Archive for January, 2012

Summer Internship Opportuinity for PSOC Undergraduates

Thursday, January 26th, 2012

Summer Student Program

The best way to lure the brightest young minds to a career in biomedical research is to give them the opportunity to work in the laboratories of some of the nation’s top scientists. Accordingly, The Methodist Hospital Research Institute (TMHRI) offers a Summer Student Program for college undergraduates and medical students. First established in 2005, the program matches students with faculty mentors in TMHRI laboratories from June to August (10 weeks) and centers on a single research project. During this time, the students also attend required weekly didactic lectures given by the mentors and invited speakers. Students present their work at the end of the program at a student retreat. The program also provides numerous opportunities for social interaction and networking, including a welcome reception, trips to local sporting and cultural events, and a dinner at the end of the program. A stipend is provided to cover living expenses while in the program. The program is directed by Dr. Patricia Chevez-Barrios and co-directed by Dr. Ching-hsuan Tung.

Some students continue working with their mentors after the end of the program in order to see the project to completion and co-author a resulting publication. Other students return for additional summers or find other research opportunities through the program. Students come from a variety of universities, both national and international, including: Colorado College, Cornell University, Duke University, Emory University, Johns Hopkins University, McGill University (Canada), Northwestern University, Reed College, Oregon, Rensselaer Polytechnic Institute, Rhodes College, Rice University, Southern Methodist University, St. Louis University, Stanford University, Tecnologico de Monterrey (Mexico), Texas A&M University, The University of Texas at Austin, Trinity University, University of California, Berkeley, University of California, Los Angeles, University of Houston, and Vanderbilt University.

The students receive $5000 to spend on living expenses and travel over the 10 week period. They are given $1000 every 2 weeks.

Pauline

Application Instructions

Students interested in the program should apply by February 14, 2012 using the program application. Applications should be submitted in a PDF format and sent to: email hidden; JavaScript is required.

Applications will not be accepted after February 14, 2012. Acceptance notifications are made in April. Please note the dates for the 2012 Summer Internship Program are June 4- August 10, 2012. All students must be able to commit to the full 10-week program. No exceptions will be made.

For more information on the program, please contact: email hidden; JavaScript is required.

Paul Davies, Ph.D. “Cancer as Metazoa 1.0″

Monday, January 23rd, 2012

Speaker: Paul Davies, Ph.D., is a theoretical physicist, cosmologist and astrobiologist. He is Director of The Beyond Center for Fundamental Concepts in Science, whose agenda encompasses foundational topics ranging from the origin of the universe to the origin of life and the nature of time. Davies is also Principal Investigator of the Center for the Convergence of Physical Science and Cancer Biology at ASU. Among his research accomplishments, Davies helped explain how black holes radiate energy, what caused the ripples in the cosmic afterglow of the big bang, and why life on Earth may have come from Mars. He has written about 30 books, most recently The Eerie Silence: Are We Alone in the Universe? His fearless championing of bold new ideas earned Davies the epithet of “The Disruptor” in a recent profile in Nature magazine.

Location: Biodesign Auditorium

Web Cast: Unavailable

Date & Time: January 26th, 2012 12:00 p.m.

Title: Cancer as Metazoa 1.0

Abstract: Cancer is widespread among eukaryotes, and can be successfully tackled only by understanding its place in the story of life itself – especially the evolution of multi-cellularity. In this seminar I will propose a new theory of cancer, drawing on insights from astrobiology. The central hypothesis is that cancer is an organized pre-programmed process driven by a cassette of highly conserved, deeply-evolved ancient genes – genes that are active in early-stage embryo development, and which become inappropriately re-awakened in the adult form. In effect, cancer tumors are atavisms, recapitulating an ancient life form – “Metazoa 1.0” – dating back to the dawn of multi-cellularity. This hypothesis differs fundamentally from the popular notion that cancers are deregulated rogue cells running amok, and explains cancer’s well-known robustness and resilience. It also offers a well-defined target for therapy.

