Indian Journal of Cancer
Home  ICS  Feedback Subscribe Top cited articles Login 
Users Online :23139
Small font sizeDefault font sizeIncrease font size
Navigate here
  Search
 
  
Resource links
 ╗  Similar in PUBMED
 ╗  Search Pubmed for
 ╗  Search in Google Scholar for
 ╗Related articles
 ╗  Article in PDF (526 KB)
 ╗  Citation Manager
 ╗  Access Statistics
 ╗  Reader Comments
 ╗  Email Alert *
 ╗  Add to My List *
* Registration required (free)  

 
  In this article
 ╗  Abstract
 ╗ Introduction
 ╗  Materials and Me...
 ╗ Results
 ╗ Discussion
 ╗ Acknowledgments
 ╗  References
 ╗  Article Figures
 ╗  Article Tables

 Article Access Statistics
    Viewed3880    
    Printed139    
    Emailed4    
    PDF Downloaded440    
    Comments [Add]    
    Cited by others 14    

Recommend this journal

 

  Table of Contents  
ORIGINAL ARTICLE
Year : 2011  |  Volume : 48  |  Issue : 3  |  Page : 298-302
 

TP53 PIN3 polymorphism associated with breast cancer risk in Iranian women


1 Department of Anatomical Sciences, Guilan University of Medical Sciences, Rasht, Iran
2 Department of Anatomical Sciences, Isfahan University of Medical Sciences, Isfahan, Iran
3 Department of Genetic, Isfahan University of Medical Sciences, Isfahan, Iran

Date of Web Publication14-Sep-2011

Correspondence Address:
M Faghani
Department of Anatomical Sciences, Guilan University of Medical Sciences, Rasht
Iran
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0019-509X.84925

Rights and Permissions

 ╗ Abstract 

Background: Breast cancer is one of the most common cancers in Iranian women. The p53 gene plays a principal role in genomic stability, and its function varies according to polymorphisms. The aim of our study was to determine the relationship between the intron3 16bp duplication polymorphism of the p53 gene and breast cancer in Iranian women. Materials and Methods: We performed a case-control study among 145 patients with invasive ductal carcinoma of the breast and 145 controls in Isfahan, Iran. The distribution of the intron3 16bp duplication polymorphism was determined by polymerase chain reaction (PCR). The relationship between clinicopathological data and the PIN3 polymorphism was examined using chi-squared analysis. Results: A significant difference was observed in the polymorphism variants in breast cancer specimens compared with controls (P < .001). Among the cancer patients, 59.9% were below the age of 50 years; and 67.5% of the patients in this group had the intron3 16bp duplication polymorphism. Conclusions: PIN3 Ins 16bp duplication polymorphism is a genetically predisposing factor for breast cancer development in Iranian women and may be causal in patients under the age of 50 years.


Keywords: Breast cancer, Iranian women, PIN3 polymorphism, TP53 genotypes


How to cite this article:
Faghani M, Ghasemi F M, Nikhbakht M, Salehi M. TP53 PIN3 polymorphism associated with breast cancer risk in Iranian women. Indian J Cancer 2011;48:298-302

How to cite this URL:
Faghani M, Ghasemi F M, Nikhbakht M, Salehi M. TP53 PIN3 polymorphism associated with breast cancer risk in Iranian women. Indian J Cancer [serial online] 2011 [cited 2019 Dec 6];48:298-302. Available from: http://www.indianjcancer.com/text.asp?2011/48/3/298/84925



 ╗ Introduction Top


The p53 tumor suppressor gene [Online Mendelian Inheritance in Man (OMIM) no. 191170] codes a 53 kilodalton (KD) protein, which plays an essential role in the cell cycle. [1] DNA damage increases p53 expression, resulting in cell cycle arrest, apoptosis and DNA repair. [2] Somatic mutations in p53 gene exist in more than half of human cancers. [3] It has been shown that mutations in the splice, donor and acceptor sites, intron and promoter elements, may be important in regulating gene expression. [4] In addition to mutation, p53 gene polymorphisms have a role in breast cancer development. [5] Among the 14 polymorphisms of p53, most studies are performed on Arg72pro (rs1042522), intron3 (rs17878362) and intron6 MspI (rs17880604). [6] There is a relationship between Arg72pro polymorphism and development of cancers. [7],[8],[9],[10],[11],[12] In addition, some researchers have reported polymorphism within introns or non-coding regions such as intron 3, 6. [13],[14],[15] ; 16 base pair (bp) duplication in intron 3 of the TP53 gene (PIN3 Ins16bp) polymorphism may be associated with cancers. [16] Some studies have reported a relationship between PIN3 p53 polymorphism and breast cancer. [15],[17] However, this is a controversial subject. [18],[19]

