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Trends in Cancer

Ruth A Franklin, Ming O Li
Macrophages are innate immune cells with evolutionarily conserved functions in tissue maintenance and host defense. As such, macrophages are among the first hematopoietic cells that seed developing tissues, and respond to inflammatory insults by in situ proliferation or de novo differentiation from monocytes. Recent studies have revealed that monocyte-derived tumor-induced macrophages represent a major tumor-associated macrophage population, which can further expand following their differentiation in tumors...
October 1, 2016: Trends in Cancer
Julian Gingold, Ruoji Zhou, Ihor R Lemischka, Dung-Fang Lee
The elucidation of cancer pathogenesis has been hindered by limited access to patient samples, tumor heterogeneity and the lack of reliable model organisms. Characterized by their ability to self-renew indefinitely and differentiate into all cell lineages of an organism, pluripotent stem cells (PSCs), including embryonic stem cells (ESCs) and induced pluripotent stem cells (iPSCs), provide a powerful and unlimited source to generate differentiated cells that can be used to study disease biology, facilitate drug discovery and development, and provide key insights for developing personalized therapies...
September 2016: Trends in Cancer
Ming Tang, Roel Gw Verhaak
The molecular basis for the clinical heterogeneity observed in patients with malignant rhabdoid tumors is unknown. Recently, two reports revealed molecular inter-tumor heterogeneity in teratoid/rhabdoid tumors (ATRTs) and extra-cranial MRTs (ecMRTs) using genomic, transcriptomic and epigenomic profiling. Distinct molecular subgroups were identified and new therapeutic targets were revealed.
May 2016: Trends in Cancer
Erika Ilagan, Brendan D Manning
The movement toward precision medicine with targeted therapeutics for cancer treatment has been hindered by both innate and acquired resistance. Understanding the molecular wiring and plasticity of oncogenic signaling networks is essential to the development of therapeutic strategies to avoid or overcome resistance. The mechanistic target of rapamycin (mTOR) complex 1 (mTORC1) represents a highly integrated signaling node that is dysregulated in the majority of human cancers. Several studies have revealed that sustained mTORC1 inhibition is essential to avoid resistance to targeted therapeutics against the driving oncogenic pathway in a given cancer...
May 2016: Trends in Cancer
Erika Langsfeld, Laimonis A Laimins
Human papillomaviruses are the causative agents of cervical, anal as well as many oropharyngeal cancers. While prophylactic vaccines have been developed, uptake is low in the US and other Western countries, and access is limited in less developed countries. A number of areas are emerging as critical for future study. These include investigation of the mechanisms regulating infection and progression to cancer at both cervical and oropharyngeal sites as these appear to be distinct. HPV-induced cancers also may be susceptible to immune therapy, revealing opportunities for treating advanced cervical disease and reducing the morbidity of treatments for oropharyngeal cancers...
May 2016: Trends in Cancer
Lindsey A Baker, Hervé Tiriac, Hans Clevers, David A Tuveson
Pancreatic ductal adenocarcinoma (PDA) is a highly lethal malignancy for which new treatment and diagnostic approaches are urgently needed. In order for such breakthroughs to be discovered, researchers require systems that accurately model the development and biology of PDA. While cell lines, genetically engineered murine models, and xenografts have all led to valuable clinical insights, organotypic culture models have emerged as tractable systems to recapitulate the complex three-dimensional organization of PDA...
April 2016: Trends in Cancer
Veronica Balatti, Mario Acunzo, Yuri Pekarky, Carlo M Croce
B-cell chronic lymphocytic leukemia (CLL) is the most common adult human leukemia. Although, the molecular alterations leading to CLL onset and progression are still under investigation (specifically, the interplay and exact role of oncogenes and tumor suppressors in CLL pathogenesis). MicroRNAs are small non-coding RNAs that regulate gene expression and are expressed in a tissue specific manner. Deregulation of microRNAs can alter expression levels of genes involved in the development and/or progression of tumors...
March 2016: Trends in Cancer
Wenyang Li, Yibin Kang
The involvement of epithelial-to-mesenchymal transition (EMT) in metastasis has long been under debate. Recent efforts to probe the occurrence and functional significance of EMT in clinical samples and animal models have produced exciting but sometimes conflicting findings. The diversity of EMT underlies the challenge in studying its role in metastasis.
February 2016: Trends in Cancer
Maria Guillamot, Luisa Cimmino, Iannis Aifantis
Aberrant DNA methylation is a characteristic feature of cancer including blood malignancies. Mutations in the DNA methylation regulators DNMT3A, TET1/2 and IDH1/2 are recurrent in leukemia and lymphoma. Specific and distinct DNA methylation patterns characterize subtypes of AML and lymphoma. Regulatory regions such as promoter CpG islands, CpG shores and enhancers show changes in methylation during transformation. However, the reported poor correlation between changes in methylation and gene expression in many mouse models and human studies reflects the complexity in the precise molecular mechanism for why aberrant DNA methylation promotes malignancies...
February 1, 2016: Trends in Cancer
Luca Antonioli, Gennady G Yegutkin, Pál Pacher, Corrado Blandizzi, György Haskó
In recent years, cancer immunotherapy made significant advances due to a better understanding of the principles underlying tumor biology and immunology. In this context, CD73 is a key molecule, since via degradation of adenosine monophosphate into adenosine, endorses the generation of an immunosuppressed and pro-angiogenic niche within the tumor microenvironment that promotes the onset and progression of cancer. Targeting CD73 results in favorable antitumor effects in pre-clinical models and combined treatments of CD73 blockade with other immune-modulating agents (i...
