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Journal articles on the topic 'P53 polymorphism'

Author: Grafiati

Published: 3 June 2025

Last updated: 31 July 2025

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1

González-Herrera, Lizbeth, Patricia Rodríguez-Morales, María del Refugio González-Losa, et al. "MTHFR/p53 Polymorphisms as Genetic Factors for Cervical Intraepithelial Neoplasia and Cervical Cancer in HPV-infected Mexican Women." International Journal of Biological Markers 29, no. 2 (2014): 142–49. http://dx.doi.org/10.5301/jbm.5000070.

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We performed a case-control association study to evaluate the association between common polymorphisms in MTHFR (C677T and A1298C) and the Arg72Pro polymorphism in the p53 gene and the risk for cervical intraepithelial neoplasia (CIN) or invasive cervical cancer (ICC) in Mexican HPV-infected women. We included 131 women with diagnosis of CIN grade I-II and 78 with CIN III or ICC; as controls we also included 274 women with normal Pap smear and negative HPV test. Genotyping for MTHFR and p53 polymorphisms was performed by PCR-RFPLs. HPV was tested by Hybrid Capture II. Odds ratios and 95% confi

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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.

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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

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3

Engin, Ayse, Bensu Karahalil, Ali Karakaya, and Atilla Engin. "Association Between XRCC1 ARG399GLN and P53 ARG72PRO Polymorphisms and the Risk of Gastric and Colorectal Cancer in Turkish Population." Archives of Industrial Hygiene and Toxicology 62, no. 3 (2011): 207–14. http://dx.doi.org/10.2478/10004-1254-62-2011-2098.

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Association Between XRCC1 ARG399GLN and P53 ARG72PRO Polymorphisms and the Risk of Gastric and Colorectal Cancer in Turkish PopulationGastric cancer is one of the most common cancers of the gastrointestinal system, and its overall five-year survival rate is still 15 % to 20 %, as it can mostly be diagnosed at an advanced stage. On the other hand, although colorectal cancer has a rather good prognosis, mortality is one half that of the incidence.As carcinogenesis is believed to involve reactive radicals that cause DNA adduct formation, impaired repair activity, and weakened tumour suppression,

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Dybikowska, A., A. Dettlaff, K. Konopa, and A. Podhajska. "p53 codon 72 polymorphism in cervical cancer patients and healthy women from Poland." Acta Biochimica Polonica 47, no. 4 (2000): 1179–82. http://dx.doi.org/10.18388/abp.2000_3970.

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A polymorphism at codon 72 of gene p53 results in the presence of either arginine or proline at this position. We investigated the distribution of p53 codon 72 polymorphism in cervical cancer patients and a control group of healthy women from Poland. Our results do not confirm the hypothesis that the p53 codon polymorphism could play a role as a factor for squamous carcinoma of the cervix.

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5

Özbey, Ulku, Hüseyin Yüce, Mustafa Namli, and Tamer Elkiran. "Investigation of Differences in P53 Gene Polymorphisms between Schizophrenia and Lung Cancer Patients in the Turkish Population." Genetics Research International 2011 (March 3, 2011): 1–9. http://dx.doi.org/10.4061/2011/483851.

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Objective. The reduced incidence of cancer observed in schizophrenia patients may be related to differences in genetic background. It has been suggested that genetic predisposition towards schizophrenia is associated with reduced vulnerability to lung cancer, and p53 gene is one of the candidate genes. In our study, we aimed to investigate polymorphisms in the BstUI in exon 4 and MspI in intron 6 restriction sites of the p53 gene in Turkish schizophrenia patients, lung cancer patients, and controls. Material and Methods. Allele and genotype incidence of these polymorphisms with their haplotype

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Shiohara, M., WS el-Deiry, M. Wada, et al. "Absence of WAF1 mutations in a variety of human malignancies." Blood 84, no. 11 (1994): 3781–84. http://dx.doi.org/10.1182/blood.v84.11.3781.bloodjournal84113781.

