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Cold Spring Harbor Symposia on Quantitative Biology

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https://www.readbyqxmd.com/read/28209717/autophagy-metabolism-and-cancer
#1
Jessie Yanxiang Guo, Eileen White
Macroautophagy (autophagy hereafter) is a process that collects cytoplasmic components, particularly mitochondria, and degrades them in lysosomes. In mammalian systems, basal autophagy levels are normally low but are profoundly stimulated by starvation and essential for survival. Cancer cells up-regulate autophagy and can be more autophagy-dependent than most normal tissues. Genetic deficiency in essential autophagy genes in tumors in many autochthonous mouse models for cancer reduces tumor growth. In K-ras(G12D)-driven non-small cell lung cancer (NSCLC) and other models, autophagy sustains metabolism and survival...
February 16, 2017: Cold Spring Harbor Symposia on Quantitative Biology
https://www.readbyqxmd.com/read/28209716/a-conversation-with-harold-varmus
#2
(no author information available yet)
No abstract text is available yet for this article.
February 16, 2017: Cold Spring Harbor Symposia on Quantitative Biology
https://www.readbyqxmd.com/read/28174256/a-time-for-myc-metabolism-and-therapy
#3
Chi V Dang
The MYC oncogene is frequently deregulated in human cancers, whereas the proto-oncogene is exquisitely, tightly regulated in normal cells. Deregulated MYC drives transcriptional imbalance, thereby altering metabolism and disrupting the circadian Bmal1-Clock E-box-dependent transcriptional circuitry. Sustained oncogenic MYC expression drives a constitutive growth program with mammalian target of rapamycin (mTOR) activation that renders cells dependent on nutrients, such that glucose or glutamine deprivation could trigger cell death and key enzymes such as lactate dehydrogenase A (LDHA) and glutaminase (GLS) amenable for targeting in cancers...
February 7, 2017: Cold Spring Harbor Symposia on Quantitative Biology
https://www.readbyqxmd.com/read/28174255/a-conversation-with-william-kaelin
#4
(no author information available yet)
No abstract text is available yet for this article.
February 7, 2017: Cold Spring Harbor Symposia on Quantitative Biology
https://www.readbyqxmd.com/read/28174254/the-essential-transcriptional-function-of-brd4-in-acute-myeloid-leukemia
#5
Jae-Seok Roe, Christopher R Vakoc
Acute myeloid leukemia (AML) is often initiated by genetic alterations of machineries that regulate chromatin and transcription, thereby blocking cell differentiation. Such mechanisms may also render leukemia cells vulnerable to perturbations of transcriptional regulators, which includes small molecules targeting the coactivator protein BRD4. Numerous studies have validated BRD4 as a therapeutic target in diverse subtypes of AML; however, the vital function of BRD4 in this disease is only beginning to be understood...
February 7, 2017: Cold Spring Harbor Symposia on Quantitative Biology
https://www.readbyqxmd.com/read/28123050/a-conversation-with-sean-morrison
#6
(no author information available yet)
No abstract text is available yet for this article.
January 25, 2017: Cold Spring Harbor Symposia on Quantitative Biology
https://www.readbyqxmd.com/read/28123049/how-cancer-genomics-drives-cancer-biology-does-synthetic-lethality-explain-mutually-exclusive-oncogenic-mutations
#7
Harold Varmus, Arun M Unni, William W Lockwood
Large-scale analyses of cancer genomes are revealing patterns of mutations that suggest biologically significant ideas about many aspects of cancer, including carcinogenesis, classification, and preventive and therapeutic strategies. Among those patterns is "mutual exclusivity," a phenomenon observed when two or more mutations that are commonly observed in samples of a type of cancer are not found combined in individual tumors. We have been studying a striking example of mutual exclusivity: the absence of coexisting mutations in the KRAS and EGFR proto-oncogenes in human lung adenocarcinomas, despite the high individual frequencies of such mutations in this common type of cancer...
