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Trends in Cancer

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https://www.readbyqxmd.com/read/28626802/cohesin-mutations-in-myeloid-malignancies
#1
Joseph B Fisher, Maureen McNulty, Michael J Burke, John D Crispino, Sridhar Rao
Acute Myeloid Leukemia (AML) is a hematologic malignancy with a poor prognosis. Recent genome-wide sequencing studies have identified frequent mutations in genes encoding members of the cohesin complex. Mutations in cohesin contribute to myeloid malignancies by conferring enhanced self-renewal of hematopoietic stem and progenitor cells but the mechanisms behind this phenotype have not been fully elucidated. Of note, cohesin mutations are highly prevalent in acute megakaryocytic leukemia associated with Down syndrome (DS-AMKL), where they occur in over half of patients...
April 2017: Trends in Cancer
https://www.readbyqxmd.com/read/28451648/necroptosis-and-cancer
#2
Ayaz Najafov, Hongbo Chen, Junying Yuan
Necroptosis is a programmed lytic cell death pathway, deregulation of which is linked to various inflammatory disorders. Escape from programmed cell death and inflammation play a significant role in cancer, and therefore, investigating the role of necroptosis in cancer has been of high interest. Necroptosis has been shown to promote cancer metastasis and T cells death. Escape from necroptosis via loss of RIPK3 expression is a feature of some cancers. While necroptosis is a promising novel target for cancer therapies, further investigation into its biological role in carcinogenesis is warranted...
April 2017: Trends in Cancer
https://www.readbyqxmd.com/read/28462395/calmodulin-and-pi3k-signaling-in-kras-cancers
#3
Ruth Nussinov, Guanqiao Wang, Chung-Jung Tsai, Hyunbum Jang, Shaoyong Lu, Avik Banerjee, Jian Zhang, Vadim Gaponenko
Calmodulin (CaM) uniquely promotes signaling of oncogenic K-Ras; but not N-Ras or H-Ras. How CaM interacts with K-Ras and how this stimulates cell proliferation are among the most challenging questions in KRAS-driven cancers. Earlier data pointed to formation of a ternary complex consisting of K-Ras, PI3Kα and CaM. Recent data point to phosphorylated CaM binding to the SH2 domains of the p85 subunit of PI3Kα and activating it. Modeling suggests that the high affinity interaction between the phosphorylated CaM tyrosine motif and PI3Kα, can promote full PI3Kα activation by oncogenic K-Ras...
March 2017: Trends in Cancer
https://www.readbyqxmd.com/read/28393116/glutamine-metabolism-in-cancer-understanding-the-heterogeneity
#4
Ahmad A Cluntun, Michael J Lukey, Richard A Cerione, Jason W Locasale
Reliance on glutamine has long been considered a hallmark of cancer cell metabolism. However, some recent studies have challenged this notion in vivo, prompting a need for further clarifications on the role of glutamine metabolism in cancer. We find that there is ample evidence of an essential role for glutamine in tumors and that a variety of factors, including tissue type, the underlying cancer genetics, the tumor microenvironment and other variables such as diet and host physiology collectively influence the role of glutamine in cancer...
March 2017: Trends in Cancer
https://www.readbyqxmd.com/read/28239669/the-heterocellular-emergence-of-colorectal-cancer
#5
REVIEW
Christopher J Tape
Tissues contain multiple different cell types and can be considered to be heterocellular systems. Signaling between different cells allows tissues to achieve phenotypes that no cell type can achieve in isolation. Such emergent tissue-level phenotypes can be said to 'supervene upon' heterocellular signaling. It is proposed here that cancer is also an emergent phenotype that supervenes upon heterocellular signaling. Using colorectal cancer (CRC) as an example, I review how heterotypic cells differentially communicate to support emergent malignancy...
February 2017: Trends in Cancer
https://www.readbyqxmd.com/read/28603778/dna-targeted-precision-medicine-have-we-been-caught-sleeping
#6
William C Reinhold, Anish Thomas, Yves Pommier
In the current drive to incorporate molecular markers into treatment-selection for precision medicine, there has been a significant and we believe ill-advised omission of the large and routinely used group of drugs whose mechanism of action is DNA damage.
January 2017: Trends in Cancer
https://www.readbyqxmd.com/read/28303264/the-strange-case-of-cdk4-6-inhibitors-mechanisms-resistance-and-combination-strategies
#7
Erik S Knudsen, Agnieszka K Witkiewicz
CDK4/6 inhibitors have emerged as a powerful class of agents with clinical activity in a number of malignancies. Targeting the cell cycle represents a core attack on a defining feature of cancer. However, the mechanisms through which selective CDK4/6 targeted agents act has few parallels in the current pharmaceutical armamentarium against cancer. Notably, CDK4/6 inhibitors act downstream of most mitogenic signaling cascades, which have implications both related to clinical efficacy and resistance. Core knowledge of cell cycle processes has provided insights into mechanisms of intrinsic resistance to CDK4/6 inhibitors; however, the basis of acquired resistance versus durable response is only beginning to emerge...
January 2017: Trends in Cancer
https://www.readbyqxmd.com/read/28630946/differentiation-and-inflammation-best-enemies-in-gastrointestinal-carcinogenesis
#8
Nathan M Krah, L Charles Murtaugh
While recent studies demonstrate that cancer can arise from mutant stem cells, this hypothesis does not explain why tissues without defined stem cell populations are susceptible to inflammation-driven tumorigenesis. We propose that chronic inflammatory diseases, such as colitis and pancreatitis, predispose to gastrointestinal (GI) adenocarcinoma by reprogramming differentiated cells. Focusing on colon and pancreas, we discuss recently discovered connections between inflammation and loss of cell differentiation, and propose that dysregulation of cell fate may be a novel rate-limiting step of tumorigenesis...