February 1, 2016: Trends in Cancer
Steve H Thorne
The identification of STING as a key cytoplasmic innate recognition molecule for DNA viruses whose function is lost in a variety of cancers has coincided with the approval of IMLYGIC for metastatic melanoma. This represents the first replication competent viral therapy approved for the treatment of any cancer in the US. The role of STING pathway in the selectivity of HSV has been addressed for the first time in Xia et al (1).
February 1, 2016: Trends in Cancer
Kamil A Lipinski, Louise J Barber, Matthew N Davies, Matthew Ashenden, Andrea Sottoriva, Marco Gerlinger
The ability to predict the future behavior of an individual cancer is crucial for precision cancer medicine. The discovery of extensive intratumor heterogeneity and ongoing clonal adaptation in human tumors substantiated the notion of cancer as an evolutionary process. Random events are inherent in evolution and tumor spatial structures hinder the efficacy of selection, which is the only deterministic evolutionary force. This review outlines how the interaction of these stochastic and deterministic processes, which have been extensively studied in evolutionary biology, limits cancer predictability and develops evolutionary strategies to improve predictions...
January 2016: Trends in Cancer
Emil Lou
The role of intercellular communication is increasingly recognized as being critical to tumoral invasion, metastasis, and development of resistance to therapy. The recent discovery of cellular protrusions - tumour microtubes - connecting cancer cells in gliomas, and tunneling nanotubes in several other forms of cancer, sheds light on a novel mechanism for molecular networking. Interrupting and disrupting vital lines of intercellular cross-talk via these membranous cellular tubes has strong potential as a novel form of cancer-directed therapy...
January 1, 2016: Trends in Cancer
Alexandra Boussommier-Calleja, Ran Li, Michelle B Chen, Siew Cheng Wong, Roger D Kamm
In recognition of the enormous potential of immunotherapies against cancer, research into the interactions between tumor and immune cells has accelerated, leading to the recent FDA approval of several drugs that reduce cancer progression. Numerous cellular and molecular interactions have been identified by which immune cells can intervene in the metastatic cascade, leading to the development of several in vivo and in vitro model systems that can recapitulate these processes. Among these, microfluidic technologies hold many advantages in terms of their unique ability to capture the essential features of multiple cell type interactions in three-dimensions while allowing tight control of the microenvironment and real-time monitoring...
January 1, 2016: Trends in Cancer
Violeta Rayon-Estrada, F Nina Papavasiliou, Dewi Harjanto
Global analyses of cancer transcriptomes demonstrate that ADAR (adenosine deaminase, RNA-specific)-mediated RNA editing dynamically contributes to genetic alterations in cancer, and directly correlates with progression and prognosis. RNA editing is abundant and frequently elevated in cancer, and affects functionally and clinically relevant sites in both coding and non-coding regions of the transcriptome. Therefore, ADAR and differentially edited transcripts may be promising biomarkers or targets for therapy...
December 2015: Trends in Cancer
Dolores Hambardzumyan, Gabriele Bergers
Glioblastomas (GBM) are one of the most recalcitrant brain tumors because of their aggressive invasive growth and resistance to therapy. They are highly heterogeneous malignancies at both the molecular and histological levels. Specific histological hallmarks including pseudopalisading necrosis and microvascular proliferation distinguish GBM from lower-grade gliomas, and make GBM one of the most hypoxic as well as angiogenic tumors. These microanatomical compartments present specific niches within the tumor microenvironment that regulate metabolic needs, immune surveillance, survival, invasion as well as cancer stem cell maintenance...
December 2015: Trends in Cancer
Natalie Saini
21 years ago, the DNA Repair Enzyme was declared "Molecule of the Year". Today, we are celebrating another "year of repair", with the 2015 Nobel Prize in Chemistry being awarded to Aziz Sancar, Tomas Lindahl and Paul Modrich for their collective work on the different DNA repair pathways.
December 1, 2015: Trends in Cancer
Mei Zhang, Jeffrey M Rosen
Breast cancer is no longer considered a single disease, but instead is made up of multiple subtypes with genetically and most likely epigenetically heterogeneous tumors composed of numerous clones. Both the hierarchical cancer stem cell and clonal evolution models have been invoked to help explain this intratumoral heterogeneity. Several recent studies have helped define the functional interactions among the different cellular subpopulations necessary for the evolution of this complex ecosystem. These interactions involve paracrine interactions that include locally acting Wnt family members, reminiscent of the signaling pathways important for normal mammary gland development and stem cell self-renewal...
December 1, 2015: Trends in Cancer
Nicholas A Willis, Emilie Rass, Ralph Scully
Chromosome rearrangement plays a causal role in tumorigenesis by contributing to the inactivation of tumor suppressor genes, the dysregulated expression or amplification of oncogenes and the generation of novel gene fusions. Chromosome breaks are important intermediates in this process. How, when and where these breaks arise and the specific mechanisms engaged in their repair strongly influence the resulting patterns of chromosome rearrangement. Here, we review recent progress in understanding how certain distinctive features of the cancer genome, including clustered mutagenesis, tandem segmental duplications, complex breakpoints, chromothripsis, chromoplexy and chromoanasynthesis may arise...
December 1, 2015: Trends in Cancer
Florian L Muller, Elisa A Aquilanti, Ronald A DePinho
Genomic deletion of tumor suppressor genes (TSG) is a rite of passage for virtually all human cancers. The synthetic lethal paradigm has provided a framework for the development of molecular targeted therapeutics that are functionally linked to the loss of specific TSG functions. In the course of genomic events that delete TSGs, a large number of genes with no apparent direct role in tumor promotion also sustain deletion as a result of chromosomal proximity to the target TSG. In this perspective, we review the novel concept of "collateral lethality", which has served to identify cancer-specific therapeutic vulnerabilities resulting from co-deletion of passenger genes neighboring TSG...
November 1, 2015: Trends in Cancer
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