Tag Archives: cancer

Recommended Readings: Titia de Lange, Ph.D.

Posted on by
Reply

Friday Lecture Series

Cancer Biology Lecture

How Telomeres Solved the End-protection Problem

Titia de Lange, Ph.D., Leon Hess Professor and head,

Laboratory of Cell Biology and Genetics,

The Rockefeller University

March 23, 2012

3:45 p.m.-5:00 p.m. (Refreshments, 3:15 p.m., Abby Lounge)

Caspary Auditorium

 

Recommended Readings:

Davoli, T., E. L. Denchi, and T. de Lange. 2010. “Persistent Telomere Damage Induces Bypass of Mitosis and Tetraploidy.” Cell 141 (1): 81-93

Davoli, T. and T. De Lange. 2011. The Causes and Consequences of Polyploidy in Normal Development and Cancer. Annual Review of Cell and Developmental Biology. Vol. 27: 585-610

De Lange, T. 2009. “How Telomeres Solve the End-Protection Problem.” Science 326 (5955): 948-952

Gong, Y. and T. de Lange. 2010. “A Shld1-Controlled POT1a Provides Support for Repression of ATR Signaling at Telomeres through RPA Exclusion.” Molecular Cell 40 (3): 377-387

Kabir, S., A. Sfeir, and T. De Lange. 2010. “Taking Apart Rap1: An Adaptor Protein with Telomeric and Non-Telomeric Functions.” Cell Cycle 9 (20): 4061-4067

Palm, W. and T. De Lange. 2008. How Shelterin Protects Mammalian Telomeres. Annual Review of Genetics. Vol. 42.

Sfeir, A., S. Kabir, M. Van Overbeek, G. B. Celli, and T. De Lange. 2010. “Loss of Rap1 Induces Telomere Recombination in the Absence of NHEJ Or a DNA Damage Signal.” Science 327 (5973): 1657-1661

Sfeir, A., S. T. Kosiyatrakul, D. Hockemeyer, S. L. MacRae, J. Karlseder, C. L. Schildkraut, and T. de Lange. 2009. “Mammalian Telomeres Resemble Fragile Sites and Require TRF1 for Efficient Replication.” Cell 138 (1): 90-103

Scherthan, H., A. Sfeir, and T. De Lange. 2011. “Rap1-Independent Telomere Attachment and Bouquet Formation in Mammalian Meiosis.” Chromosoma 120 (2): 151-157

Share

Recommended Readings: Jason Cyster, Ph.D.

Posted on by
Reply

Friday Lecture Series

Sphingolipids and Oxysterols in B Cell Immunity and Cancer

Jason Cyster, Ph.D., Professor, Department of Microbiology and Immunology,

University of California, San Francisco

March 16, 2012

3:45 p.m.-5:00 p.m. (Refreshments, 3:15 p.m., Abby Lounge)

Caspary Auditorium

 

Recommended Readings:

Cinamon, G., M. A. Zachariah, O. M. Lam, F. W. Foss Jr., and J. G. Cyster. 2008. Follicular shuttling of marginal zone B cells facilitates antigen transport. Nature immunology 9, (1): 54-62

Cyster, J. G. 2005. Chemokines, sphingosine-1-phosphate, and cell migration in secondary lymphoid organs. Annual Review of Immunology 23 , pp. 127-159

Okada, T., and J. G. Cyster. 2006. B cell migration and interactions in the early phase of antibody responses. Current opinion in immunology 18, (3): 278-285

Pappu, R., S. R. Schwab, I. Cornelissen, J. P. Pereira, J. B. Regard, Y. Xu, E. Camerer, et al. 2007. Promotion of lymphocyte egress into blood and lymph by distinct sources of sphingosine-1-phosphate. Science 316, (5822): 295-298

Pham, T. H. M., P. Baluk, Y. Xu, I. Grigorova, A. J. Bankovich, R. Pappu, S. R. Coughlin, D. M. McDonald, S. R. Schwab, and J. G. Cyster. 2010. Lymphatic endothelial cell sphingosine kinase activity is required for lymphocyte egress and lymphatic patterning. Journal of Experimental Medicine 207, (1): 17-27

Randall, K. L., T. Lambe, A. Johnson, B. Treanor, E. Kucharska, H. Domaschenz, B. Whittle, et al. 2009. Dock8 mutations cripple B cell immunological synapses, germinal centers and long-lived antibody production. Nature immunology 10, (12): 1283-1291

Share

Recommended Readings: Elaine Fuchs, Ph.D.

