvard, Vancouver, ISO, and other styles

41

Cooper, Melissa, Shu-Qiu Li, Tajinder Bhardwaj, Thomas Rohan, and Rita A. Kandel. "Evaluation of Oligonucleotide Arrays for Sequencing of the p53 Gene in DNA from Formalin-Fixed, Paraffin-Embedded Breast Cancer Specimens." Clinical Chemistry 50, no. 3 (2004): 500–508. http://dx.doi.org/10.1373/clinchem.2003.025221.

Full text

Abstract:

Abstract Background: Routine tissue processing has generated banks of paraffin-embedded tissue that could be used in retrospective cohort studies to study the molecular changes that occur during cancer development. The purpose of this study was to determine whether a p53 microarray could be used to sequence the p53 gene in DNA extracted from formalin-fixed, paraffin-embedded (FFPE) tissues. Methods: DNA was extracted from 70 FFPE breast cancer tissue specimens. p53 was sequenced with an oligonucleotide microarray (p53 GeneChip®; Affymetrix), and the results were compared with the results obtai

APA, Harvard, Vancouver, ISO, and other styles

42

Lee, Hun Ju, Miguel Gallardo, Xiaorui Zhang, Alfonso Quintas-Cardama, and Sean M. Post. "p53 Pathway Alterations Influence Survival and Treatment Response In Chronic Lymphocytic Leukemia." Blood 122, no. 21 (2013): 2885. http://dx.doi.org/10.1182/blood.v122.21.2885.2885.

Full text

Abstract:

Abstract Chronic lymphocytic leukemia (CLL) is a heterogeneous malignancy, with survival rates that range from months to decades. Numerous genetic markers have been identifying that predict for poor survival outcomes. One of the most significant prognostic risk factors is loss of integrity of the p53 pathway. It is well known that loss of the short arm of chromosome 17 (17p-), containing the p53 locus, is a major predictor poor outcome in CLL, however, there is a lack of clarity how specific p53 mutations influence cancer progression. It is our contention that understanding the impact of p53 m

APA, Harvard, Vancouver, ISO, and other styles

43

Yoo, Jinyoung, Sonya Park, Chang Suk Kang, Seok Jin Kang, and Byung Kee Kim. "Expression of E-Cadherin and p53 Proteins in Human Soft Tissue Sarcomas." Archives of Pathology & Laboratory Medicine 126, no. 1 (2002): 33–38. http://dx.doi.org/10.5858/2002-126-0033-eoecap.

Full text

Abstract:

Abstract Objective.—To investigate the expression of E-cadherin in human soft tissue sarcomas and its potential relationship to p53 alterations. Design.—Tissue sections of 91 soft tissue sarcomas were analyzed by immunohistochemistry for E-cadherin and p53 proteins. Sixty-one tumors were investigated further by the application of the polymerase chain reaction technique and a direct sequence analysis procedure of exons 5 through 8 in the p53 gene. Setting.—Tertiary-care teaching hospital. Patients.—Ninety-one patients with soft tissue tumor were treated surgically. Thirteen of these patients ha

APA, Harvard, Vancouver, ISO, and other styles

44

Sugimoto, K., H. Toyoshima, R. Sakai, et al. "Mutations of the p53 gene in lymphoid leukemia." Blood 77, no. 6 (1991): 1153–56. http://dx.doi.org/10.1182/blood.v77.6.1153.1153.

Full text

Abstract:

Abstract p53 is currently considered to be a tumor suppressor gene product, and its alterations are suggested to be involved in several human malignancies. Here we show evidence of the possible involvement of p53 gene mutations in lymphoid leukemias studied by reverse transcriptase- polymerase chain reaction, single strand conformation polymorphism analysis, and nucleotide sequencing. Fourteen patients with various leukemias were examined and two with acute lymphoblastic leukemia and one with Waldenstrom's macroglobulinemia were identified to have mutations in the coding region of the p53 gene

APA, Harvard, Vancouver, ISO, and other styles

45

Sugimoto, K., H. Toyoshima, R. Sakai, et al. "Mutations of the p53 gene in lymphoid leukemia." Blood 77, no. 6 (1991): 1153–56. http://dx.doi.org/10.1182/blood.v77.6.1153.bloodjournal7761153.

Full text

Abstract:

p53 is currently considered to be a tumor suppressor gene product, and its alterations are suggested to be involved in several human malignancies. Here we show evidence of the possible involvement of p53 gene mutations in lymphoid leukemias studied by reverse transcriptase- polymerase chain reaction, single strand conformation polymorphism analysis, and nucleotide sequencing. Fourteen patients with various leukemias were examined and two with acute lymphoblastic leukemia and one with Waldenstrom's macroglobulinemia were identified to have mutations in the coding region of the p53 gene. These m

APA, Harvard, Vancouver, ISO, and other styles

46

Marks, D. I., B. W. Kurz, M. P. Link, et al. "Altered expression of p53 and mdm-2 proteins at diagnosis is associated with early treatment failure in childhood acute lymphoblastic leukemia." Journal of Clinical Oncology 15, no. 3 (1997): 1158–62. http://dx.doi.org/10.1200/jco.1997.15.3.1158.

