Esophageal squamous cell carcinomas with DNA replication errors (RER + ) are associated with p16/pRb loss and wild-type p53

2001 ◽  
Vol 127 (10) ◽  
pp. 603-612 ◽  
Author(s):  
Robin Mathew ◽  
Sonia Arora ◽  
Meera Mathur ◽  
Ranju Ralhan ◽  
Tushar Chattopadhyay
2000 ◽  
Vol 7 (5) ◽  
pp. 749-756 ◽  
Author(s):  
Lisa S St. John ◽  
Edward R Sauter ◽  
Meenhard Herlyn ◽  
Samuel Litwin ◽  
Karen Adler-Storthz

2020 ◽  
Vol 21 (21) ◽  
pp. 8091
Author(s):  
Natalia Rakislova ◽  
Laia Alemany ◽  
Omar Clavero ◽  
Adela Saco ◽  
Aureli Torné ◽  
...  

Human papillomavirus (HPV)-independent vulvar squamous cell carcinomas (VSCC) and its precursors frequently harbour TP53 mutations. Recently, six p53 immunohistochemical (IHC) patterns have been defined, which have shown strong correlation with TP53 mutation status. However, few studies have applied this new six-pattern framework and none of them exhaustively compared p53 IHC positivity and patterns between invasive VSCC and adjacent skin lesion. We performed p53 IHC in a series of 779 HPV-independent VSCC with adjacent skin and evaluated the IHC slides following the newly described classification. Some 74.1% invasive VSCC showed abnormal p53 IHC staining. A skin lesion was identified in 450 cases (57.8%), including 254 intraepithelial precursors and 196 inflammatory/reactive lesions. Two hundred and ten of 450 (47%) VSCC with associated skin lesions showed an abnormal p53 IHC stain, with an identical staining pattern between the VSCC and the adjacent skin lesion in 80% of the cases. A total of 144/450 (32%) VSCC showed wild-type p53 IHC both in the invasive VSCC and adjacent skin lesion. Finally, 96/450 (21%) VSCC showed p53 IHC abnormal staining in the invasive VSCC but a wild-type p53 staining in the skin lesion. Most of the discordant cases (70/96; 73%) showed adjacent inflammatory lesions. In conclusion, the p53 IHC staining and pattern are usually identical in the VSCC and the intraepithelial precursor.


Genetics ◽  
1996 ◽  
Vol 142 (3) ◽  
pp. 717-726 ◽  
Author(s):  
Polina V Shcherbakova ◽  
Youri I Pavlov

Abstract The base analog 6-N-hydroxylaminopurine (HAP) induces bidirectional GC → AT and AT → GC transitions that are enhanced in DNA polymerase ϵ and δ 3′ → 5′ exonuclease-deficient yeast mutants, pol2-4 and pol3-01, respectively. We have constructed a set of isogenic strains to determine whether the DNA polymerases δ and ϵ contribute equally to proofreading of replication errors provoked by HAP during leading and lagging strand DNA synthesis. Site-specific GC → AT and AT → GC transitions in a Pol→, pol2-4 or pol3-01 genetic background were scored as reversions of ura3 missense alleles. At each site, reversion was increased in only one proofreading-deficient mutant, either pol2-4 or pol3-01, depending on the DNA strand in which HAP incorporation presumably occurred. Measurement of the HAP-induced reversion frequency of the ura3 alleles placed into chromosome III near to the defined active replication origin ARS306 in two orientations indicated that DNA polymerases ϵ and δ correct HAP-induced DNA replication errors on opposite DNA strands.


Author(s):  
Rafael Rosell ◽  
Alex Pifarré ◽  
Mariano Monzó ◽  
Julio Astudillo ◽  
M. Paz López-Cabrerizo ◽  
...  

PROTEOMICS ◽  
2015 ◽  
Vol 15 (17) ◽  
pp. 3087-3100 ◽  
Author(s):  
Lihong Hao ◽  
Xin Zhou ◽  
Shuqing Liu ◽  
Mingzhong Sun ◽  
Yang Song ◽  
...  

2002 ◽  
Vol 296 (1) ◽  
pp. 152-155 ◽  
Author(s):  
Tomoki Ishizuka ◽  
Chikako Tanabe ◽  
Hiromi Sakamoto ◽  
Kazuhiko Aoyagi ◽  
Masahiko Maekawa ◽  
...  

2014 ◽  
pp. 1753 ◽  
Author(s):  
Judong Luo ◽  
LiLi Cao ◽  
Xin Jiang ◽  
Kejun Dai ◽  
Shuyu Zhang ◽  
...  

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