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A newly cloned gene named wild-type p53-activated fragment 1 (WAF1; also known as p21, Pic-1, Cip-1, or SDI1) is directly regulated by p53 and can itself suppress tumor cell growth in culture. Induction of expression of WAF1 may be an important means by which cells with DNA injury arrest their growth to repair DNA or undergo apoptosis. Based on the hypothesis that mutations of this gene may play a role in carcinogenesis, we have studied 351 DNAs from 14 kinds of malignancies, as well as 36 human transformed cell lines, for alterations of WAF1 gene by single-strand conformation polymorphism ana

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7

Yi, Ke, LingYun Yang, Zhu Lan, and MingRong Xi. "The Association Between p53 Codon 72 Polymorphism and Endometrial Cancer Risk: A System Review and Meta-analysis." International Journal of Gynecologic Cancer 26, no. 6 (2016): 1121–28. http://dx.doi.org/10.1097/igc.0000000000000725.

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AbstractPolymorphism of p53 codon 72 plays an important role in pathogenesis and development of cancer. Published data on the association between the p53 codon 72 polymorphism and endometrial cancer risk are controversial. A meta-analysis was performed to assess whether the polymorphism of p53 codon 72 is associated with endometrial cancer risk. Medline, Embase, China National Knowledge Infrastructure, and Chinese Biomedicine Databases were searched to identify eligible studies. Pooled odds ratios (ORs) and 95% confidence intervals (CIs) for p53 codon 72 polymorphism and endometrial cancer wer

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8

Zhang, Shengliang, and Wafik S. El-Deiry. "Abstract 2604: Functional analysis of p53 codon 72 polymorphism with cysteine substitution in cancer cells." Cancer Research 83, no. 7_Supplement (2023): 2604. http://dx.doi.org/10.1158/1538-7445.am2023-2604.

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Abstract The p53 codon p72 polymorphism with proline (p53P72)/arginine (p53R72) substitution is associated with cancer incidence. Cysteine(C) substitution at p53 codon 72 polymorphism (p53C72) is rarely studied in cancer patients. A patient who developed AML and who carries p53C72 was described (El-Deiry, 2022 WIN Symposium). The patient’s family has high rates of cancer susceptibility in the women some of whom carry FANCC alterations and other alleles. To examine the functional characteristics of different p53 alterations at codon 72, we generated plasmids expressing p53C72, p53 R72 or p53P72

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Jafari Nedooshan, Jamal, Mohammad Forat Yazdi, Hossein Neamatzadeh, Masoud Zare Shehneh, Saeed Kargar, and Niloofar Seddighi. "Association between TP53 codon 72 G>C Polymorphism and Thyroid Carcinoma Risk: An Up-to-Date Meta-Analysis." Asian Pacific Journal of Cancer Biology 1, no. 4 (2016): 89–95. http://dx.doi.org/10.31557/apjcb.2016.1.4.89-95.

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Objective: Many published data on the association between p53 codon 72 G>C polymorphism and thyroid carcinoma risk showed inconclusive results. The aim this study was to assess the association between p53 codon 72 G>C polymorphism and thyroid cancer risk. Methods: A literature search of PubMed, EMBASE, Google scholar and Web of Science databases for case–control studies examining the association between p53 codon 72 G>C polymorphism and thyroid cancer susceptibility up October 2016 was performed. Odds ratios (OR) with 95 % confidence intervals (95 % CI) were used to assess the strengt

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10

Helland, Aslaug, and Anne-Lise Børresen-Dale. "p53 polymorphism and cervical cancer." Lancet 354, no. 9189 (1999): 1561–62. http://dx.doi.org/10.1016/s0140-6736(05)76596-x.

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11

Zehbe, Ingeborg, Gianfranco Voglino, Erik Wilander, Franco Genta, and Massimo Tommasino. "p53 polymorphism and cervical cancer." Lancet 354, no. 9189 (1999): 1562. http://dx.doi.org/10.1016/s0140-6736(05)76597-1.

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12

Hashemi, Seyed, Atena Farsi, Gholamreza Bahari, Hoseinali Danesh, and Kamran Roudini. "Evaluation of 40-bp deletion/insertion polymorphism of mdm2 and 16-bp deletion/insertion polymorphism of p53 gene in patients with lymphoma in a Persian population." Genetika 53, no. 3 (2021): 997–1005. http://dx.doi.org/10.2298/gensr2103997h.

