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  • Regulatory T Cells in Cancer
    Annu. Rev. Cancer Biol. (IF 5.413) Pub Date : 2020-03-09
    George Plitas; Alexander Y. Rudensky

    The immune system has evolved complex effector mechanisms to protect the host against a diversity of pathogenic organisms and regulatory adaptations that can curtail pathological sequelae of inflammatory events, prevent autoimmunity, and assist in tissue repair. Cancers, by virtue of their local manifestations of tissue dysfunction and destruction, inflammation, and genomic instability, can evoke these

    更新日期:2020-03-09
  • The Role of Translation Control in Tumorigenesis and Its Therapeutic Implications
    Annu. Rev. Cancer Biol. (IF 5.413) Pub Date : 2020-03-09
    Yichen Xu; Davide Ruggero

    As a convergent mechanism downstream of most oncogenic signals, control of mRNA translation has emerged as a key driver in establishing and tuning gene expression at specific steps in cancer development. Translation control is the most energetically expensive molecular process in the cell that needs to be modulated upon adaption to limited cellular resources, such as cellular stress. It thereby serves

    更新日期:2020-03-09
  • The Pleiotropic Role of the KEAP1/NRF2 Pathway in Cancer
    Annu. Rev. Cancer Biol. (IF 5.413) Pub Date : 2020-03-09
    Warren L. Wu; Thales Papagiannakopoulos

    The unregulated proliferative capacity of many tumors is dependent on dysfunctional nutrient utilization and ROS (reactive oxygen species) signaling to sustain a deranged metabolic state. Although it is clear that cancers broadly rely on these survival and signaling pathways, how they achieve these aims varies dramatically. Mutations in the KEAP1/NRF2 pathway represent a potent cancer adaptation to

    更新日期:2020-03-09
  • Cancer-Associated Cachexia: A Systemic Consequence of Cancer Progression
    Annu. Rev. Cancer Biol. (IF 5.413) Pub Date : 2020-03-09
    Anup K. Biswas; Swarnali Acharyya

    Cancer is a life-threatening disease that has plagued humans for centuries. The vast majority of cancer-related mortality results from metastasis. Indeed, the invasive growth of metastatic cancer cells in vital organs causes fatal organ dysfunction, but metastasis-related deaths also result from cachexia, a debilitating wasting syndrome characterized by an involuntary loss of skeletal muscle mass and

    更新日期:2020-03-09
  • The Neural Regulation of Cancer
    Annu. Rev. Cancer Biol. (IF 5.413) Pub Date : 2020-03-09
    Shawn Gillespie; Michelle Monje

    The nervous system is intimately involved in physiological processes from development and growth to tissue homeostasis and repair throughout the body. It logically follows that the nervous system has the potential to play analogous roles in the context of cancer. Progress toward understanding the crucial role of the nervous system in cancer has accelerated in recent years, but much remains to be learned

    更新日期:2020-03-09
  • Immune-Based Approaches for the Treatment of Pediatric Malignancies
    Annu. Rev. Cancer Biol. (IF 5.413) Pub Date : 2020-03-09
    Kristopher R. Bosse; Robbie G. Majzner; Crystal L. Mackall; John M. Maris

    Immune-based therapies have now been credentialed for pediatric cancers with the robust efficacy of chimeric antigen receptor (CAR) T cells for pediatric B cell acute lymphocytic leukemia (ALL), offering a chance of a cure for children with previously lethal disease and a potentially more targeted therapy to limit treatment-related morbidities. The developmental origins of most pediatric cancers make

    更新日期:2020-03-09
  • Biomarkers for Response to Immune Checkpoint Blockade
    Annu. Rev. Cancer Biol. (IF 5.413) Pub Date : 2020-03-09
    Shridar Ganesan; Janice Mehnert

    Immune checkpoint blockade (ICB) has significant clinical activity in diverse cancer classes and can induce durable remissions in even refractory advanced disease. However, only a minority of cancer patients treated with ICB have long-term benefits, and ICB treatment is associated with significant, potentially life-threatening, autoimmune side effects. There is a great need to develop biomarkers of

    更新日期:2020-03-09
  • Nongenetic Mechanisms of Drug Resistance in Melanoma
    Annu. Rev. Cancer Biol. (IF 5.413) Pub Date : 2020-03-09
    Vito W. Rebecca; Meenhard Herlyn

    Resistance to targeted and immune-based therapies limits cures in patients with metastatic melanoma. A growing number of reports have identified nongenetic primary resistance mechanisms including intrinsic microenvironment- and lineage plasticity–mediated processes serving critical functions in the persistence of disease throughout therapy. There is a temporally shifting spectrum of cellular identities