January 25, 2017: Cold Spring Harbor Symposia on Quantitative Biology
https://www.readbyqxmd.com/read/28123048/a-conversation-with-christopher-vakoc
#8
(no author information available yet)
No abstract text is available yet for this article.
January 25, 2017: Cold Spring Harbor Symposia on Quantitative Biology
https://www.readbyqxmd.com/read/28123047/a-conversation-with-eileen-white
#9
(no author information available yet)
No abstract text is available yet for this article.
January 25, 2017: Cold Spring Harbor Symposia on Quantitative Biology
https://www.readbyqxmd.com/read/28104828/a-conversation-with-robert-weinberg
#10
(no author information available yet)
No abstract text is available yet for this article.
January 19, 2017: Cold Spring Harbor Symposia on Quantitative Biology
https://www.readbyqxmd.com/read/28104827/a-conversation-with-elaine-mardis
#11
(no author information available yet)
No abstract text is available yet for this article.
January 19, 2017: Cold Spring Harbor Symposia on Quantitative Biology
https://www.readbyqxmd.com/read/28082378/cancer-oxidative-stress-and-metastasis
#12
Jennifer G Gill, Elena Piskounova, Sean J Morrison
Reactive oxygen species (ROS) are highly reactive molecules that arise from a number of cellular sources, including oxidative metabolism in mitochondria. At low levels they can be advantageous to cells, activating signaling pathways that promote proliferation or survival. At higher levels, ROS can damage or kill cells by oxidizing proteins, lipids, and nucleic acids. It was hypothesized that antioxidants might benefit high-risk patients by reducing the rate of ROS-induced mutations and delaying cancer initiation...
January 12, 2017: Cold Spring Harbor Symposia on Quantitative Biology
https://www.readbyqxmd.com/read/28062533/bet-bromodomain-proteins-as-cancer-therapeutic-targets
#13
Shaokun Shu, Kornelia Polyak
Epigenetic regulators are emerging therapeutic targets in a wide variety of human cancers. BET bromodomain proteins have been identified as key regulators of oncogenic transcription factors including MYC; therefore, their inhibition might provide a way to block these "undruggable" targets. Several BET bromodomain inhibitors are in clinical development with promising preliminary findings. However, tumors acquire resistance to these agents in several different ways. In this review, we summarize the role that BET bromodomain proteins play in tumorigenesis as well as the molecular mechanisms underlying therapeutic responses and resistance to their inhibition with emphasis on BRD4 and breast cancer...
January 6, 2017: Cold Spring Harbor Symposia on Quantitative Biology
https://www.readbyqxmd.com/read/28062532/lipid-synthesis-is-a-metabolic-liability-of-non-small-cell-lung-cancer
#14
Robert U Svensson, Reuben J Shaw
The renaissance in the study of cancer metabolism has refocused efforts to identify and target metabolic dependencies of tumors as an approach for cancer therapy. One of the unique metabolic requirements that cancer cells possess to sustain their biosynthetic growth demands is altered fatty acid metabolism, in particular the synthesis of de novo fatty acids that are required as cellular building blocks to support cell division. Enhanced fatty acid synthesis that is observed in many tumor types has been postulated to open a therapeutic window for cancer therapy and, correspondingly, efforts to pharmacologically inhibit key enzymes of fatty acid synthesis are being pursued...
January 6, 2017: Cold Spring Harbor Symposia on Quantitative Biology
https://www.readbyqxmd.com/read/28057849/a-conversation-with-daniel-haber
#15
(no author information available yet)
No abstract text is available yet for this article.
January 5, 2017: Cold Spring Harbor Symposia on Quantitative Biology
https://www.readbyqxmd.com/read/28057848/a-pipeline-for-drug-target-identification-and-validation
#16
Eusebio Manchado, Chun-Hao Huang, Nilgun Tasdemir, Darjus F Tschaharganeh, John E Wilkinson, Scott W Lowe
Rapid and affordable tumor profiling has led to an explosion of genomic data that is facilitating the development of new cancer therapies. The potential of therapeutic strategies aimed at inactivating the oncogenic lesions that contribute to the aberrant survival and proliferation of tumor cells has yielded remarkable success in some malignancies such as BRAF-mutant melanoma and BCR-ABL expressing chronic myeloid leukemia. However, the direct inhibition of several well-established oncoproteins in some of these cancers is not possible or produces only transient benefits...