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Considering the importance of lymphoma and its prevalence in communities as well as its relationship with genetic factors (P53 & MDM2) as well as contradictory results about the possible role of deletion/insertion of polymorphisms in different types of cancer. The aim of this study was to investigate the deletion/insertion of 40 bp of mdm2 polymorphism and 16-bp of p53 polymorphism in patients with lymphoma. In this case-control study, 152 non-Hodgkin's lymphoma patients and 155 healthy individuals were selected by convenience sampling method. MDM2 and P53 polymorphisms were examined by PC

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13

Shen, Chiung-Chyi. "DNAR-04. BOTH P53 CODON 72 ARG/ARG AND PRO/ARG GENOTYPES IN GLIOBLASTOMA MULTIFORME PATIENTS HAVE A BETTER PROGNOSIS IN BEVACIZUMAB TREATMENT." Neuro-Oncology 24, Supplement_7 (2022): vii91. http://dx.doi.org/10.1093/neuonc/noac209.336.

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Abstract BACKGROUND In glioblastoma multiforme (GBM), bevacizumab increased progression-free survival but it has failed to improve overall survival (OS) in controlled trials. This study, therefore, aimed to retrospectively analyze the polymorphisms of p53 codon 72 and the clinical characteristics of GBM specimens from Taiwanese patients. METHODS The polymorphisms of p53 codon 72 in 99 patients with GBM treated at Taichung Veterans General Hospital in Taiwan from 2007 to 2017 were analyzed using direct DNA sequencing and PCR-RFLP analysis. RESULTS We found that among these GBM patients, the pol

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14

Mahmood, Silvia, Monika Sivoňová, Tatiana Matáková, et al. "Association of EGF and p53 gene polymorphisms and colorectal cancer risk in the Slovak population." Open Medicine 9, no. 3 (2014): 405–16. http://dx.doi.org/10.2478/s11536-013-0300-4.

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AbstractDuring the transformation process single nucleotide polymorphisms (SNPs) of key genes, such as p53 Arg72Pro or EGF A61G, may mediate various cellular processes. These variants may be associated with colorectal cancer risk (CRC), but conflicting findings have been reported. The purpose of this study was to determine the association of the SNPs in 5′ UTR of EGF A61G and p53 Arg72Pro and CRC in the Slovak population. The present case-control study was carried out in 173 confirmed CRC patients and 303 healthy subjects. Genotyping was performed by PCR-RFLP methods. Significant association w

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15

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.

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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

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Das, Mandakini, Santanu Kumar Sharma, Gaganpreet Singh Sekhon, Jagadish Mahanta, Rup Kumar Phukan, and Bimal Kumar Jalan. "p16 gene silencing along with p53 single-nucleotide polymorphism and risk of esophageal cancer in Northeast India." Tumor Biology 39, no. 5 (2017): 101042831769838. http://dx.doi.org/10.1177/1010428317698384.

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The high incidence of esophageal cancer in Northeast India and the unique ethnic background and dietary habits provide a great opportunity to study the molecular genetics behind esophageal squamous cell carcinoma in this part of the region. We hypothesized that in addition to currently known environmental risk factors for esophageal cancer, genetic and epigenetic factors are also involved in esophageal carcinogenesis in Northeast India. Therefore, in this study, we explored the possible association between the two important G1 cell cycle regulatory genes p16 and p53 and environmental risk fact

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Pillai, RadhakrishnaMadhavan, and SAsha Nair. "Polymorphism of p53 in cancer prognosis." Indian Journal of Medical Research 144, no. 3 (2016): 314. http://dx.doi.org/10.4103/0971-5916.198683.

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18

de la Calle-Martin, Oscar, Virginia Fabregat, Matilde Romero, Jesus Soler, Jordi Vives, and Jordi Yagüe. "Accll polymorphism of the p53 gene." Nucleic Acids Research 18, no. 16 (1990): 4963. http://dx.doi.org/10.1093/nar/18.16.4963.

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19

Min-Min, H., X. Ming-Rong, C. Ze-Yi, Y. Kai-Xuan, and S. Zhi-Lin. "Analysis of p53 codon 72 polymorphism and its association with human papillomavirus 16 and 18 E6 in Chinese cervical lesions." International Journal of Gynecologic Cancer 16, no. 6 (2006): 2004–8. http://dx.doi.org/10.1111/j.1525-1438.2006.00733.x.