    更新日期:2020-03-09
  • Toward Targeting Antiapoptotic MCL-1 for Cancer Therapy
    Annu. Rev. Cancer Biol. (IF 5.413) Pub Date : 2020-03-09
    Gemma L. Kelly; Andreas Strasser

    Apoptosis is critical for embryonic development, tissue homeostasis, and the removal of infected or otherwise dangerous cells. It is controlled by three subgroups of the BCL-2 protein family—the BH3-only proteins that initiate cell death; the effectors of cell killing, BAX and BAK; and the antiapoptotic guardians, including MCL-1 and BCL-2. Defects in apoptosis can promote tumorigenesis and render

    更新日期:2020-03-09
  • Acquired Resistance in Lung Cancer
    Annu. Rev. Cancer Biol. (IF 5.413) Pub Date : 2020-03-09
    Asmin Tulpule; Trever G. Bivona

    The last decade has witnessed a transformation in the treatment of advanced-stage lung cancer from a largely palliative approach to one where long-term durable remissions and even cures might be within reach. In this review, we discuss the current state of oncogene-directed precision medicine therapies in lung cancer and focus on the major cause of mortality for lung cancer patients: acquired resistance

    更新日期:2020-03-09
  • Deregulation of Chromosome Segregation and Cancer
    Annu. Rev. Cancer Biol. (IF 5.413) Pub Date : 2020-03-09
    Natalie L. Curtis; Gian Filippo Ruda; Paul Brennan; Victor M. Bolanos-Garcia

    The mitotic spindle assembly checkpoint (SAC) is an intricate cell signaling system that ensures the high fidelity and timely segregation of chromosomes during cell division. Mistakes in this process can lead to the loss, gain, or rearrangement of the genetic material. Gross chromosomal aberrations are usually lethal but can cause birth and development defects as well as cancer. Despite advances in

    更新日期:2020-03-09
  • Is There a Clinical Future for IDO1 Inhibitors After the Failure of Epacadostat in Melanoma?
    Annu. Rev. Cancer Biol. (IF 5.413) Pub Date : 2020-03-09
    Benoit J. Van den Eynde; Nicolas van Baren; Jean-François Baurain

    Indoleamine-2,3 dioxygenase 1 (IDO1) contributes to tumor immunosuppression by enzymatically degrading tryptophan, which is required for T cell activity, and producing kynurenine. Small-molecule inhibitors, such as epacadostat, have been developed to block IDO1 activity. In preclinical models, they can restore antitumoral T cell immunity and synergize with immune checkpoint inhibitors or cancer vaccines

    更新日期:2020-03-09
  • RNA Modifications in Cancer: Functions, Mechanisms, and Therapeutic Implications
    Annu. Rev. Cancer Biol. (IF 5.413) Pub Date : 2020-03-09
    Huilin Huang; Hengyou Weng; Xiaolan Deng; Jianjun Chen

    Over 170 chemical modifications have been identified in protein-coding and noncoding RNAs and shown to exhibit broad impacts on gene expression. Dysregulation of RNA modifications caused by aberrant expression of or mutations in RNA modifiers aberrantly reprograms the epitranscriptome and skews global gene expression, which in turn leads to tumorigenesis and drug resistance. Here we review current

    更新日期:2020-03-09
  • The Epithelial-to-Mesenchymal Transition in Development and Cancer
    Annu. Rev. Cancer Biol. (IF 5.413) Pub Date : 2020-03-09
    Alexandre Francou; Kathryn V. Anderson

    Epithelial-to-mesenchymal transitions (EMTs) are complex cellular processes where cells undergo dramatic changes in signaling, transcriptional programming, and cell shape, while directing the exit of cells from the epithelium and promoting migratory properties of the resulting mesenchyme. EMTs are essential for morphogenesis during development and are also a critical step in cancer progression and

    更新日期:2020-03-09
  • WNT and β-Catenin in Cancer: Genes and Therapy
    Annu. Rev. Cancer Biol. (IF 5.413) Pub Date : 2020-03-09
    Rene Jackstadt; Michael Charles Hodder; Owen James Sansom

    The WNT pathway is a pleiotropic signaling pathway that controls developmental processes, tissue homeostasis, and cancer. The WNT pathway is commonly mutated in many cancers, leading to widespread research into the role of WNT signaling in carcinogenesis. Understanding which cancers are reliant upon WNT activation and which components of the WNT signaling pathway are mutated is paramount to advancing