Breast cancer is the most common cancer in women and the second leading cause of death worldwide. [20] According to the World Health Organization, 2.1 million cases are identified yearly. [21] Breast cancer is the first cancer to have been diagnosed in Iranian women (21.4% of all cancers) and the first cause of cancer-related death. [22] The age at diagnosis of breast cancer in Iranian women is approximately one decade lower than that in women of other countries, [23] and approximately 10% of these cancers have been reported in Isfahan. [24] There have been studies on the Arg72pro polymorphism in breast cancer among Iranian women, [11],[25],[26] but there is no report about the PIN3 polymorphism in Iran. Thus we aimed to study the relationship, if any, between the PIN3 polymorphism of the p53 gene and the risk of breast cancer in Iranian women in Isfahan.


 ╗ Materials and Methods Top


Blood samples were obtained from 145 patients with invasive ductal breast carcinoma (average age, 23-79 years; mean age, 50 years), referred by the hospital of Isfahan University of Medical Sciences in the period 2003-2006. All cases were histologically confirmed by our Pathology Department. Control group consisted of 145 age-matched women without known malignancy or autoimmune disease, from whom blood was also taken. Prior to commencement of the study, all patients provided informed consent and the study was approved by our institutional ethics committee, Samples were divided into two groups: 86 patients were premenopausal, and 59 were postmenopausal; and among controls, the corresponding numbers were 87 and 58, respectively.

Using high pure polymerase chain reaction (PCR) template preparation DNA isolation kit (Roche), genomic DNA was extracted from blood samples, according to manufacturer's instructions. As much as 100 to 300 ng of DNA was used as template in a 25- mL PCR reaction mixture containing 1.5 mmol MgCl 2 , 1 U Taq polymerase (Cinnagen, Iran) and 2 mmol either of the primer pairs. For negative control, no DNA was added or included in each run. The forward and reverse primers sequences were used to amplify the TP53 PIN3 Ins16bp polymorphism in intron3 as follows [27] :

F: 5'-CTGAAAACAACGTTCTGGTA-3'

R: 5'-AAGGGGGACTGTAGATGGGTG-3'

PCR cycling conditions were implemented with an initial denaturation step for 5 minutes at 95°C, followed by 35 cycles: Denaturation at 94°C for 30 seconds, annealing at 60°C for 30 seconds with extension at 72°C for 60 seconds. A final extension step was performed at 72°C for 5 minutes. The PCR product was electrophoresed on 15% polyacrylamide gels and stained with ethidium bromide. For detection of intron3 polymorphism, we considered that the amplification yielded 119 or A1 allele (no duplication) and the variant 135-bp fragments or A2 allele (with 16-bp duplication) for the wild-type, depending on the absence or the presence of the 16-bp duplication in the genomic DNA. We observed both bands in the heterozygote [Figure 1]. Data such as tumor grade and size, family history, date of diagnosis, lymph node metastasis, and progesterone and estrogen receptor were also recorded.
Figure 1: Detection of the P53 PIN3 polymorphism by PCR amplification. The PCR products were electrophoresed on 15% polyacrylamide gel and were stained with ethidium bromide. Lanes 1, 2, 3: Positive for A1 allele (no duplication) Lanes 4, 5: Positive for A2 allele (16-bp duplication) and A1 allele Lane N: Negative control. L: Gene ruler TM DNA ladder. The sizes of the bands are indicated beside the gel photo

Click here to view


For statistical analysis, we used both SPSS (version 16) program and Hardy-Weinberg Equilibrium calculator. The Pearson chi-squared test was used to assess statistical significance. The odds ratio with 95% confidence interval (95% CI) was used to confirm the association between TP53 polymorphic genotypes and breast cancer risk. We used Kruskal-Wallis ANOVA test to determine the correlation between clinicopathological data and PIN3 polymorphisms. The distribution of two alleles in our groups was tested by Hardy-Weinberg Equilibrium calculator (http://ihg.gsf.de/cgi-bin/hw/hwa1.p1.).


