Annual Review of Cancer Biology-Series最新文献_第8页

Organoid Models for Cancer Research 癌症研究的类器官模型

IF 7.7 2区医学

Annual Review of Cancer Biology-Series Pub Date : 2019-03-04 DOI: 10.1146/ANNUREV-CANCERBIO-030518-055702

H. Clevers, D. Tuveson

引用次数: 42

Biology and Therapy of Dominant Fusion Oncoproteins Involving Transcription Factor and Chromatin Regulators in Sarcomas 肉瘤中涉及转录因子和染色质调节因子的显性融合癌蛋白的生物学和治疗

IF 7.7 2区医学

Annual Review of Cancer Biology-Series Pub Date : 2019-03-04 DOI: 10.1146/ANNUREV-CANCERBIO-030518-055710

J. Perry, B. Seong, K. Stegmaier

引用次数: 18

Taming the Heterogeneity of Aggressive Lymphomas for Precision Therapy 控制侵袭性淋巴瘤的异质性以进行精确治疗

IF 7.7 2区医学

Annual Review of Cancer Biology-Series Pub Date : 2019-03-04 DOI: 10.1146/ANNUREV-CANCERBIO-030518-055734

R. Young, J. Phelan, A. Shaffer, George W. Wright, D. Huang, R. Schmitz, Calvin A. Johnson, T. Oellerich, W. Wilson, L. Staudt

引用次数: 17

Cancer Immunotherapy: Beyond Checkpoint Blockade. 癌症免疫治疗:超越检查点封锁。

IF 7.7 2区医学

Annual Review of Cancer Biology-Series Pub Date : 2019-03-01 DOI: 10.1146/annurev-cancerbio-030518-055552

Michael Dougan, Glenn Dranoff, Stephanie K Dougan

{"title":"Cancer Immunotherapy: Beyond Checkpoint Blockade.","authors":"Michael Dougan, Glenn Dranoff, Stephanie K Dougan","doi":"10.1146/annurev-cancerbio-030518-055552","DOIUrl":"https://doi.org/10.1146/annurev-cancerbio-030518-055552","url":null,"abstract":"Blocking antibodies to the immune checkpoint receptors or their ligands have revolutionized the treatment of diverse malignancies. Many tumors are recognized by adaptive immunity, but these adaptive responses can be inhibited by immunosuppressive mechanisms within the tumor, often through pathways outside of the currently targeted checkpoints. For this reason, only a minority of cancer patients achieve durable responses to current immunotherapies. Multiple novel approaches strive to expand immunotherapy's reach. These may include targeting alternative immune checkpoints. However, many investigational strategies look beyond checkpoint blockade. These include cellular therapies to bypass endogenous immunity and efforts to stimulate new adaptive antitumor responses using vaccines, adjuvants, and combinations with cytotoxic therapy, as well as strategies to inhibit innate immune suppression and modulate metabolism within the tumor microenvironment. The challenge for immunotherapy going forward will be to select rational strategies for overcoming barriers to effective antitumor responses from the myriad possible targets.","PeriodicalId":54233,"journal":{"name":"Annual Review of Cancer Biology-Series","volume":"3 ","pages":"55-75"},"PeriodicalIF":7.7,"publicationDate":"2019-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1146/annurev-cancerbio-030518-055552","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10302301","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 101

A Joint Odyssey into Cancer Genetics 共同探索癌症遗传学

IF 7.7 2区医学

Annual Review of Cancer Biology-Series Pub Date : 2019-03-01 DOI: 10.1146/ANNUREV-CANCERBIO-030518-055543

S. Cory, Jerry M. Adams

引用次数: 4

MiT/TFE Family of Transcription Factors, Lysosomes, and Cancer. 转录因子、溶酶体和癌症的MiT/TFE家族。

IF 4.7 2区医学

Annual Review of Cancer Biology-Series Pub Date : 2019-03-01 Epub Date: 2018-11-28 DOI: 10.1146/annurev-cancerbio-030518-055835

Rushika M Perera, Chiara Di Malta, Andrea Ballabio

{"title":"MiT/TFE Family of Transcription Factors, Lysosomes, and Cancer.","authors":"Rushika M Perera, Chiara Di Malta, Andrea Ballabio","doi":"10.1146/annurev-cancerbio-030518-055835","DOIUrl":"10.1146/annurev-cancerbio-030518-055835","url":null,"abstract":"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. Here, we focus on the MiT/TFE family of transcription factors, which control transcriptional programs for autophagy and lysosome biogenesis and have emerged as regulators of energy metabolism in cancer. These new findings complement earlier reports that chromosomal translocations and amplifications involving the MiT/TFE genes contribute to the etiology and pathophysiology of renal cell carcinoma, melanoma, and sarcoma, suggesting pleiotropic roles for these factors in a wider array of cancers. Understanding the interplay between the oncogenic and stress-adaptive roles of MiT/TFE factors could shed light on fundamental mechanisms of cellular homeostasis and point to new strategies for cancer treatment.","PeriodicalId":54233,"journal":{"name":"Annual Review of Cancer Biology-Series","volume":"3 ","pages":"203-222"},"PeriodicalIF":4.7,"publicationDate":"2019-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6812561/pdf/nihms-1041567.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41220062","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Aberrant RNA Splicing in Cancer. 癌症中的RNA剪接异常