    更新日期:2020-03-09
  • Reactivation of Endogenous Retroelements in Cancer Development and Therapy
    Annu. Rev. Cancer Biol. (IF 5.413) Pub Date : 2020-03-09
    Charles A. Ishak; Daniel D. De Carvalho

    Domesticated retroelements contribute extensively as regulatory elements within host gene networks. Upon germline integration, retroelement mobilization is restricted through epigenetic silencing, mutational degradation, and innate immune defenses described as the viral mimicry response. Recent discoveries reveal how early events in tumorigenesis reactivate retroelements to facilitate onco-exaptation

    更新日期:2020-03-09
  • Lactate and Acidity in the Cancer Microenvironment
    Annu. Rev. Cancer Biol. (IF 5.413) Pub Date : 2020-03-09
    Scott K. Parks; Wolfgang Mueller-Klieser; Jacques Pouysségur

    Fermentative glycolysis, an ancient evolved metabolic pathway, is exploited by rapidly growing tissues and tumors but also occurs in response to the nutritional and energetic demands of differentiated tissues. The lactic acid it produces is transported across cell membranes through reversible H+/lactate− symporters (MCT1 and MCT4) and is recycled in organs as a major metabolic precursor of gluconeogenesis

    更新日期:2020-03-09
  • Engineering T Cells to Treat Cancer: The Convergence of Immuno-Oncology and Synthetic Biology
    Annu. Rev. Cancer Biol. (IF 5.413) Pub Date : 2020-03-09
    Joseph H. Choe; Jasper Z. Williams; Wendell A. Lim

    T cells engineered to recognize and kill tumor cells have emerged as powerful agents for combating cancer. Nonetheless, our ability to engineer T cells remains relatively primitive. Aside from CAR T cells for treating B cell malignancies, most T cell therapies are risky, toxic, and often ineffective, especially those that target solid cancers. To fulfill the promise of cell-based therapies, we must

    更新日期:2020-03-09
  • Investigating Tumor Heterogeneity in Mouse Models
    Annu. Rev. Cancer Biol. (IF 5.413) Pub Date : 2020-03-09
    Tuomas Tammela; Julien Sage

    Cancer arises from a single cell through a series of acquired mutations and epigenetic alterations. Tumors gradually develop into a complex tissue comprised of phenotypically heterogeneous cancer cell populations, as well as noncancer cells that make up the tumor microenvironment. The phenotype, or state, of each cancer and stromal cell is influenced by a plethora of cell-intrinsic and cell-extrinsic

    更新日期:2020-03-09
  • Metabolic Drivers in Hereditary Cancer Syndromes
    Annu. Rev. Cancer Biol. (IF 5.413) Pub Date : 2020-03-09
    Marco Sciacovelli; Christina Schmidt; Eamonn R. Maher; Christian Frezza

    Cancer is a multifaceted disease in which inherited genetic variants can be important drivers of tumorigenesis. The discovery that germline mutations of metabolic genes predispose to familial forms of cancer caused a shift in our understanding of how metabolism contributes to tumorigenesis, providing evidence that metabolic alterations can be oncogenic. In this review, we focus on mitochondrial enzymes

    更新日期:2020-03-09
  • Targeting MYC Proteins for Tumor Therapy
    Annu. Rev. Cancer Biol. (IF 5.413) Pub Date : 2020-03-09
    Elmar Wolf; Martin Eilers

    Targeting the function of MYC oncoproteins holds the promise of achieving conceptually new and effective anticancer therapies that can be applied to a broad range of tumors. The nature of the target however—a broadly, possibly universally acting transcription factor that has no enzymatic activity and is largely unstructured unless complexed with partner proteins—has so far defied the development of

    更新日期:2020-03-09
  • Mitophagy and Mitochondrial Dysfunction in Cancer
    Annu. Rev. Cancer Biol. (IF 5.413) Pub Date : 2020-03-09
    Kay F. Macleod

    The process of mitophagy, in which mitochondria are selectively turned over at the autophagolysosome, plays a central role in both eliminating dysfunctional mitochondria and reducing mitochondrial mass as an adaptive response to key physiological stresses, such as hypoxia, nutrient deprivation, and DNA damage. Defects in mitophagy have been linked to altered mitochondrial metabolism, production of

    更新日期:2020-03-09
  • Metabolism in the Tumor Microenvironment
    Annu. Rev. Cancer Biol. (IF 5.413) Pub Date : 2020-03-09
    Allison N. Lau; Matthew G. Vander Heiden