Full text

Abstract:

PURPOSE To determine whether potential alteration in p53 function through p53 gene mutation or mdm-2 overexpression correlates with early treatment failure in childhood acute lymphoblastic leukemia (ALL). PATIENTS AND METHODS Diagnostic marrow samples from 34 children were analyzed for p53 gene alterations by western blot and SSCP/DNA sequence analysis and for mdm-2 overexpression by western blot analysis. These samples were derived from two groups of children with ALL: 17 good outcome patients who are in long-term continuous complete remission and 17 poor outcome patients who did not achieve

APA, Harvard, Vancouver, ISO, and other styles

47

Salvatore, Domenico, Angela Celetti, Nicole Fabien, et al. "Low frequency of p53 mutations in human thyroid tumors; p53 and Ras mutation in two out of fifty-six thyroid tumours." European Journal of Endocrinology 134, no. 2 (1996): 177–83. http://dx.doi.org/10.1530/eje.0.1340177.

Full text

Abstract:

Salvatore D, Celetti A, Fabien N, Paulin C, Martelli ML, Battaglia C, Califano D, Monaco C, Viglietto G, Santoro M, Fusco A. Low frequency of p53 mutations in human thyroid tumors; p53 and Ras mutation in two out of fifty-six thyroid tumours. Eur J Endocrinol 1996;134:177–83. ISSN 0804–4643 Objective: p53 is a well-known nuclear phosphoprotein encoded by a suppressor gene known to be mutated in various kinds of human tumours. A relationship between p53 gene mutation and tumour progression seems to be a common feature of several neoplasias. Desing: In order to investigate the role of p53 mutati

APA, Harvard, Vancouver, ISO, and other styles

48

Pant, Vinod, Neeraj K. Aryal, Shunbin Xiong, Gilda P. Chau, Natalie W. Fowlkes, and Guillermina Lozano. "Alterations of the Mdm2 C-Terminus Differentially Impact Its Function In Vivo." Cancer Research 82, no. 7 (2022): 1313–20. http://dx.doi.org/10.1158/0008-5472.can-21-2381.

Full text

Abstract:

Abstract Murine double minute 2 (Mdm2) is the principal E3-ubiquitin ligase for p53 and contains a C2H2C4 type RING domain wherein the last cysteine residue is followed by an evolutionarily conserved 13 amino acid C-terminal tail. Previous studies have indicated that integrity of the C-terminal tail is critical for Mdm2 function. Recently, a mutation extending the MDM2 length by five amino acids was identified and associated with enhanced p53 response in fibroblasts and premature aging in a human patient. To investigate the importance of the conserved Mdm2 C-terminal length on p53 regulatory f

APA, Harvard, Vancouver, ISO, and other styles

49

Lupien, Leslie, Veronica Rendo, Eric Morin, et al. "DIPG-54. p53 pathway reactivation as a therapeutic strategy in diffuse intrinsic pontine glioma." Neuro-Oncology 24, Supplement_1 (2022): i31. http://dx.doi.org/10.1093/neuonc/noac079.111.

Full text

Abstract:

Abstract TP53 is the most frequently mutated tumor suppressor with somatic alterations found in approximately 50% of all human cancers. In the remaining TP53 wild-type (WT) tumors, functional inactivation of the p53 pathway may be achieved through a variety of other mechanisms, including gene deletion, epigenetic silencing, and/or alterations in prominent negative regulators, including MDM2/MDM4 and PPM1D. These alterations block p53 activity and lead to uncontrolled cell proliferation and oncogenesis in a majority of cancers, including the highly aggressive, universally fatal glial cell tumor

APA, Harvard, Vancouver, ISO, and other styles

50

Boldrini, Laura, Barbara Loggini, Silvia Gisfredi, et al. "Mutations of Fas (APO-1/CD95) and p53 Genes in Nonmelanoma Skin Cancer." Journal of Cutaneous Medicine and Surgery 7, no. 2 (2003): 112–18. http://dx.doi.org/10.1177/120347540300700203.

Full text

Abstract:

Background: There is considerable evidence that apoptosis plays an important role in the pathogenesis of a wide variety of skin diseases. Apoptosis failure may ensure the survival of transformed cells prone to sustain further genetic damage and it plays an important part in the development of tumors. Genetic alterations of Fas and p53, with consequent inactivation of gene protein products, may be involved in transcriptional downregulation of Fas. Objective: We investigated Fas and its ligand expression in 30 cases of nonmelanoma skin cancer, 19 basal cell and 11 squamous cell carcinomas, and w

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!