 ╗ Results Top


The distribution of PIN3 genotype frequencies among the two groups is not in agreement with that expected under Hardy-Weinberg Equilibrium [Table 1]. Histopathologic tumor grade, tumor size, and other clinicopathological data are presented in [Table 2]. There was a statistically significant difference in the distribution of the A1 and A2 alleles between the case and control groups. The genotype distribution for insertion of the 16-bp duplication polymorphism was 14.5% for homozygotes (NoIns), 85.5% for heterozygotes and 0% for homozygotes (Ins) in breast cancer patients [Table 1]. In the control group, the genotype distribution was 42.8%, 57.2% and 0% for the homozygotes (NoIns), heterozygotes and homozygotes (Ins), respectively. We found that the A1/A2 genotype carriers had a 4.41-fold (95% CI, 2.5-7.78; P < .001) increased risk of breast cancer. The allelic frequency was strongly associated with the A1/A2 genotype (P = .001; odds ratio= 1.85, 1.37-2.5). In addition, out of 145 patients, we used the data of 77 (53.1%) patients with lymph node metastasis; 70.5% of these had the A1/A2 genotype.
Table 1: Demographics of breast cancer patients (n = 145) and controls (n = 145)

Click here to view
Table 2: Association of clinicopathological variables with p53 PIN3 genotypes

Click here to view


Our data showed that neither estrogen nor progesterone receptor expression was associated with the presence of a specific genotype [Table 2]. On the other hand, we considered the relationship between the PIN3 polymorphism and menopause, tumor grade and tumor size. No relationship was found between histologic type and tumor size, genotype and menopause (P > .05). These data showed that 64.1% of cancer patients were in the "before menopause" age category and 67.5% of this group had the A1/A2 genotype. The Chi-squared test revealed no significant differences between the two menopausal groups and the genotypes of the p53 gene (OR = 1.02; 95% CI, 0.64-1.64; P = .5).


 ╗ Discussion Top


Breast cancer is a heterogeneous disease, reflected in the varying responses to adjuvant therapy. [28] Molecular changes, including the P53 gene mutation and polymorphism, are related to growth and development of different cancers. [29] Researchers have shown that the Arg72pro P53 gene polymorphism is a risk factor in lung, colorectal, bladder and breast cancers. [7],[9],[19],[30],[31] Polymorphisms can affect protein function or expression; polymorphisms in genes involved in DNA repair, cell-cycle control, estrogen production and carcinogen metabolism could predispose individuals to developing breast malignancy. [27] Past studies have reported that genetic variants in the promoter or intron regions could alter gene expression; this variant may not have direct functional implications but can be linked to other polymorphisms and can affect the function related to wild-type sequence. [27]

Our results are in agreement with those of the study by Sayhan and Wn, who described the association between PIN3 Ins 16-bp duplication polymorphisms and risk of ovarian and lung cancer. [32],[14] However, contrary to the finding of our study, there was no correlation reported about this polymorphism in Caucasian Americans with ovarian or bladder cancer or in Turkish women with breast cancer. [33],[15]

Hrstka and Trifa could not find a relationship between the PIN3 polymorphism and breast cancer, and attributed differences to race or geographical distribution. [18],[19]

In our study, we investigated the frequency of 16 bp duplication polymorphism intron3 of p53 in 145 female patients with invasive ductal breast carcinoma and 145 healthy controls from the central part (Isfahan province) of Iran. We observed an association between the A1/A2 genotype and higher risk of breast cancer among patients, showing that TP53 PIN3 Ins 16-bp duplication polymorphism increased susceptibility for breast cancer in Iranian women. The frequency of the inherited 16bp insertion statistically differed between patients and controls. Our results confirmed those of studies performed on ovarian, lung and breast cancers, [14],[32],[34] but were contrary to those of other studies. [15],[33] The age range of patients was 23-79 years, and most of the younger women (<50 years) had the TP53 PIN3 Ins 16-bp duplication polymorphism. Data in Iranian patients shows that age of patients at diagnosis of breast cancer in Iran is lower than that of patients in other countries and that tumors are more aggressive compared to those in patients in other countries. [23],[35] Our data, which showed a high level of lymph node metastasis (53.1%), confirmed this claim.