Thank you and if you have questions please contact Amanda Wilber! And don’t forget, coffee will be served!

Amanda Wilber, Center for the Convergence of Physical Science and Cancer Biology

Arizona State University | P.O. Box 871504 | Tempe, AZ 85287

480.965.3860 | Fax: 480.965.6362
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ASU PSOC Workshop, Thursday February 9th – Friday February 10th 2012

Wednesday, January 18th, 2012

Evolution, Development and Cancer: Connecting the Dots

Cancer is widespread among eukaryotes, and can be successfully tackled only by understanding its place in the story of life itself – especially the evolution of multi-cellularity. There is general agreement that the roots of cancer date back hundreds of millions of years. The ancient genes responsible for cancer are retained because they play a key role in embryo development. Normally these genes are subsequently silenced, but if they become re-awakened in the adult form, cancer is the result. The workshop is an ambitious attempt to connect the dots of evolutionary biology, developmental biology and cancer biology, bringing together three distinct communities in the search for hidden links that may form the basis of a radically new theory of cancer.
Listen to Audio Interviews and Read Transcripts (more…)

Sanjay Kumar, M.D., Ph.D., UC Berkeley – Mechanobiological control of tumor and stem cell behavior: Lessons from the brain

Tuesday, January 17th, 2012

Speaker: Sanjay Kumar, M.D., Ph.D., is Associate Professor of Bioengineering at the University of California, Berkeley. Dr. Kumar also holds appointments as a Faculty Scientist at Lawrence Berkeley National Laboratory and Supernumerary (Visiting) Professor at The University of Navarra in Spain. He earned a B.S. in chemical engineering from the University of Minnesota in 1996, and both a Ph.D. in molecular biophysics and an M.D. from Johns Hopkins University in 2003. From 2003-2005, he served as an NIH research fellow at Children’s Hospital Boston and Harvard Medical School. Since joining the faculty at UC Berkeley in 2005, Dr. Kumar has been recognized with the Presidential Early Career Award for Scientists and Engineers (PECASE) through the Department of Defense, The NSF CAREER Award, The NIH Director’s New Innovator Award, and The Arnold and Mabel Beckman Young Investigator Award.

Location: CPCOM 120

Web Cast: View Web Cast

Date & Time: March 8th, 2012 12:00 p.m.

Title: Mechanobiological control of tumor and stem cell behavior: Lessons from the brain

Abstract: One of the most exciting breakthroughs in cell biology over the past decade is the recognition that micromechanical inputs to cells from the solid-state extracellular matrix (ECM), such as those encoded in ECM geometry, topography, and elasticity, can influence cell and tissue physiology and pathology in profound and specific ways. This “physical microenvironment” bears direct relevance to the pathogenesis of diseases of the nervous system in which cells alter their structure, motility, or compliance, including neuronal and glial tumors and neurodegenerative disorders, and suggests that specific cell behaviors may be engineered by directly manipulating the underlying molecular systems. In this talk, I will discuss efforts my group has taken to elucidate the importance of the physical microenvironment in regulating tumor and stem cell biology in the central nervous system. This includes efforts to probe the molecular basis of the relationship between ECM mechanics, topology, and cellular motility and force generation in malignant glioma cells in two- and three-dimensional culture. In the case of adult neural stem cells, these approaches have enabled us to dissect and manipulate neurogenic commitment and maturation in vitro and in vivo by controlling both physical properties of the stem cell niche and the cellular signaling systems that interface with this niche. An important lesson from this work is that adult neural stem cells sense time-sensitive biomechanical signals from the microenvironment that are processed through Rho family GTPases, produce changes in cellular contractile signaling, and strongly influence neurogenic lineage commitment.

Thank you and if you have questions please contact Amanda Wilber! And don’t forget, coffee will be served!

