5 results match your criteria Annual review of cancer biology[Journal]

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The Fanconi Anemia Pathway in Cancer.

Annu Rev Cancer Biol 2019 Mar 3;3:457-478. Epub 2018 Dec 3.

Department of Radiation Oncology and Center for DNA Damage and Repair, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA;

Fanconi anemia (FA) is a complex genetic disorder characterized by bone marrow failure (BMF), congenital defects, inability to repair DNA interstrand cross-links (ICLs), and cancer predisposition. FA presents two seemingly opposite characteristics: () massive cell death of the hematopoietic stem and progenitor cell (HSPC) compartment due to extensive genomic instability, leading to BMF, and () uncontrolled cell proliferation leading to FA-associated malignancies. The canonical function of the FA proteins is to collaborate with several other DNA repair proteins to eliminate clastogenic (chromosome-breaking) effects of DNA ICLs. Read More

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http://dx.doi.org/10.1146/annurev-cancerbio-030617-050422DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6417835PMC

Homology-Directed Repair and the Role of BRCA1, BRCA2, and Related Proteins in Genome Integrity and Cancer.

Annu Rev Cancer Biol 2018 Mar 1;2:313-336. Epub 2017 Dec 1.

Developmental Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065.

Germ-line and somatic mutations in genes that promote homology-directed repair (HDR), especially and , are frequently observed in several cancers, in particular, breast and ovary but also prostate and other cancers. HDR is critical for the error-free repair of DNA double-strand breaks and other lesions, and HDR factors also protect stalled replication forks. As a result, loss of BRCA1 or BRCA2 poses significant risks to genome integrity, leading not only to cancer predisposition but also to sensitivity to DNA-damaging agents, affecting therapeutic approaches. Read More

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http://www.annualreviews.org/doi/10.1146/annurev-cancerbio-0
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http://dx.doi.org/10.1146/annurev-cancerbio-030617-050502DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6193498PMC
March 2018
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Lineage Plasticity in Cancer Progression and Treatment.

Annu Rev Cancer Biol 2018 Mar 1;2:271-289. Epub 2017 Dec 1.

Department of Urology and Medicine, Herbert Irving Comprehensive Cancer Center, Columbia University Medical Center, New York, NY 10032, USA.

Historically, it has been widely presumed that differentiated cells are determined during development and become irreversibly committed to their designated fates. In certain circumstances, however, differentiated cells can display plasticity by changing their identity, either by dedifferentiation to a progenitor-like state or by transdifferentiation to an alternative differentiated cell type. Such cellular plasticity can be triggered by physiological or oncogenic stress, or it can be experimentally induced through cellular reprogramming. Read More

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http://dx.doi.org/10.1146/annurev-cancerbio-030617-050224DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5942183PMC

Stress-Induced Mutagenesis: Implications in Cancer and Drug Resistance.

Annu Rev Cancer Biol 2017 Mar;1:119-140

Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas 77030.

Genomic instability underlies many cancers and generates genetic variation that drives cancer initiation, progression, and therapy resistance. In contrast with classical assumptions that mutations occur purely stochastically at constant, gradual rates, microbes, plants, flies, and human cancer cells possess mechanisms of mutagenesis that are upregulated by stress responses. These generate transient, genetic-diversity bursts that can propel evolution, specifically when cells are poorly adapted to their environments-that is, when stressed. Read More

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http://dx.doi.org/10.1146/annurev-cancerbio-050216-121919DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5794033PMC
March 2017
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p53: Multiple Facets of a Rubik's Cube.

Annu Rev Cancer Biol 2017 Mar 17;1:185-201. Epub 2016 Oct 17.

Department of Genetics, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030.

The p53 tumor suppressor has been studied for decades, and still there are many questions left unanswered. In this review, we first describe the current understanding of the wild-type p53 functions that determine cell survival or death, and regulation of the protein, with a particular focus on the negative regulators, the murine double minute family of proteins. We also summarize tissue-, stress-, and age-specific p53 activities and the potential underlying mechanisms. Read More

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http://dx.doi.org/10.1146/annurev-cancerbio-050216-121926DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6374046PMC
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