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The aim of this study was to analysis the relationship between p53 codon 72 polymorphism with human papillomavirus (HPV) 16 and 18 E6 in Chinese cervical cancer. A total of 81 cervical squamous cancer (specimens of G1, G2, and G3 are 13, 24, and 44, respectively; and of stage IB, IIA, IIB, and IIIA are 15, 37, 24, and 5, respectively), 18 cervical adenocarcinoma, 88 cervical intraepithelial neoplasm (CIN) (specimens of CIN II and III are 30 and 58), and 60 normal cervical specimens were included in this study. Polymerase chain reaction was used to examine p53 genotypes and HPV 16 and 18 E6. Th

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Olkova, MV, VS Petrushenko, and GYu Ponomarev. "Analysis of 13 TP53 and WRAP53 polymorphism frequencies in russian populations." Features of HIV and SARS-CoV-2 coinfection in a pandemic, no. 2021(1) (January 2021): 30–39. http://dx.doi.org/10.24075/brsmu.2021.001.

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In the last decade the search for and annotation of human genome polymorphisms associated with phenotype have become particularly important concerning the opportunity of their use in medical and population genetics, pharmacogenomics and evolutionary biology. The study was aimed to calculate the frequencies and analyze the prevalence of 13 germline polymorphisms of two genes, ТР53 encoding the genome-keeper p53 protein and WRAP53 involved in regulation of p53 production, in 28 Russian populations. We obtained data on 9 exonic ТР53 variants (rs587781663, rs17882252, rs150293825, rs112431538, rs1

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Pandima Devi, K., B. Sivamaruthi, PV Kiruthiga, and S. Karutha Pandian. "Study of p53 codon 72 polymorphism and codon 249 mutations in Southern India in relation to age, alcohol drinking and smoking habits." Human & Experimental Toxicology 29, no. 6 (2009): 451–58. http://dx.doi.org/10.1177/0960327109354938.

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Germline polymorphisms of genes involved in different steps of tumorigenesis like p53, the tumor suppressor gene, are reported to determine the individual susceptibility to cancer. Lung cancer is one of the most common and lethal cancers and tobacco smoking remains its most important etiologic factors. The most frequently p53 mutated codons of lung cancer are 72 (exon 4) and 249 (exon 7). Since mutations in the p53 gene are present in ∼40% of all human lung cancers and are more common in smokers than in nonsmokers, we aimed to detect the status of p53 at codon 72 for Arg/Arg or Arg/Pro or Pro/

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Lima, Igor, Ambuja Navalkar, Samir K. Maji, Jerson L. Silva, Guilherme A. P. de Oliveira, and Elio A. Cino. "Biophysical characterization of p53 core domain aggregates." Biochemical Journal 477, no. 1 (2020): 111–20. http://dx.doi.org/10.1042/bcj20190778.

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Aggregation is the cause of numerous protein conformation diseases. A common facet of these maladies is the transition of a protein from its functional native state into higher order forms, such as oligomers and amyloid fibrils. p53 is an essential tumor suppressor that is prone to such conformational transitions, resulting in its compromised ability to avert cancer. This work explores the biophysical properties of early-, mid-, and late-stage p53 core domain (p53C) aggregates. Atomistic and coarse-grained molecular dynamics (MD) simulations suggest that early- and mid-stage p53C aggregates ha

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Vieira, Jussane, Afonso Nazário, and João Pesquero. "Abstract PO3-15-02: TP53 GENE POLYMORPHISM AT CODON 72 AS A RESPONSE PREDICTOR FOR NEOADJUVANT CHEMOTHERAPY." Cancer Research 84, no. 9_Supplement (2024): PO3–15–02—PO3–15–02. http://dx.doi.org/10.1158/1538-7445.sabcs23-po3-15-02.

