scholarly journals Deep sequencing of 3 cancer cell lines on 2 sequencing platforms

2019 ◽  
Author(s):  
Kanika Arora ◽  
Minita Shah ◽  
Molly Johnson ◽  
Rashesh Sanghvi ◽  
Jennifer Shelton ◽  
...  

AbstractTo test the performance of a new sequencing platform, develop an updated somatic calling pipeline and establish a reference for future benchmarking experiments, we sequenced 3 common cancer cell lines along with their matched normal cell lines to great sequencing depths (up to 278X coverage) on both Illumina HiSeqX and NovaSeq sequencing instruments. Somatic calling was generally consistent between the two platforms despite minor differences at the read level. We designed and implemented a novel pipeline for the analysis of tumor-normal samples, using multiple variant callers. We show that coupled with a high-confidence filtering strategy, it improves the accuracy of somatic calls. We also demonstrate the utility of the dataset by creating an artificial purity ladder to evaluate the somatic pipeline and benchmark methods for estimating purity and ploidy from tumor-normal pairs. The data and results of the pipeline are made accessible to the cancer genomics community.

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Kanika Arora ◽  
Minita Shah ◽  
Molly Johnson ◽  
Rashesh Sanghvi ◽  
Jennifer Shelton ◽  
...  

AbstractTo test the performance of a new sequencing platform, develop an updated somatic calling pipeline and establish a reference for future benchmarking experiments, we performed whole-genome sequencing of 3 common cancer cell lines (COLO-829, HCC-1143 and HCC-1187) along with their matched normal cell lines to great sequencing depths (up to 278x coverage) on both Illumina HiSeqX and NovaSeq sequencing instruments. Somatic calling was generally consistent between the two platforms despite minor differences at the read level. We designed and implemented a novel pipeline for the analysis of tumor-normal samples, using multiple variant callers. We show that coupled with a high-confidence filtering strategy, the use of combination of tools improves the accuracy of somatic variant calling. We also demonstrate the utility of the dataset by creating an artificial purity ladder to evaluate the somatic pipeline and benchmark methods for estimating purity and ploidy from tumor-normal pairs. The data and results of the pipeline are made accessible to the cancer genomics community.


2016 ◽  
Vol 63 (3) ◽  
Author(s):  
Karolina Kowalska ◽  
Magdalena Nowakowska ◽  
Kamila Domińska ◽  
Agnieszka W. Piastowska-Ciesielska

The aim of this study was to evaluate the coexpression of caveolin-1 (CAV-1), angiotensin II type 1 receptor (AT1-R) and forkhead box Ml (FOXM1) in prostate and breast cancer cell lines, in comparison with normal cell lines. CAV-1, AT1-R and FOXM1 expression was determined by reverse transcription-quantitative polymerase chain reaction and western blot analysis in the prostate cancer cell lines PC3, DU145 and LNCaP; prostate normal cell line PNT1A; breast cancer cell lines MCF-7 and MDA-MB-231; and the normal breast cell line 184A1. A correlation between the expression levels of the investigated genes and their metastatic properties was determined by the Spearman's rank test (P<0.05) and Aspin-Welsch t-test, respectively. In prostate cell lines, a significant correlation was noted between CAV-1 and AT1-R expression and between FOXM1 and CAV-1 expression. A correlation between the expression levels of the investigated genes and their metastatic potential was also observed, with relatively high expression of all the investigated genes in the normal prostate cell line PNT1A. In comparison to prostate cancer cell lines, an adverse dependency between CAV-1, AT1-R, FOXM1 expression and metastatic potential was observed in the breast cancer cell lines. Relatively high expression of all tested genes was observed in the normal breast cell line 184A1, which was decreasing respectively with increasing metastatic potential of breast cancer cell lines. The results obtained here indicate that CAV-1, FOXM1 and AT1-R may be potential markers of tumorigenesis in certain types of cancer in vitro.


2018 ◽  
Vol 33 (1) ◽  
pp. e4692 ◽  
Author(s):  
Ambarish Mondal ◽  
Rajat K. Tripathy ◽  
Parul Dutta ◽  
Manas Kumar Santra ◽  
Anvarhusein A. Isab ◽  
...  