Amanda Wilber, Center for the Convergence of Physical Science and Cancer Biology

Arizona State University | P.O. Box 871504 | Tempe, AZ 85287

480.965.3860 | Fax: 480.965.6362
email hidden; JavaScript is required

John Pepper, National Cancer Institute – Cancer as a failure of multicellularity

Tuesday, January 17th, 2012

Speaker: John W. Pepper, Ph.D. received his Ph.D. in biology from the University of Michigan in 1966. He was a postdoctoral fellow at the Santa Fe Institute, where he now serves as a member of the External Research Faculty. He is also a biologist at the National Cancer
Institute. His research focuses on the theory of multilevel selection and evolution, and on applications of this theory. Currently, he is working primarily on applications of evolutionary theory to complex diseases, including cancer. His major goal is to bring scientific understanding of evolution to bear in understanding the role of somatic cell-level evolution in the origin and progression of cancer. Pepper’s 31 peer-reviewed publications in behavioral ecology, evolutionary theory and its applications, and in cancer biology have been cited an average of 25 times each.

Location: Biodesign Auditorium

Web Cast: View Web Cast

Date & Time: February 9th, 2012 12:00 p.m.

Title: Cancer as a failure of multicellularity

Abstract: Cancer results from a process of cellular evolution. Key cancer defenses and vulnerabilities
both arose from the ancient evolutionary transition from single-celled to multicellular
organisms. Because cellular evolution leads inexorably to cancer, organismal evolution has
led to adaptations that organize cell reproduction into patterns that are less subject to cellular
evolution. We used an agent-based computational model of evolution inside tissues to test the
hypothesis that cell differentiation is crucial to suppressing cellular evolution within the body.
The hypothesis was supported. If this most basic safeguard is compromised, all the obstacles
to cancer built by organismal evolution are quickly dismantled by cellular evolution within the
organism.

Thank you and if you have questions please contact Amanda Wilber! And don’t forget, coffee will be served!

Amanda Wilber, Center for the Convergence of Physical Science and Cancer Biology

Arizona State University | P.O. Box 871504 | Tempe, AZ 85287

480.965.3860 | Fax: 480.965.6362
email hidden; JavaScript is required

John W. Pepper – Cancer as a failure of multicellularity

Friday, January 13th, 2012

Speaker: John W. Pepper, Ph.D. received his Ph.D. in biology from the University of Michigan in 1966. He was a postdoctoral fellow at the Santa Fe Institute, where he now serves as a member of the External Research Faculty. He is also a biologist at the National Cancer Institute. . His research focuses on the theory of multilevel selection and evolution, and on applications of this theory. Currently, he is working primarily on applications of evolutionary theory to complex diseases, including cancer. His major goal is to bring scientific understanding of evolution to bear in understanding the role of somatic cell-level evolution in the origin and progression of cancer. Pepper’s 31 peer-reviewed publications in behavioral ecology, evolutionary theory and its applications, and in cancer biology have been cited an average of 25 times each.

Location: Biodesign Auditorium

Web Cast: View Web Cast

Date & Time: February 9th, 2012 12:00 p.m.

Title: Cancer as a failure of multicellularity

Abstract: Cancer results from a process of cellular evolution. Key cancer defenses and vulnerabilities both arose from the ancient evolutionary transition from single-celled to multicellular organisms. Because cellular evolution leads inexorably to cancer, organismal evolution has led to adaptations that organize cell reproduction into patterns that are less subject to cellular evolution. We used an agent-based computational model of evolution inside tissues to test the hypothesis that cell differentiation is crucial to suppressing cellular evolution within the body. The hypothesis was supported. If this most basic safeguard is compromised, all the obstacles to cancer built by organismal evolution are quickly dismantled by cellular evolution within the organism.

Thank you and if you have questions please contact Amanda Wilber! And don’t forget, coffee will be served!