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Abstract Introduction: Breast cancer is one of the most prevalent in women in the world and has shown extensive changes in treatment in recent decades. More patients are undergoing neoadjuvant chemotherapy in order to achieve pathological complete response (CPR) and perform less aggressive surgeries. CPR increases overall and disease-free survival and the decrease in tumor size increases the chances of conservative surgery. We have numerous studies that propose to discover CPR markers. Predictive factors of response to chemotherapy are important for treatment planning and the P53 gene, apoptos

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Klumb, Claudete Esteves Nogueira Pinto, Lídia Maria Magalhães de Resende, Eloísa Helena Tajara, Erika Cristina Pavarino Bertelli, Vivian Mary Rumjanek, and Raquel Ciuvalschi Maia. "p53 gene analysis in childhood B non - Hodgkin's lymphoma." Sao Paulo Medical Journal 119, no. 6 (2001): 212–15. http://dx.doi.org/10.1590/s1516-31802001000600006.

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CONTEXT: Mutations or deletions in the tumor-suppressor gene p53 are among the commonest genetic changes found in human neoplasms including breast, lung and bowel cancers. In hematological malignancies, p53 is most often mutated in Burkitt's lymphoma, with p53 mutations present in 30 to 40% of tumor samples and in 70% of cell lines. OBJECTIVE: To analyze the p53 gene alterations in child patients with B non-Hodgkin's lymphoma. DESIGN: Descriptive study. SETTING: Tertiary oncology care center. PARTICIPANTS: The study investigated 12 patients with childhood B non-Hodgkin's lymphoma (Burkitt's ly

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Arbel-Alon, S., J. Menczer, N. Feldman, M. Glezerman, L. Yeremin, and E. Friedman. "Codon 72 polymorphism of p53 in Israeli Jewish cervical cancer patients and healthy women." International Journal of Gynecologic Cancer 12, no. 6 (2002): 741–44. http://dx.doi.org/10.1136/ijgc-00009577-200211000-00009.

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Recently it has been found that the presence of homozygous arginine polymorphism at codon 72 of p53, represents a significant risk factor in the development of HPV-associated cervical cancer. The incidence of cervical carcinoma is persistently very low in Israeli Jewish women for unknown reasons. The incidence among those of North African origin is relatively higher. The aim of the present study was to assess the frequency distribution of the p53 homozygous arginine polymorphism in cervical cancer patients and in a population sample of healthy Israeli Jewish women in order to determine whether

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Jeong, J., Y. Chae, J. Kim, et al. "Association between P53 expression or TP53 codon 72 polymorphism and prognosis in patients with operated invasive breast cancer." Journal of Clinical Oncology 27, no. 15_suppl (2009): e22175-e22175. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.e22175.

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e22175 Background: The present study analyzed the impact of p53 expression and TP53 codon 72 polymorphism on the prognosis in patients with operated invasive breast cancer. Methods: Two hundred thirty-four patients with ductal breast cancer who underwent surgery with curative intent were enrolled in the present study. The tumor expressions of p53, ER, PR, and HER2 were graded immunohistochemically and TP53 codon 72 polymorphism was determined by a PCR-RFLP assay using genomic DNA extracted from paraffin-embedded tissue. Results: The median age was 49 (range, 24–82) years, and 134 (57.3%) patie

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Hayati, Lusia, and Siska Delvia. "Polymorphism of p53 Codon 72 Gene on Cervical Cancer Incidence in Malay Population." Archives of The Medicine and Case Reports 1, no. 1 (2020): 21–25. http://dx.doi.org/10.37275/amcr.v1i1.511.

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In Indonesia, the cases of cervical cancer are estimated at around 50 per 100.000 people. It was estimatedthattherearemore than1 millionwomenworldwidewho have cervical cancer,andmostofthemhave not been diagnosed yet or do not have access to screening and medical treatment. P53 codon 72 polymorphism can affect the risk of cervical cancerthrough the regulationofproliferationandcellapoptosis.The purpose of this research was to investigate the association between p53 codon 72 polymorphism and cases of cervical cancer. This research was observational analytic research. The research was done by exam

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Knabe, Lucie, Jessica Varilh, Anne Bergougnoux, et al. "CCSP G38A polymorphism environment interactions regulate CCSP levels differentially in COPD." American Journal of Physiology-Lung Cellular and Molecular Physiology 311, no. 4 (2016): L696—L703. http://dx.doi.org/10.1152/ajplung.00280.2016.