It has been suggested that PIN3 Ins 16-bp duplication polymorphism and other polymorphisms of p53 (72Arg) affect the DNA repair gene, resulting in alteration of p53 function. Some investigators have reported that the Arg-A2 haplotype has a positive association with cancer [14],[36] and that the A2 allele is associated with decreased apoptotic and DNA repair functions. [34] Due to the high frequency of the A2 (42.8%) and Arg (75.4%) alleles (data not shown) in our patients, it appears that linkage between the two aforementioned factors possibly has greater effect in the development of invasive cancers such as ductal carcinoma in Iranian (Isfahanian) women. In addition, in our previous work we showed that the Arg/Arg polymorphism of p53 codon 72 is related to breast cancer development (data not shown). [11]

In conclusion, our findings indicate that Iranian women with TP53 PIN3 Ins16bp polymorphism and Arg/Arg polymorphism may have a higher risk for developing breast cancer; these findings require confirmation with a larger sample size. Because polymorphisms can be considered potent factors for breast cancer development, this data can be considered as part of a genetic profile in high-risk women and would create an effective approach to aid in early diagnosis and treatment.


 ╗ Acknowledgments Top


We thank the Deputy Research Isfahan University of Medical Sciences for financial support under grant number 185191. We also thank the faculty of the Biotechnology Department of Pharmacy, Isfahan University of Medical Sciences; and Ms. Fatemeh Moazzen for their technical support.

 
 ╗ References Top

1.Williams C, Norberg T, Ahmadian A, Pontén F, Bergh J, Inganäs M, et al. Assessment of sequence-based p53 gene analysis in human breast cancer: Messenger RNA in comparison with genomic DNA targets. Clin Chem 1998;44:455-62.  Back to cited text no. 1
    
2.Rahko E, Blanco G, Bloigu R, Soini Y, Talvensaari-Mattila A, Jukkola A. Adverse outcome and resistance to adjuvant antiestrogen therapy in node-positive postmenopausal breast cancer patients-The role of p53. Breast 2006;15:69-75.  Back to cited text no. 2
    
3.Soussi T, Béroud C. Assessing TP53 status in human tumours to evaluate clinical outcome. Nat Rev Cancer 2001;1:233-40.  Back to cited text no. 3
    
4.Lozano G, Levine AJ. Tissue-specific expression of p53 in transgenic mice is regulated by intron sequences. Mol Carcinog 1991;4:3-9.  Back to cited text no. 4
    
5.Bai L, Zhu W-G. P53: Structure, Function and Therapeutic Applications. J Cancer Mol 2006;2:141-53.  Back to cited text no. 5
    
6.Gemignani F, Moreno V, Landi S, Moullan N, Chabrier A, Gutiérrez-Enríquez S, et al. A TP53 polymorphism is associated with increased risk of colorectal cancer and with reduced levels of TP53 mRNA. Oncogene 2004;11;23:1954-6.  Back to cited text no. 6
    
7.Zehbe I, Voglino G, Wilander E, Genta F, Tommasino M. Codon 72 polymorphism of p53 and its association with cervical cancer. Lancet 1999;17;354:218-9.  Back to cited text no. 7
    
8.Fan R, Wu MT, Miller D, Wain JC, Kelsey KT, Wiencke JK, et al. The p53 codon 72 polymorphism and lung cancer risk. Cancer Epidemiol Biomarkers Prev 2000;9:1037-42.  Back to cited text no. 8
    
9.Soulitzis N, Sourvinos G, Dokianakis DN, Spandidos DA. P53 codon 72 polymorphism and its association with bladder cancer. Cancer Lett 2002;28;179:175-83.  Back to cited text no. 9
    
10.Buyru N, Tigli H, Dalay N. P53 codon 72 polymorphism in breast cancer. Oncol Rep 2003;10:711-4.  Back to cited text no. 10
    