IF 7.7 2区医学

Annual Review of Cancer Biology-Series Pub Date : 2019-03-01 Epub Date: 2018-11-28 DOI: 10.1146/annurev-cancerbio-030617-050407

Luisa Escobar-Hoyos, Katherine Knorr, Omar Abdel-Wahab

引用次数: 0

The Fanconi Anemia Pathway in Cancer. 癌症中的范可尼贫血途径。

IF 7.7 2区医学

Annual Review of Cancer Biology-Series Pub Date : 2019-03-01 DOI: 10.1146/annurev-cancerbio-030617-050422

Joshi Niraj, Anniina Färkkilä, Alan D D'Andrea

{"title":"The Fanconi Anemia Pathway in Cancer.","authors":"Joshi Niraj, Anniina Färkkilä, Alan D D'Andrea","doi":"10.1146/annurev-cancerbio-030617-050422","DOIUrl":"https://doi.org/10.1146/annurev-cancerbio-030617-050422","url":null,"abstract":"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 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. Recent discoveries reveal that the FA pathway functions in a critical tumor-suppressor network to preserve genomic integrity by stabilizing replication forks, mitigating replication stress, and regulating cytokinesis. Homozygous germline mutations (biallelic) in 22 FANC genes cause FA, whereas heterozygous germline mutations in some of the FANC genes (monoallelic), such as BRCA1 and BRCA2, do not cause FA but significantly increase cancer susceptibility sporadically in the general population. In this review, we discuss our current understanding of the functions of the FA pathway in the maintenance of genomic stability, and we present an overview of the prevalence and clinical relevance of somatic mutations in FA genes.","PeriodicalId":54233,"journal":{"name":"Annual Review of Cancer Biology-Series","volume":"3 ","pages":"457-478"},"PeriodicalIF":7.7,"publicationDate":"2019-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1146/annurev-cancerbio-030617-050422","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10326078","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 239

Homology-Directed Repair and the Role of BRCA1, BRCA2, and Related Proteins in Genome Integrity and Cancer. 同源定向修复以及 BRCA1、BRCA2 和相关蛋白在基因组完整性和癌症中的作用。

IF 7.7 2区医学

Annual Review of Cancer Biology-Series Pub Date : 2018-03-01 Epub Date: 2017-12-01 DOI: 10.1146/annurev-cancerbio-030617-050502

Chun-Chin Chen, Weiran Feng, Pei Xin Lim, Elizabeth M Kass, Maria Jasin

{"title":"Homology-Directed Repair and the Role of BRCA1, BRCA2, and Related Proteins in Genome Integrity and Cancer.","authors":"Chun-Chin Chen, Weiran Feng, Pei Xin Lim, Elizabeth M Kass, Maria Jasin","doi":"10.1146/annurev-cancerbio-030617-050502","DOIUrl":"10.1146/annurev-cancerbio-030617-050502","url":null,"abstract":"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 BRCA2 poses significant risks to genome integrity, leading not only to cancer predisposition but also to sensitivity to DNA-damaging agents, affecting therapeutic approaches. Here we review recent advances in our understanding of BRCA1 and BRCA2, including how they genetically interact with other repair factors, how they protect stalled replication forks, how they affect the response to aldehydes, and how loss of their functions links to mutation signatures. Importantly, given the recent advances with poly(ADP-ribose) polymerase inhibitors (PARPi) for the treatment of HDR-deficient tumors, we discuss mechanisms by which BRCA-deficient tumors acquire resistance to PARPi and other agents.","PeriodicalId":54233,"journal":{"name":"Annual Review of Cancer Biology-Series","volume":"2 ","pages":"313-336"},"PeriodicalIF":7.7,"publicationDate":"2018-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6193498/pdf/nihms958408.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36604734","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Lineage Plasticity in Cancer Progression and Treatment. 癌症进展和治疗中的血统可塑性

IF 7.7 2区医学

Annual Review of Cancer Biology-Series Pub Date : 2018-03-01 Epub Date: 2017-12-01 DOI: 10.1146/annurev-cancerbio-030617-050224

Clémentine Le Magnen, Michael M Shen, Cory Abate-Shen

{"title":"Lineage Plasticity in Cancer Progression and Treatment.","authors":"Clémentine Le Magnen, Michael M Shen, Cory Abate-Shen","doi":"10.1146/annurev-cancerbio-030617-050224","DOIUrl":"10.1146/annurev-cancerbio-030617-050224","url":null,"abstract":"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. Notably, physiological stresses that promote plasticity, such as severe tissue damage, inflammation, or senescence, also represent hallmarks of cancer. Furthermore, key drivers of cellular plasticity include major oncogenic and tumor suppressor pathways and can be exacerbated by drug treatment. Thus, plasticity may help cancer cells evade detection and treatment. We propose that cancer can be considered as a disease of excess plasticity, a notion that has important implications for intervention and treatment.","PeriodicalId":54233,"journal":{"name":"Annual Review of Cancer Biology-Series","volume":"2 ","pages":"271-289"},"PeriodicalIF":7.7,"publicationDate":"2018-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5942183/pdf/nihms962734.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36094820","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0