December 2016: Trends in Cancer
https://www.readbyqxmd.com/read/28626801/b-lymphocytes-and-cancer-a-love-hate-relationship
#9
Grace J Yuen, Ezana Demissie, Shiv Pillai
No abstract text is available yet for this article.
December 2016: Trends in Cancer
https://www.readbyqxmd.com/read/28138568/cancer-prevention-lessons-learned-and-future-directions
#10
Barbara K Dunn, Barnett S Kramer
In this review, we address selected areas that are central to the state-of-the-art of cancer prevention science. The emphasis on prevention as a viable and critical approach to decreasing cancer mortality has gained traction in recent years, evidenced by its inclusion in the US Vice President's Cancer Initiative (also termed 'Moonshot'). Cancer prevention occurs by arresting, slowing down, or reversing the carcinogenic process before invasion into surrounding tissue or by avoiding or blocking causative exposure...
December 2016: Trends in Cancer
https://www.readbyqxmd.com/read/28607951/pgc-1-coactivators-shepherding-the-mitochondrial-biogenesis-of-tumors
#11
Chi Luo, Hans R Widlund, Pere Puigserver
As coordinators of energy demands and nutritional supplies, the PGC-1 family of transcriptional coactivators regulates mitochondrial biogenesis to control the cellular bioenergetic state. Aside from maintaining normal and adapted cell physiology, recent studies indicate that PGC-1 coactivators also serve important functions in cancer cells. In fact, by balancing mitochondrial energy production with demands for cell proliferation, these factors are involved in almost every step of tumorigenesis. In this review, we discuss the interplay between PGC-1 coactivators and cancer pathogenesis, including tumor initiation, metastatic spread, and response to treatment...
October 2016: Trends in Cancer
https://www.readbyqxmd.com/read/28439564/the-evolution-of-lifespan-and-age-dependent-cancer-risk
#12
Andrii I Rozhok, James DeGregori
The Armitage-Doll multi-stage model of carcinogenesis tremendously refocused cancer science by postulating that carcinogenesis is driven by a sequence of genetic changes in cells. Age-dependent cancer incidence thus has been explained in terms of the time necessary for oncogenic mutations to occur. While the multi-step nature of cancer evolution is well-supported by evidence, the mutation-centric theory is unable to explain a number of phenomena, such as the disproportion between cancer frequency and animal body size or the scaling of cancer incidence to animal lifespan...
October 2016: Trends in Cancer
https://www.readbyqxmd.com/read/27917404/the-emerging-role-of-cdk5-in-cancer
#13
Karine Pozo, James A Bibb
Cdk5 is an atypical cyclin-dependent kinase that is well characterized for its role in the central nervous system rather than in the cell cycle. However Cdk5 has been recently implicated in the development and progression of a variety of cancers including breast, lung, colon, pancreatic, melanoma, thyroid and brain tumors. This broad pro-tumorigenic role makes Cdk5 a promising drug target for the development of new cancer therapies. Here we review the contribution of Cdk5 to molecular mechanisms that confer upon tumors the ability to grow, proliferate and disseminate to secondary organs, as well as resistance to chemotherapies...
October 2016: Trends in Cancer
https://www.readbyqxmd.com/read/27904887/paul-workman-drugging-the-cancer-genome
#14
(no author information available yet)
No abstract text is available yet for this article.
October 2016: Trends in Cancer
https://www.readbyqxmd.com/read/27904886/mel-greaves-cancer-through-the-lens-of-evolution
#15
(no author information available yet)
No abstract text is available yet for this article.
October 2016: Trends in Cancer
https://www.readbyqxmd.com/read/26949745/ontogeny-of-tumor-associated-macrophages-and-its-implication-in-cancer-regulation
#16
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
https://www.readbyqxmd.com/read/28603777/malignant-mesothelioma-time-to-translate
#17
Andrea Napolitano, Michele Carbone
Malignant mesothelioma is an aggressive cancer largely associated with asbestos exposure. In this review, we will discuss the significant advancements in our understanding of its genetics and molecular biology and their translational relevance. Remarkable findings included the discovery of germline and somatic mutations of BRCA1 associated protein-1 (BAP1) in patients, and the genome-wide characterization of pathways altered in mesothelioma that could be potentially exploited to design novel therapeutic approaches...
September 2016: Trends in Cancer
https://www.readbyqxmd.com/read/28459108/cachexia-brown-fat-a-burning-issue-in-cancer
#18
Serkan Kir, Bruce M Spiegelman
Cachexia, a progressive weight loss in cancer patients that results from tumor-induced energy wasting, is a serious problem that interferes with response to treatment and affects quality of life. Recent studies suggest that thermogenesis of adipose tissues is involved in energy wasting and also point to a link between the atrophy of fat and muscle. Tumor-derived PTHrP has emerged as a key molecule playing multiple roles in cachexia, from fat "browning" factor to potential therapeutic target.
September 2016: Trends in Cancer
https://www.readbyqxmd.com/read/28210711/intergenically-spliced-chimeric-rnas-in-cancer
#19
Yuemeng Jia, Zhongqiu Xie, Hui Li
Gene fusions and their encoded products (fusion RNAs and proteins) are viewed as one of the hallmarks of cancer. Traditionally, they were thought to be generated solely by chromosomal rearrangements. However, recent discoveries of trans-splicing and cis-splicing events between neighboring genes, suggest that there are other mechanisms to generate chimeric fusion RNAs without corresponding changes in DNA. In addition, chimeric RNAs have been detected in normal physiology, complicating the use of fusions in cancer detection and therapy...
September 2016: Trends in Cancer
https://www.readbyqxmd.com/read/27722205/modeling-cancer-with-pluripotent-stem-cells
#20
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
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