    Experiments in culture systems where one cell type is provided with abundant nutrients and oxygen have been used to inform much of our understanding of cancer metabolism. However, many differences have been observed between the metabolism of tumors and the metabolism of cancer cells grown in monoculture. These differences reflect, at least in part, the presence of nonmalignant cells in the tumor microenvironment

    更新日期:2020-03-09
  • AMP-Activated Protein Kinase: Friend or Foe in Cancer?
    Annu. Rev. Cancer Biol. (IF 5.413) Pub Date : 2020-03-09
    Diana Vara-Ciruelos; Madhumita Dandapani; D. Grahame Hardie

    The AMP-activated protein kinase (AMPK) is activated by energy stress and restores homeostasis by switching on catabolism, while switching off cell growth and proliferation. Findings that AMPK acts downstream of the tumor suppressor LKB1 have suggested that AMPK might also suppress tumorigenesis. In mouse models of B and T cell lymphoma in which genetic loss of AMPK occurred before tumor initiation

    更新日期:2020-03-09
  • MiT/TFE Family of Transcription Factors, Lysosomes, and Cancer.
    Annu. Rev. Cancer Biol. (IF 5.413) Pub Date : 2019-10-28
    Rushika M Perera,Chiara Di Malta,Andrea Ballabio

    Cancer cells have an increased demand for energy sources to support accelerated rates of growth. When nutrients become limiting, cancer cells may switch to nonconventional energy sources that are mobilized through nutrient scavenging pathways involving autophagy and the lysosome. Thus, several cancers are highly reliant on constitutive activation of these pathways to degrade and recycle cellular materials

    更新日期:2019-11-01
  • The Fanconi Anemia Pathway in Cancer.
    Annu. Rev. Cancer Biol. (IF 5.413) Pub Date : 2019-03-19
    Joshi Niraj,Anniina Färkkilä,Alan D D'Andrea

    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: (a) massive cell death of the hematopoietic stem and progenitor cell (HSPC) compartment due to extensive genomic instability, leading to BMF, and (b) uncontrolled

    更新日期:2019-11-01
  • Homology-Directed Repair and the Role of BRCA1, BRCA2, and Related Proteins in Genome Integrity and Cancer.
    Annu. Rev. Cancer Biol. (IF 5.413) Pub Date : 2018-10-23
    Chun-Chin Chen,Weiran Feng,Pei Xin Lim,Elizabeth M Kass,Maria Jasin

    Germ-line and somatic mutations in genes that promote homology-directed repair (HDR), especially BRCA1 and BRCA2, 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

    更新日期:2019-11-01
  • Lineage Plasticity in Cancer Progression and Treatment.
    Annu. Rev. Cancer Biol. (IF 5.413) Pub Date : 2018-05-15
    Clémentine Le Magnen,Michael M Shen,Cory Abate-Shen

    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

    更新日期:2019-11-01
  • Stress-Induced Mutagenesis: Implications in Cancer and Drug Resistance.
    Annu. Rev. Cancer Biol. (IF 5.413) Pub Date : 2018-02-06
    Devon M Fitzgerald,P J Hastings,Susan M Rosenberg

    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

    更新日期:2019-11-01
  • p53: Multiple Facets of a Rubik's Cube.
    Annu. Rev. Cancer Biol. (IF 5.413) Pub Date : 2017-03-01
    Yun Zhang,Guillermina Lozano

    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-,

    更新日期:2019-11-01
  • The Role of Autophagy in Cancer.
    Annu. Rev. Cancer Biol. (IF 5.413) Pub Date : 2017-03-01
    Naiara Santana-Codina,Joseph D Mancias,Alec C Kimmelman

    Autophagy is a highly conserved and regulated process that targets proteins and damaged organelles for lysosomal degradation to maintain cell metabolism, genomic integrity, and cell survival. The role of autophagy in cancer is dynamic and depends, in part, on tumor type and stage. Although autophagy constrains tumor initiation in normal tissue, some tumors rely on autophagy for tumor promotion and

    更新日期:2019-11-01
  • Aberrant RNA Splicing in Cancer.
    Annu. Rev. Cancer Biol. (IF 5.413) Pub Date : 2018-11-28
    Luisa Escobar-Hoyos,Katherine Knorr,Omar Abdel-Wahab

    RNA splicing, the enzymatic process of removing segments of premature RNA to produce mature RNA, is a key mediator of proteome diversity and regulator of gene expression. Increased systematic sequencing of the genome and transcriptome of cancers has identified a variety of means by which RNA splicing is altered in cancer relative to normal cells. These findings, in combination with the discovery of

    更新日期:2018-11-28
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