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Impaired airway homeostasis in chronic obstructive pulmonary disease (COPD) could be partly related to club cell secretory protein (CCSP) deficiency. We hypothesize that CCSP G38A polymorphism is involved and aim to examine the influence of the CCSP G38A polymorphism on CCSP transcription levels and its regulatory mechanisms. CCSP genotype and CCSP levels in serum and sputum were assessed in 66 subjects with stable COPD included in a 1-yr observational study. Forty-nine of them had an exacerbation. In an in vitro study, the impact on the CCSP promoter of 38G wild-type or 38A variant was assess

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Macdonald, Kimberley A., Maylis de Suremain, Zuoyu Zheng, Geoffrey A. Porter, Duane L. Guernsey, and Alan G. Casson. "P52 The p53 codon 72 polymorphism and risk for esophageal adenocarcinoma." Journal of Clinical Gastroenterology 40, Supplement 4 (2006): S209. http://dx.doi.org/10.1097/00004836-200609001-00137.

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Tortola, Silvia, Eugenio Marcuello, Isabel González, et al. "p53 and K-ras Gene Mutations Correlate With Tumor Aggressiveness But Are Not of Routine Prognostic Value in Colorectal Cancer." Journal of Clinical Oncology 17, no. 5 (1999): 1375. http://dx.doi.org/10.1200/jco.1999.17.5.1375.

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PURPOSE: p53 gene and K-ras mutations are among the most common genetic alterations present in colorectal cancer. The prognostic utility of such mutations remains controversial. The purpose of this study was to prospectively evaluate the prognostic significance of p53 and K-ras gene mutations in colorectal cancer. PATIENTS AND METHODS: One hundred forty patients were analyzed. Tumors belonging to the microsatellite mutator phenotype were excluded (n = 8). Mutations at the K-ras and p53 genes were detected and characterized by restriction fragment length polymorphism, single-strand conformation

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Beckman, G., R. Birgander, A. Själander, et al. "Is p53 Polymorphism Maintained by Natural Selection?" Human Heredity 44, no. 5 (1994): 266–70. http://dx.doi.org/10.1159/000154228.

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32

Helland, Åslaug, Anita Langerød, Hilde Johnsen, Anne O. Olsen, Eva Skovlund, and Anne-Lise Børresen-Dale. "p53 polymorphism and risk of cervical cancer." Nature 396, no. 6711 (1998): 530–31. http://dx.doi.org/10.1038/25034.

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Josefsson, Agnetha M., Patrik K. E. Magnusson, Nathalie Ylitalo, et al. "p53 polymorphism and risk of cervical cancer." Nature 396, no. 6711 (1998): 531. http://dx.doi.org/10.1038/25037.

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Hildesheim, Allan, Mark Schiffman, Louise A. Brinton, et al. "p53 polymorphism and risk of cervical cancer." Nature 396, no. 6711 (1998): 531–32. http://dx.doi.org/10.1038/25040.

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Storey, Alan, Miranda Thomas, Ann Kalita, et al. "p53 polymorphism and risk of cervical cancer." Nature 396, no. 6711 (1998): 532. http://dx.doi.org/10.1038/25043.

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Lancaster, J. M., H. A. Brownlee, R. W. Wiseman, and J. Taylor. "p53 polymorphism in ovarian and bladder cancer." Lancet 346, no. 8968 (1995): 182. http://dx.doi.org/10.1016/s0140-6736(95)91239-8.

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Campbell, IanG, DianaM Eccles, Bridget Dunn, Michael Davis, and Vivien Leake. "p53 polymorphism in ovarian and breast cancer." Lancet 347, no. 8998 (1996): 393–94. http://dx.doi.org/10.1016/s0140-6736(96)90569-3.

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Lanham, Stuart, Ian Campbell, Peter Watt, and Robert Gornall. "p53 polymorphism and risk of cervical cancer." Lancet 352, no. 9140 (1998): 1631. http://dx.doi.org/10.1016/s0140-6736(05)61083-5.

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Breda, Eduardo, Raquel Catarino, Hugo Sousa, Alexandra Maria Barros Santos, Daniela Pinto, and Rui Medeiros. "P017: P53 Polymorphism: Susceptibility to Nasopharyngeal Cancer." Otolaryngology–Head and Neck Surgery 137, no. 2_suppl (2007): P218. http://dx.doi.org/10.1016/j.otohns.2007.06.528.

