Multiscale Modeling of Inflammation-Induced Tumorigenesis Reveals Competing Oncogenic and Oncoprotective Roles for Inflammation DOI Open Access
Yucheng Guo, Qing Nie, Adam L. MacLean

et al.

Cancer Research, Journal Year: 2017, Volume and Issue: 77(22), P. 6429 - 6441

Published: Sept. 27, 2017

Chronic inflammation is a serious risk factor for cancer; however, the routes from to cancer are poorly understood. On basis of processes implicated by frequently mutated genes associated with and in three organs (stomach, colon, liver) extracted Gene Expression Omnibus, The Cancer Genome Atlas, Ontology databases, we present multiscale model long-term evolutionary dynamics leading tumorigenesis. incorporates cross-talk among interactions on several scales, including responses DNA damage, gene mutation, cell-cycle behavior, population dynamics, inflammation, metabolism-immune balance. Model simulations revealed two stages inflammation-induced tumorigenesis: precancerous state was mainly caused mutations cell proliferation pathway; transition tumorigenic states induced pathways apoptosis, differentiation, We identified opposing effects Mild removed cells damage through damage-induced death, whereas severe accelerated accumulation hence promoted These results provide insight into tumorigenesis highlight combinatorial This approach establishes methods quantifying risk, discovery driver tumorigenesis, has direct relevance early detection prevention development new treatment regimes. Res; 77(22); 6429-41. ©2017 AACR.

Language: Английский

Eleven grand challenges in single-cell data science DOI Creative Commons

David Lähnemann,

Johannes Köster, Ewa Szczurek

et al.

Genome biology, Journal Year: 2020, Volume and Issue: 21(1)

Published: Feb. 7, 2020

Abstract The recent boom in microfluidics and combinatorial indexing strategies, combined with low sequencing costs, has empowered single-cell technology. Thousands—or even millions—of cells analyzed a single experiment amount to data revolution biology pose unique science problems. Here, we outline eleven challenges that will be central bringing this emerging field of forward. For each challenge, highlight motivating research questions, review prior work, formulate open This compendium is for established researchers, newcomers, students alike, highlighting interesting rewarding problems the coming years.

Language: Английский

Citations

1037

Resolving genetic heterogeneity in cancer DOI
Samra Turajlic, Andrea Sottoriva, Trevor A. Graham

et al.

Nature Reviews Genetics, Journal Year: 2019, Volume and Issue: 20(7), P. 404 - 416

Published: March 27, 2019

Language: Английский

Citations

559

Pancreatic cancer biology and genetics from an evolutionary perspective DOI Open Access
Alvin Makohon‐Moore, Christine A. Iacobuzio‐Donahue

Nature reviews. Cancer, Journal Year: 2016, Volume and Issue: 16(9), P. 553 - 565

Published: July 22, 2016

Language: Английский

Citations

371

Unravelling biology and shifting paradigms in cancer with single-cell sequencing DOI
Timour Baslan, James Hicks

Nature reviews. Cancer, Journal Year: 2017, Volume and Issue: 17(9), P. 557 - 569

Published: Aug. 24, 2017

Language: Английский

Citations

342

The evolution of tumour phylogenetics: principles and practice DOI
Russell Schwartz, Alejandro A. Schäffer

Nature Reviews Genetics, Journal Year: 2017, Volume and Issue: 18(4), P. 213 - 229

Published: Feb. 13, 2017

Language: Английский

Citations

287

Minimal functional driver gene heterogeneity among untreated metastases DOI Open Access
Johannes G. Reiter, Alvin Makohon‐Moore, Jeffrey M. Gerold

et al.

Science, Journal Year: 2018, Volume and Issue: 361(6406), P. 1033 - 1037

Published: Sept. 6, 2018

Metastases are responsible for the majority of cancer-related deaths. Although genomic heterogeneity within primary tumors is associated with relapse, among treatment-naïve metastases has not been comprehensively assessed. We analyzed sequencing data 76 untreated from 20 patients and inferred cancer phylogenies breast, colorectal, endometrial, gastric, lung, melanoma, pancreatic, prostate cancers. found that individual patients, a large driver gene mutations common to all metastases. Further analysis revealed were shared by unlikely have functional consequences. A mathematical model tumor evolution metastasis formation provides an explanation observed homogeneity. Thus, single biopsies capture most functionally important in therefore provide essential information therapeutic decision-making.

Language: Английский

Citations

272

Therapy-induced mutations drive the genomic landscape of relapsed acute lymphoblastic leukemia DOI Open Access

Benshang Li,

Samuel W. Brady, Xiaotu Ma

et al.

Blood, Journal Year: 2019, Volume and Issue: 135(1), P. 41 - 55

Published: Oct. 24, 2019

Language: Английский

Citations

236

A general memristor-based partial differential equation solver DOI
Mohammed A. Zidan, YeonJoo Jeong, Jihang Lee

et al.

Nature Electronics, Journal Year: 2018, Volume and Issue: 1(7), P. 411 - 420

Published: July 9, 2018

Language: Английский

Citations

217

Assessing the interactions between radiotherapy and antitumour immunity DOI
Clemens Grassberger, Susannah G. Ellsworth,

Moses Q. Wilks

et al.

Nature Reviews Clinical Oncology, Journal Year: 2019, Volume and Issue: 16(12), P. 729 - 745

Published: June 26, 2019

Language: Английский

Citations

207

Increased stem cell proliferation in atherosclerosis accelerates clonal hematopoiesis DOI Creative Commons
Alexander Heyde, David Rohde, Cameron S. McAlpine

et al.

Cell, Journal Year: 2021, Volume and Issue: 184(5), P. 1348 - 1361.e22

Published: Feb. 25, 2021

Language: Английский

Citations

205