Posted on by
Reply

Friday Lecture Series

Skin Stem Cells: In Morphogenesis, Wound Repair and Cancer

Elaine Fuchs, Ph.D., Rebecca C. Lancefield Professor,

The Rockefeller University

March 2, 2012

3:45 p.m.-5:00 p.m. (Refreshments, 3:15 p.m., Abby Lounge)

Caspary Auditorium

 

Recommended Readings:

Blanpain, C., and E. Fuchs. 2009. Epidermal homeostasis: A balancing act of stem cells in the skin. Nature Reviews Molecular Cell Biology 10, (3): 207-217

Ezhkova, E., W. -H Lien, N. Stokes, H. A. Pasolli, J. M. Silva, and E. Fuchs. 2011. EZH1 and EZH2 cogovern histone H3K27 trimethylation and are essential for hair follicle homeostasis and wound repair. Genes and Development 25, (5): 485-498

Fuchs, E. 2007. Scratching the surface of skin development. Nature 445, (7130): 834-842

Guasch, G., M. Schober, H. A. Pasolli, E. B. Conn, L. Polak, and E. Fuchs. 2007. Loss of TGFβ signaling destabilizes homeostasis and promotes squamous cell carcinomas in stratified epithelia. Cancer Cell 12, (4): 313-327

Kobielak, A., and E. Fuchs. 2006. Links between α-catenin, NF-κB, and squamous cell carcinoma in skin. Proceedings of the National Academy of Sciences of the United States of America 103, (7): 2322-2327

Williams, S. E., S. Beronja, H. A. Pasolli, and E. Fuchs. 2011. Asymmetric cell divisions promote notch-dependent epidermal differentiation. Nature 470, (7334): 353-358

Yi, R., and E. Fuchs. 2010. MicroRNA-mediated control in the skin. Cell death and differentiation 17, (2): 229-235

Share

Understanding The Relationship Between Inflammation and Cancer

Posted on by
Reply

The relationship between cancer and inflammation—the immune system’s response to infection, irritation, or injury—is a bit like that between the chicken and the egg. The two seem to occur together, but scientists aren’t really sure which comes first or whether one causes the other.  

A recent discovery by a team of researchers in the tumor biology section at the NIDCD, and scientists at SUNY Buffalo and the U.S. Food and Drug Administration (FDA) in Bethesda, Md., could help shine a welcome light on this quandary. The finding is the first to show that inflammatory factors produced during the development of head and neck tumors play an active role in coordinating a series of cellular events that allow cancer cells to grow and multiply unimpeded. Their findings are published in the September 20 early online edition of Cancer Research.

Share

Critical Review: The Origin of Cancer Robustness and Evolvability

Posted on by
Reply

This article, one of the most highly viewed and downloaded articles among Royal Society publications  in the past month, challenges our approaches to cancer which have failed to achieved expected improvements in dieases outcomes.   The authors suggest that a better understanding of underlying tumor robustness might lead to more successful research directions.

Share

Cancer Drug Candidate Leads to Proteomics Method

Posted on by
Reply

Scientists at Memorial Sloan-Kettering Cancer Center and Weill Cornell Medical have devised an affinity capture-based proteomics technique that could be used to identify and map dysregulated protein pathways in a number of different cancers.

The technique, which was detailed in a paper published Nature Chemical Biology, relies on the inhibitor PU-H71 – a small molecule that selectively binds tumor-enriched Hsp90 proteins, enabling pulldown of Hsp90-bound oncogenic client proteins. According to MSK researcher Gabriela Chiosis ― one of the developers of the method ― measurement of these captured proteins combined with bioinformatic analysis could provide a better understanding of tumor biology.

Share

Cancers Outwit Immune System by Silencing Signaling Mechanism

Posted on by
Reply

Scientists at Stanford University’s School of Medicine have shown that muting a key voice in the conversation between human immune cells as they coordinate an effort to fight off infection is an early step in the progression of human cancers.    The study, published May 18 in the Proceedings of the National Academy of Sciences, shows that the interferon pathway may harbor a general immune defect in many kinds of cancer. That may help explain the immune dysfunctions seen in numerous cancer patients, and why cancer immunotherapies are often ineffective.

Share

Understanding metastasis: Collective Cell Migration Controlled by Wnt and Fgf Signaling

Posted on by
Reply

In the November 11, 2008 issue of Developmental Cell, investigators from the University of Utah School of Medicine report the results of their studies in an article entitled Wnt/B-Catenin and Fgf Signaling Control Collective Cell Migration by Restricting Chemokine Receptor Expression.  These studies demonstrate a link between Wnt and Fgf signaling pathways in zebrafish and their impact on collective cell migration. 

The Wnt pathway regulates cell-to-cell communication in embryogenesis and cancer and Fgf influences embryongenesis, healing, and cell proliferation.  Piotrowski and Aman demonstrate for the first time that the interaction between Wnt and Fgf pathways is critical for collective cell migration.  Each pathway can restrict chemokine receptor expression and thereby elucidate how some types of cancer metastisize. 

Extracted from Developmental Cell and ScienceDaily.

Share

Wistar Raises Hopes for Block on Cancer

Posted on by
Reply

In an article published Aug. 31 in Nature online, researchers at The Wistar Institute have elucidated an active region of telomerase, an enzyme that plays a major role in the development of most human cancers.  This discovery could open the door for discovering new drugs that shut down telomerase.  The enzyme is inactive in most normal cells.

The research provides the first full-length view of the telomerase active region and how its configuration works to replicate the ends of chromosomes.  The enzyme has a complex structure of multiple protein domains and a stretch of RNA.  Many cancer cells hijack the telomerase system to promote their uninhibited growth.  Deactivating the enzyme could likely work against cancers, with few side effects.

Extracted from BBC News, Medical News Today, and Nature

Share