January 5, 2017: Cold Spring Harbor Symposia on Quantitative Biology
https://www.readbyqxmd.com/read/28057847/ron-signaling-is-a-key-mediator-of-tumor-progression-in-many-human-cancers
#17
Najme Faham, Alana L Welm
With an increasing body of literature covering RON receptor tyrosine kinase function in different types of human cancers, it is becoming clear that RON has prominent roles in both cancer cells and in the tumor-associated microenvironment. RON not only activates several oncogenic signaling pathways in cancer cells, leading to more aggressive behavior, but also promotes an immunosuppressive, alternatively activated phenotype in macrophages and limits the antitumor immune response. These two unique functions of this oncogene, the strong correlation between RON expression and poor outcomes in cancer, and the high tolerability of a new RON inhibitor make it an exciting therapeutic target, the blocking of which offers an advantage toward improving the survival of cancer patients...
January 5, 2017: Cold Spring Harbor Symposia on Quantitative Biology
https://www.readbyqxmd.com/read/28057846/beyond-the-oncogene-revolution-four-new-ways-to-combat-cancer
#18
Thorsten Berger, Mary E Saunders, Tak W Mak
It has become clear that tumorigenesis results from much more than just the activation of an oncogene and/or the inactivation of a tumor-suppressor gene, and that the cancer cell genome contains many more alterations than can be specifically targeted at once. This observation has led our group to a search for alternative ways to kill cancer cells (while sparing normal cells) by focusing on properties unique to the former. We have identified four approaches with the potential to generate new anticancer therapies: combatting the tactics by which cancers evade antitumor immune responses, targeting metabolic adaptations that tumor cells use to survive conditions that would kill normal cells, manipulating a cancer cell's response to excessive oxidative stress, and exploiting aneuploidy...
January 5, 2017: Cold Spring Harbor Symposia on Quantitative Biology
https://www.readbyqxmd.com/read/28057845/targeting-the-epithelial-to-mesenchymal-transition-the-case-for-differentiation-based-therapy
#19
Diwakar R Pattabiraman, Robert A Weinberg
Although important strides have been made in targeted therapy for certain leukemias and subtypes of breast cancer, the standard of care for most carcinomas still involves chemotherapy, radiotherapy, surgery, or a combination of these. Two processes serve as obstacles to the successful treatment of carcinomas. First, a majority of deaths from these types of cancers occurs as a result of distant metastases and not the primary tumors themselves. Second, subsets of cells that are able to survive conventional therapy drive the aggressive relapse of the tumors, often in forms that are resistant to treatment...
January 5, 2017: Cold Spring Harbor Symposia on Quantitative Biology
https://www.readbyqxmd.com/read/27932568/targeting-hif2-in-clear-cell-renal-cell-carcinoma
#20
Hyejin Cho, William G Kaelin
Inactivation of the von Hippel-Lindau tumor-suppressor protein (pVHL) is the signature "truncal" event in clear cell renal cell carcinoma, which is the most common form of kidney cancer. pVHL is part of a ubiquitin ligase the targets the α subunit of the hypoxia-inducible factor (HIF) transcription factor for destruction when oxygen is available. Preclinical studies strongly suggest that deregulation of HIF, and particularly HIF2, drives pVHL-defective renal carcinogenesis. Although HIF2α was classically considered undruggable, structural and chemical work by Rick Bruick and Kevin Gardner at University of Texas Southwestern laid the foundation for the development of small molecule direct HIF2α antagonists (PT2385 and the related tool compound PT2399) by Peloton Therapeutics that block the dimerization of HIF2α with its partner protein ARNT1...
December 8, 2016: Cold Spring Harbor Symposia on Quantitative Biology
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