2013 ◽  
Vol 781-784 ◽  
pp. 1107-1110
Author(s):  
Xu Jian Luo ◽  
Qi Pin Qin ◽  
Yu Lan Li ◽  
Yan Cheng Liu

A new phenanthroimidazole platinum (II) complex has been synthesized and characterized by IR, NMR, ESI-MS, element analysis. The affinities of the complex toward ct-DNA was determined by circular dichroism absorption (CD), UV-Vis absorption. Results indicate that the complex interact with ct-DNA by classical intercalating mode. The cytotoxicities of the complex was screened against four cancer cell lines and normal cells of HL-7702 in comparison to cisplatin and it showed a higher activity than cisplatin, with IC50 values in the range 8.7417.11 μmol/L. Furthermore, the complex displayed lower cytotoxic activities to HL-7702 (normal cell) compared with the cancer cell lines.


2019 ◽  
Author(s):  
Neetha Nanoth Vellichirammal ◽  
Abrar Albahrani ◽  
Jasjit K. Banwait ◽  
You Li ◽  
Babu Guda

2019 ◽  
Author(s):  
Neetha Nanoth Vellichirammal ◽  
Abrar Albahrani ◽  
Jasjit K. Banwait ◽  
You Li ◽  
Babu Guda

Author(s):  
Han Chang ◽  
Donald G. Jackson ◽  
Paul S. Kayne ◽  
Petra B. Ross-Macdonald ◽  
Rolf-Peter Ryseck ◽  
...  

2013 ◽  
Vol 781-784 ◽  
pp. 1130-1133
Author(s):  
Qi Pin Qin ◽  
Yu Lan Li ◽  
Yan Cheng Liu ◽  
Xu Jian Luo

A platinum (II) complex has been synthesized and characterized. The complex binding properties with G-quadruplex DNA and ds26 were examined by FID and CD spectroscopic methods. The results revealed that the platinum (II) complex can induce the antiparallel G-quadruplex structure of HTG21 conformation in the absence of added K+ with selectivity over other G-quadruplex DNA and duplex DNA. The cytotoxicity of the platinum (II) was screened against four cancer cell lines and normal cells of HL-7702 in comparison to cisplatin and it showed a higher activity than cisplatin, with inhibition rates ranging from (40.06±1.65)% to (89.47±1.14)%. Furthermore, the platinum (II) complex displayed lower cytotoxic activities to HL-7702 (normal cell) compared with the cancer cell lines.


2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Sherry X. Yang ◽  
Melinda Hollingshead ◽  
Larry Rubinstein ◽  
Dat Nguyen ◽  
Angelo B. A. Larenjeira ◽  
...  

Abstract Background Challenges remain on the selection of patients who potentially respond to a class of drugs that target epigenetics for cancer treatment. This study aims to investigate TET2/DNMT3A mutations and antitumor activity of a novel epigenetic agent in multiple human cancer cell lines and animal models. Methods Seventeen cancer cell lines and multiple xenograft models bearing representative human solid tumors were subjected to 4′-thio-2′-deoxycytidine (T-dCyd) or control treatment. Gene mutations in cell lines were examined by whole exome and/or Sanger sequencing. Specific gene expression was measured in cells and xenograft tumor samples by Western blotting and immunohistochemistry. TET2/DNMT3A mutation status in 47,571 human tumor samples was analyzed at cBioPortal for Cancer Genomics. Results Cell survival was significantly inhibited by T-dCyd in breast BT549, lung NCI-H23, melanoma SKMEL5 and renal ACHN cancer lines harboring deleterious TET2 and nonsynonymous DNMT3A mutations compared to 13 lines without such mutation pattern (P = 0.007). The treatment upregulated p21 and induced cell cycle arrest in NCI-H23 cells, and dramatically inhibited their xenograft tumor growth versus wildtype models. T-dCyd administrations led to a significant p21 increase and near eradication of tumor cells in the double-mutant xenografts by histological evaluation. TET2/DNMT3A was co-mutated in human lung, breast, skin and kidney cancers and frequently in angioimmunoblastic and peripheral T cell lymphomas and several types of leukemia. Conclusions Cell and animal models with concurrent mutations in TET2 and DNMT3A were sensitive to T-dCyd treatment. The mutations were detectable in human solid tumors and frequently occur in some hematological malignancies.


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