11.Faghani M, Nikhbakht M, Salehi M, Rabbani M, Talebi A, SoleimanieB, etal. Investigation of p53 codon 72 polymorphism in breast cancer in isfahan. Vol. 84. Isfahan, Iran: Isfahan University of Medical Sciences; 2007. p. 26-33.  Back to cited text no. 11
    
12.Pérez LO, Abba MC, Dulout FN, Golijow CD. Evaluation of p53 codon 72 polymorphism in adenocarcinomas of the colon and rectum in La Plata, Argentina. World J Gastroenterol 2006;7;12:1426-9.  Back to cited text no. 12
    
13.Tommiska J, Eerola H, Heinonen M, Salonen L, Kaare M, Tallila J, et al. Breast cancer patients with p53 Pro72 homozygous genotype have a poorer survival. Clin Cancer Res 2005;11:5098-103.  Back to cited text no. 13
    
14.Wu X, Zhao H, Amos CI, Shete S, Makan N, Hong WK, et al. P53 Genotypes and Haplotypes Associated With Lung Cancer Susceptibility and Ethnicity. J Natl Cancer Inst 2002;94:681-90.  Back to cited text no. 14
    
15.Buyru N, Altinisik J, Demokan S, Dalay N. P53 genotypes and haplotypes associated with risk of breast cancer. Cancer Detect Prev 2007;31:207-13.  Back to cited text no. 15
    
16.Birgander R, Själander A, Rannug A, Alexandrie AK, Sundberg MI, Seidegård J, et al. P53 polymorphisms and haplotypes in lung cancer. Carcinogenesis 1995;16:2233-6.  Back to cited text no. 16
    
17.Själander A, Birgander R, Hallmans G, Cajander S, Lenner P, Athlin L, et al. P53 polymorphisms and haplotypes in breast cancer. Carcinogenesis 1996;17:1313-6.  Back to cited text no. 17
    
18.Hrstka R, Beranek M, Klocova K, Nenutil R, Vojtesek B. Intronic polymorphisms in TP53 indicate lymph node metastasis in breast cancer. Oncol Rep 2009;22:1205-11.  Back to cited text no. 18
    
19.Trifa F, Karray-Chouayekh S, Mabrouk I, Baccouche S, Khabir A, Sellami-Boudawara T, et al. Haplotype analysis of p53 polymorphisms: Arg72Pro, Ins16bp and G13964C in Tunisian patients with familial or sporadic breast cancer. Cancer Epidemiol 2010;34:184-8.  Back to cited text no. 19
    
20.Parkin DM, Bray F, Ferlay J, Pisani P. Global cancer statistics, 2002. CA Cancer J Clin 2005;55:74-108.  Back to cited text no. 20
    
21.Jemal A, Murray T, Ward E, Samuels A, Tiwari RC, Ghafoor A, et al. Cancer statistics 2005. CA Cancer J Clin 2005;55:10-30.  Back to cited text no. 21
    
22.Behjati F, Atri M, Najmabadi H, Nouri K, Zamani M, Mehdipour P. Prognostic value of chromosome 1 and 8 copy number in invasive ductal breast carcinoma among Iranian women: An interphase FISH analysis. Pathol Oncol Res 2005;11:157-63.  Back to cited text no. 22
    
23.Atri M, Jafarimojarrad E, Javidroozi M, Mehdipour P. Lack of association between early onset of breast cancer and numbers of affected relatives in an Iranian population. Fam Cancer 2003;2:117-8.  Back to cited text no. 23
    
24.Asadpour, [Isfahan: First degree of cancer in Iran], in Jame jam journal 2006;15-16. (In Persian)   Back to cited text no. 24
    
25.Khadang B, Fattahi MJ, Talei A, Dehaghani AS, Ghaderi A. Polymorphism of TP53 codon 72 showed no association with breast cancer in Iranian women. Cancer Genet Cytogenet 2007;173:38-42.  Back to cited text no. 25
    
26.Kazemi M, Salehi Z, Chakosari RJ. TP53 codon 72 polymorphism and breast cancer in northern Iran. Oncol Res 2009;18:25-30.  Back to cited text no. 26
    
27.Powell BL, van Staveren IL, Roosken P, Grieu F, Berns EM, Iacopetta B. Associations between common polymorphisms in TP53 and p21WAF1/Cip1 and phenotypic features of breast cancer. Carcinogenesis 2002;23:311-5.  Back to cited text no. 27
    