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Gomes de Souza, Lessileia, Jacqueline Miranda de Lima, Ismael Dale Cotrim Guerreiro da Silva, and Nora Manoukian Forones. "P53 Arg72Pro Polymorphism in Gastric Cancer Patients." Journal of Gastrointestinal Cancer 40, no. 1-2 (2009): 41–45. http://dx.doi.org/10.1007/s12029-009-9078-7.

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Yung, W. C. W., M. H. Ng, J. S. T. Sham, and D. T. K. Choy. "p53 codon 72 polymorphism in nasopharyngeal carcinoma." Cancer Genetics and Cytogenetics 93, no. 2 (1997): 181–82. http://dx.doi.org/10.1016/s0165-4608(96)00219-1.

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Di Renzo, Laura, Santo Gratteri, Francesca Sarlo, Andrea Cabibbo, Carmen Colica, and Antonino De Lorenzo. "Individually Tailored Screening of Susceptibility to Sarcopenia Using p53 Codon 72 Polymorphism, Phenotypes, and Conventional Risk Factors." Disease Markers 2014 (2014): 1–10. http://dx.doi.org/10.1155/2014/743634.

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Background and Aim.p53 activity plays a role in muscle homeostasis and skeletal muscle differentiation; all pathways that lead to sarcopenia are related to p53 activities. We investigate the allelic frequency of the TP53 codon 72 in exon 4 polymorphism in the Italian female population and the association with appendicular skeletal muscle mass index in normal weight (NW), normal weight obese (NWO), and preobese-obese (Preob-Ob) subjects.Methods.We evaluated anthropometry, body composition, and p53 polymorphism in 140 women distinguished in NW, NWO, and Preob-Ob.Results.Arg*/Arg*genotype increas

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Calhoun, Eric S., Renee M. McGovern, Carol A. Janney, et al. "Host Genetic Polymorphism Analysis in Cervical Cancer." Clinical Chemistry 48, no. 8 (2002): 1218–24. http://dx.doi.org/10.1093/clinchem/48.8.1218.

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Abstract Background: The natural history of cervical cancer comprises a latency period that probably involves long-term immunologic tolerance of human papillomavirus infection. Identifying host determinants of viral persistence may help to better understand the mechanisms of tolerance and may lead to the development of tests that can allow more focused follow-up of high-risk individuals. Methods: Genotypic frequencies of 12 polymorphic loci in four candidate genes from 127 cervical cancer patients were compared with a control group of 108 female blood donors. Genotypes were determined by PCR a

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Hernandez, L., T. Fest, M. Cazorla, et al. "p53 gene mutations and protein overexpression are associated with aggressive variants of mantle cell lymphomas." Blood 87, no. 8 (1996): 3351–59. http://dx.doi.org/10.1182/blood.v87.8.3351.bloodjournal8783351.

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Mantle cell lymphoma (MCL) is molecularly characterized by bcl-1 rearrangement and cyclin D1/PRAD-1 gene overexpression. Some aggressive variants have been recognized with a blastic or large cell morphology, higher proliferative activity, and shorter survival. p53 gene mutations in lymphoid neoplasms have been detected mainly in high grade lymphomas and have been associated with tumor progression in follicular and small lymphocytic lymphomas. To determine the role of p53 alterations in MCL, we examined 35 typical and 8 aggressive variants (5 blastic and 3 large cell) of MCLs by a combination o

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Schiller, Joan H., Sudeshna Adak, Richard H. Feins, et al. "Lack of Prognostic Significance of p53 and K-ras Mutations in Primary Resected Non–Small-Cell Lung Cancer on E4592: A Laboratory Ancillary Study on an Eastern Cooperative Oncology Group Prospective Randomized Trial of Postoperative Adjuvant Therapy." Journal of Clinical Oncology 19, no. 2 (2001): 448–57. http://dx.doi.org/10.1200/jco.2001.19.2.448.

