journal
MENU ▼
Read by QxMD icon Read
search

Cold Spring Harbor Symposia on Quantitative Biology

journal
https://www.readbyqxmd.com/read/28104828/a-conversation-with-robert-weinberg
#1
(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
#2
(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
#3
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
#4
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
#5
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
#6
(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
#7
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
#8
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
#9
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
#10
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
#11
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
https://www.readbyqxmd.com/read/27932567/a-conversation-with-david-tuveson
#12
(no author information available yet)
No abstract text is available yet for this article.
December 8, 2016: Cold Spring Harbor Symposia on Quantitative Biology
https://www.readbyqxmd.com/read/27932566/a-conversation-with-guillermina-gigi-lozano
#13
(no author information available yet)
No abstract text is available yet for this article.
December 8, 2016: Cold Spring Harbor Symposia on Quantitative Biology
https://www.readbyqxmd.com/read/27932565/a-conversation-with-gerard-evan
#14
(no author information available yet)
No abstract text is available yet for this article.
December 8, 2016: Cold Spring Harbor Symposia on Quantitative Biology
https://www.readbyqxmd.com/read/27932564/a-conversation-with-benjamin-neel
#15
(no author information available yet)
No abstract text is available yet for this article.
December 8, 2016: Cold Spring Harbor Symposia on Quantitative Biology
https://www.readbyqxmd.com/read/27932563/the-enigma-of-p53
#16
Guillermina Lozano
This perspective will focus on the physiological impact of wild-type and mutant p53 activities. In particular, the tissue-specific nature of activation of p53 targets and their subsequent effects on cell behavior will be discussed. Because mutations in p53 are common in human cancers, the regulation and physiological consequences of mutant p53 proteins will also be discussed.
December 8, 2016: Cold Spring Harbor Symposia on Quantitative Biology
https://www.readbyqxmd.com/read/27815544/functional-genomic-characterization-of-cancer-genomes
#17
Thomas P Howard, Francisca Vazquez, Aviad Tsherniak, Andrew L Hong, Mik Rinne, Andrew J Aguirre, Jesse S Boehm, William C Hahn
International efforts to sequence cancer genomes now provide an overview of the major genetic alterations that occur in most human cancers. These studies have identified many highly recurrent alterations in specific cancer subtypes but have also identified mutations that occur at lower frequency and unstudied variants of known cancer-associated genes. To elucidate the function of such cancer alleles, we have developed several approaches to systematically interrogate genomic changes found in human tumors. In general, we have taken two complementary approaches...
November 4, 2016: Cold Spring Harbor Symposia on Quantitative Biology
https://www.readbyqxmd.com/read/27815543/genetic-dissection-of-cancer-development-therapy-response-and-resistance-in-mouse-models-of-breast-cancer
#18
Stefano Annunziato, Marco Barazas, Sven Rottenberg, Jos Jonkers
The cancer genomics revolution has rapidly expanded the inventory of somatic mutations characterizing human malignancies, highlighting a previously underappreciated extent of molecular variability between and within patients. Also in breast cancer, the most commonly diagnosed malignancy in women, this heterogeneity complicates the understanding of the stepwise sequence of pathogenic events and the design of effective and long-lasting target therapies. To disentangle this complexity and pinpoint which molecular perturbations are crucial to hijack the cellular machinery and lead to tumorigenesis and drug resistance, functional studies are needed in model systems that faithfully and comprehensively recapitulate all the salient aspects of their cognate human counterparts...
November 4, 2016: Cold Spring Harbor Symposia on Quantitative Biology
https://www.readbyqxmd.com/read/27815542/cell-of-origin-and-cancer-stem-cells-in-tumor-suppressor-mouse-models-of-glioblastoma
#19
Sheila R Alcantara Llaguno, Xuanhua Xie, Luis F Parada
The cellular origins and the mechanisms of progression, maintenance of tumorigenicity, and therapeutic resistance are central questions in the glioblastoma multiforme (GBM) field. Using tumor suppressor mouse models, our group recently reported two independent populations of adult GBM-initiating central nervous system progenitors. We found different functional and molecular subtypes depending on the tumor-initiating cell lineage, indicating that the cell of origin is a driver of GBM subtype diversity. Using an in vivo model, we also showed that GBM cancer stem cells (CSCs) or glioma stem cells (GSCs) contribute to resistance to chemotherapeutic agents and that genetic ablation of GSCs leads to a delay in tumor progression...
November 4, 2016: Cold Spring Harbor Symposia on Quantitative Biology
https://www.readbyqxmd.com/read/27811212/to-prime-or-not-to-prime-that-is-the-question
#20
Danielle S Potter, Anthony Letai
Mitochondrial priming is regulated by the B-cell lymphoma 2 (BCL-2) family of proteins and determines a cell's "readiness" for apoptosis. A highly primed cell will undergo apoptosis more easily than an unprimed cell in response to apoptotic stimuli via the intrinsic apoptotic pathway. Priming can be measured via BH3 profiling, which uses BH3 peptides derived from the BH3 domain of pro-apoptotic BH3-only BCL-2 family members to provoke a response from viable mitochondria. BH3 profiling can be performed on tumor cells and can identify mechanisms a cell uses to evade apoptosis and anti-apoptotic dependency to the anti-apoptotic BCL-2 family members...
November 3, 2016: Cold Spring Harbor Symposia on Quantitative Biology
journal
journal
25235
1
2
Fetch more papers »
Fetching more papers... Fetching...
Read by QxMD. Sign in or create an account to discover new knowledge that matter to you.
Remove bar
Read by QxMD icon Read
×

Search Tips

Use Boolean operators: AND/OR

diabetic AND foot
diabetes OR diabetic

Exclude a word using the 'minus' sign

Virchow -triad

Use Parentheses

water AND (cup OR glass)

Add an asterisk (*) at end of a word to include word stems

Neuro* will search for Neurology, Neuroscientist, Neurological, and so on

Use quotes to search for an exact phrase

"primary prevention of cancer"
(heart or cardiac or cardio*) AND arrest -"American Heart Association"