28.Perou CM, Sørlie T, Eisen MB, van de Rijn M, Jeffrey SS, Rees CA, et al. Molecular portraits of human breast tumours. Nature 2000;17;406:747-52.  Back to cited text no. 28
    
29.Brankovic-Magic MV, Jankovic RN, Dobricic JD, Borojevic ND, ZM, Radulovic SS. TP53 mutations in breast cancer: Association with ductal histology and early relapse of disease. Int J Biol Markers 2008;23:147-53.  Back to cited text no. 29
    
30.Mahasneh AA, Abdel-Hafiz SS. Polymorphism of p53 gene in Jordanian population and possible associations with breast cancer and lung adenocarcinoma. Saudi Med J 2004;25:1568-73.  Back to cited text no. 30
    
31.Zhang Z, Wang M, Wu D, Wang M, Tong N, Tian Y, et al. P53 codon 72 polymorphism contributes to breast cancer risk: A meta-analysis based on 39 case-control studies. Breast Cancer Res Treat 2010;120:509-17.  Back to cited text no. 31
    
32.Sayhan N, Yazici H, Budak M, Bitisik O, Dalay N. P53 codon 72 genotypes in colon cancer. Association with human papillomavirus infection. Res Commun Mol Pathol Pharmacol 2001;109:25-34.  Back to cited text no. 32
    
33.Lancaster JM, Brownlee HA, Wiseman RW, Taylor J. P53 polymorphism in ovarian and bladder cancer. Lancet 1995;346:182.  Back to cited text no. 33
    
34.Wang-Gohrke S, Becher H, Kreienberg R, Runnebaum IB, Chang-Claude J. Intron 3 16 bp duplication polymorphism of p53 is associated with an increased risk for breast cancer by the age of 50 years. Pharmacogenetics 2002;12:269-72.  Back to cited text no. 34
    
35.Montazeri A, Ebrahimi M, Mehrdad N, Ansari M, Sajadian A. Delayed presentation in breast cancer: A study in Iranian women. BMC Womens Health 2003;3:4.  Back to cited text no. 35
    
36.Weston A, Pan CF, Ksieski HB, Wallenstein S, Berkowitz GS, Tartter PI, et al. P53 haplotype determination in breast cancer. Cancer Epidemiol Biomarkers Prev 1997;6:105-12.  Back to cited text no. 36
    


    Figures

  [Figure 1]
 
 
    Tables

  [Table 1], [Table 2]