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PURPOSE: To determine the prognostic and predictive significance of p53 and K-ras mutations in patients with completely resected non–small-cell lung cancer (NSCLC). PATIENTS AND METHODS: Patients were randomized preoperatively to receive adjuvant postoperative radiotherapy (Arm A) or radiotherapy plus concurrent chemotherapy (Arm B). p53 protein expression was studied by immunohistochemistry (IHC) and p53 mutations in exons 5 to 8 were evaluated by single-strand conformational analysis. K-ras mutations in codons 12, 13, and 61 were determined using engineered restriction fragment length polymo

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Babiker, Nihad Elsadig. "Detection of p53 codon 72 polymorphisms among Sudanese women with recurrent spontaneous abortion." Science Progress and Research 2, no. 2 (2022): 588–93. http://dx.doi.org/10.52152/spr/2022.175.

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Recurrent Spontaneous abortion (RSA) is defined as consecutive pregnancy loss before 20 weeks of gestation. This study aimed to detect p53 codon 72 polymorphisms among Sudanese women with recurrent spontaneous abortion. A case-control study was conducted at the national centre of neurological sciences, Khartoum, Sudan. All patients attending the obese and gaina unit at Ibraheim Malike teaching hospital and diagnosed with recurrent spontaneous were included. In addition, healthy women with no history of abortion were selected as a control group. 5 ml of blood for each participant was collected

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Du, M., H. Peng, N. Singh, PG Isaacson, and L. Pan. "The accumulation of p53 abnormalities is associated with progression of mucosa-associated lymphoid tissue lymphoma." Blood 86, no. 12 (1995): 4587–93. http://dx.doi.org/10.1182/blood.v86.12.4587.bloodjournal86124587.

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The genetic mechanisms underlying the genesis of low-grade mucosa- associated lymphoid tissue (MALT) lymphomas and their transformation into high-grade lymphoma are poorly understood. p53 inactivation, commonly caused by mutation and allele loss, has been shown to play an important role in the early development and/or the late disease progression of many human tumors including lymphoid malignancies and, thus, may also be important in MALT lymphomagenesis. We examined 75 cases (48 low grade and 27 high grade) of MALT lymphoma for p53 allele loss and mutation as well as protein accumulation. DNA

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Verheijen, F. M., M. Sprong, J. M. E. Kloosterman, G. Blaauw, J. H. H. Thijssen, and M. A. Blankenstein. "TP53 Mutations in Human Meningiomas." International Journal of Biological Markers 17, no. 1 (2002): 42–48. http://dx.doi.org/10.1177/172460080201700105.

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Overexpression of p53 has been reported to play a role in the development of neoplasms of the central nervous system. Meningiomas are generally benign intracranial tumors originating from the meninges. Overexpression of the p53 protein in meningiomas and an association with histological type and recurrence has been reported. Mutation of the TP53 gene leads to a more stable p53 protein in quantities high enough for detection by immunohistochemistry. In the search for these mutations the core domain of the TP53 gene of meningiomas has been analyzed. Only a very low incidence of mutations was rep

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Haque, Shabirul, Jennifer Nieto, Hyunjoo Lee, Nicholas Chiorazzi, and Patricia Mongini. "Evidence for Allelic Exclusion of p53 within Single Sorted Human B Cells." Blood 118, no. 21 (2011): 1122. http://dx.doi.org/10.1182/blood.v118.21.1122.1122.

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Abstract Abstract 1122 The survival of replicating B cells, with DNA damage arising from oxidative stress and/or activation-induced cytosine deaminase (AID), appears in part to be under p53 control. Importantly, a common C>G single nucleotide polymorphism (SNP) within codon 72 of p53 influences p53 function. Among other differences, p53-72R (CGC=Arginine) is notably more effective than p53-72P (CCC=Proline) at inducing apoptosis. The SNP has been linked to clinical outcome in multiple settings, including malignancy. Most individuals in the US population display heterozygosity. In this study

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Matlashewski, G. J., S. Tuck, D. Pim, P. Lamb, J. Schneider, and L. V. Crawford. "Primary structure polymorphism at amino acid residue 72 of human p53." Molecular and Cellular Biology 7, no. 2 (1987): 961–63. http://dx.doi.org/10.1128/mcb.7.2.961-963.1987.

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We analyzed p53 cDNA and genomic clones from a variety of normal and transformed cells. Sequence analysis of these clones revealed that amino acid residue 72 can be an arginine, proline, or cysteine. This single codon difference results in electrophoretically distinct forms of human p53 seen in normal and transformed cells.

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