This article has been cited by
1 Evaluation of clinical utility of P53 gene variations in repeated implantation failure
Milad Mohammadzadeh,Saeid Ghorbian,Mohammad Nouri
Molecular Biology Reports. 2019; 46(3): 2885
[Pubmed] | [DOI]
2 Transcriptome profiling revealed multiple genes and ECM-receptor interaction pathways that may be associated with breast cancer
Yulong Bao,Li Wang,Lin Shi,Fen Yun,Xia Liu,Yongxia Chen,Chen Chen,Yanni Ren,Yongfeng Jia
Cellular & Molecular Biology Letters. 2019; 24(1)
[Pubmed] | [DOI]
3 Association between polymorphisms in TP53 and MDM2 genes and susceptibility to prostate cancer
Mohammad Hashemi,Shadi Amininia,Mahboubeh Ebrahimi,Nasser Simforoosh,Abbas Basiri,Seyed Amir Mohsen Ziaee,Behzad Narouie,Mehdi Sotoudeh,Mohammad Javad Mollakouchekian,Esmaeil Rezghi Maleki,Hamideh Hanafi-Bojd,Maryam Rezaei,Gholamreza Bahari,Mohsen Taheri,Saeid Ghavami
Oncology Letters. 2017; 13(4): 2483
[Pubmed] | [DOI]
4 Effect of TP53 16-bp and ▀-TrCP 9-bp INS/DEL polymorphisms in relation to risk of breast cancer
Ebrahim Eskandari-Nasab,Mohammad Hashemi,Shadi Amininia,Mahboubeh Ebrahimi,Maryam Rezaei,Seyed Mehdi Hashemi
Gene. 2015; 568(2): 181
[Pubmed] | [DOI]
5 Differences in Incidence, Mortality and Survival of Breast Cancer by Regions and Countries in Asia and Contributing Factors
Yeonju Kim,Keun-Young Yoo,Marc T Goodman
Asian Pacific Journal of Cancer Prevention. 2015; 16(7): 2857
[Pubmed] | [DOI]
6 Association of TP53 PIN3 polymorphism with breast cancer in Moroccan population
Chaymaa Marouf,Amal Tazzite,Brehima DiakitÚ,Hassan Jouhadi,Abdellatif Benider,Sellama Nadifi
Tumor Biology. 2014;
[Pubmed] | [DOI]
7 Intronic polymorphisms of antionkogene TP53 in patients with indolent variants of non-Hodgkin lymphomas
E. N. Voropaeva,M. I. Voevoda,T. I. Pospelova,V. N. Maksimov
Advances in Gerontology. 2014; 4(1): 42
[Pubmed] | [DOI]
8 Association of P53 (-16ins-Pro) Haplotype with the Decreased Risk of Differentiated Thyroid Carcinoma in Iranian-Azeri Patients
Roghayeh Dehghan,Mohammad Ali Hosseinpour Feizi,Nasser Pouladi,Esmaeil Babaei,Vahid Montazeri,Ashraf Fakhrjoo,Ayda Sedaei,Parvin Azarfam,Masoumeh Nemati
Pathology & Oncology Research. 2014;
[Pubmed] | [DOI]
9 TP53 Polymorphisms in Sporadic North Indian Breast Cancer Patients
Sarika Sharma,Vasudha Sambyal,Kamlesh Guleria,Mridu Manjari,Meena Sudan,Manjit Singh Uppal,Neeti Rajan Singh,Darpan Bansal,Arun Gupta
Asian Pacific Journal of Cancer Prevention. 2014; 15(16): 6871
[Pubmed] | [DOI]
10 Lack of Association of Intron 3 16 bp Polymorphism of TP53 with Breast Cancer among Iranian-Azeri Patients
Nasser Pouladi,Shideh Montasser Kouhsari,Mohammadali Hosseinpour Feizi,Roghayeh Dehghan,Parvin Azarfam,Davoud Farajzadeh
Asian Pacific Journal of Cancer Prevention. 2014; 15(6): 2631
[Pubmed] | [DOI]
11 Intron 3 Sixteen Base Pairs Duplication Polymorphism of P53 Contributes to Breast Cancer Susceptibility: Evidence from Meta-Analysis
Wu, D. and Zhang, Z. and Chu, H. and Xu, M. and Xue, Y. and Zhu, H. and Zhang, Z.
PLoS ONE. 2013; 8(4)
[Pubmed]
12 Intron 3 Sixteen Base Pairs Duplication Polymorphism of P53 Contributes to Breast Cancer Susceptibility: Evidence from Meta-Analysis
Dongmei Wu,Zhizhong Zhang,Haiyan Chu,Ming Xu,Yao Xue,Haixia Zhu,Zhengdong Zhang,Gayle E. Woloschak
PLoS ONE. 2013; 8(4): e61662
[Pubmed] | [DOI]
13 p.R72P, PIN3 Ins16bp Polymorphisms of TP53 and CCR5Δ32 in North Indian breast cancer patients
Guleria, K. and Sharma, S. and Manjari, M. and Uppal, M.S. and Singh, N.R. and Sambyal, V.
Asian Pacific Journal of Cancer Prevention. 2012; 13(7): 3305-3311
[Pubmed]
14 p.R72P, PIN3 Ins16bp Polymorphisms of TP53 and CCR5?32 in North Indian Breast Cancer Patients
Kamlesh Guleria,Sarika Sharma,Mridu Manjari,Manjit Singh Uppal,Neeti Rajan Singh,Vasudha Sambyal
Asian Pacific Journal of Cancer Prevention. 2012; 13(7): 3305
[Pubmed] | [DOI]



 

Top
Print this article  Email this article
 

    

  Site Map | What's new | Copyright and Disclaimer
  Online since 1st April '07
  ę 2007 - Indian Journal of Cancer | Published by Wolters Kluwer - Medknow