Amanda Wilber, Center for the Convergence of Physical Science and Cancer Biology

Arizona State University | P.O. Box 871504 | Tempe, AZ 85287

480.965.3860 | Fax: 480.965.6362
email hidden; JavaScript is required

Paul Davies’s Research Papers

Friday, January 13th, 2012

Targeting cancer’s weaknesses (not its strengths): Therapeutic strategies suggested by the atavistic model, BioEsays, September 2014

Targeting cancer’s weaknesses (not its strengths): Therapeutic strategies suggested by the atavistic model

‘Mitochondria and the evolutionary roots of cancer’ with Alfonso F Davila and Pedro Zamorano, Physical Biology 026008 10, (2013)

Mitochondria and the evolutionary roots of cancer PDF

Self-Orginization and Entropy Production in a Living Cell with E. Rieper & J.A. Tuszynski, BioSystems 111, 1(2013)

Self Orginization and Entropy Production in a Living Cell PDF

A physical sciences network characterization of non-tumorigenic and metastatic cells. Sci Rep. 2013
A physical sciences network characterization of non-tumorigenic and metastatic cells.

‘Isotropic 3D Nuclear Morphometry of normal, fibrocystic and malignant breast epithelial cells reveals novel structural alterations’ with Vivek Nandakumar, Laimonas Kelbauskas, Kathryn Hernandez, Kelly Lintecum, Patti Senechal, Kimberly Bussey, Roger Johnson and Deirdre Meldrum, PLoS ONE (2012).

Isotropic 3D Nuclear Morphometry of normal, fibrocystic and malignant breast epithelial cells reveals novel structural alterations PDF

‘Cancer as a dynamical phase transition’ with Lloyd Demetrius and Jack A Tuszynski, Theoretical Biology and Medical Modelling 8 1, 30 (2011).

Cancer as a dynamical phase transition PDF

‘Epigenetics and top-down causation’, Interface Focus 2, 42-48 (2011).

Epigenetics and top-down causation PDF

‘Cancer tumors as Metazoa 1.0: tapping genes of ancient ancestors’ with C H Lineweaver, Physical Biology 015001 8, (2011)

AFM Stiffness Nanotomography of Normal, Metaplastic and Dysplastic Human Esophageal Cells. Phys. Biol. February 2011.
AFM stiffness nanotomography of normal, metaplastic and dysplastic human esophageal cells.

Cancer tumors as Metazoa 1 0 tapping genes of ancient ancestors PDF

 

Roger Johnson talks about PSOC cancer project on KTAR

Wednesday, January 11th, 2012

New cancer technology study conducted at ASU
by Bob McClay/KTAR (January 10th, 2012 @ 5:00am)

Tempe, Ariz. – Technology being studied at Arizona State University could one day lead to an earlier diagnosis of breast cancer.

Researchers at ASU’s Biodesign Institute are working with a new 3D Imaging technology that pinpoints subtle changes in the nuclear structure of cells.

“The texture or the arrangement of the DNA in the nucleus is known to affect gene expression, which means which genes are more turned off or turned on, which changes as a function of disease state,” said Roger Johnson, a Research Laborator Manager at ASU and a co-author of a study of the technology.

Johnson went on to describe the technology.

“It’s kind of like a CAT Scanner, where the imaging is reduced to a sub-micron scale,” he said. “So it’s kind of like a cat-scanner for individual cells.

“Our hope is that these technologies will offer us the opportunity for early cancer detection,” said Johnson. “So that we can alert patients at the very early stages when the disease is still treatable.”

The technology was developed by a company called Visiongate, which hopes to get FDA approval this year. If it does, Johnson says the technology could be available in clinics around the country in two to three years.

Paul Davies on NPR

Monday, January 9th, 2012

Listen to Paul Davies on NPR discussing how his study of time travel and search for life in the universe informs his cancer research.

Steve Goldstein, left, host of "Here and Now" on KJZZ radio, interviewed ASU Regents' Professor Paul Davies on topics ranging from time travel to cancer research during the Dec. 21 show. Photo by: Carol Hughes

Time travel, SETI and cancer research are focus for ASU astrobiologist
December 21, 2011

“What do cancer research, time travel theories and the possibilities of life on other planets all have in common? For one thing, Paul Davies,” said Steve Goldstein, host of the radio show “Here and Now” on KJZZ (91.5 FM) in metropolitan Phoenix.

Davies, a theoretical physicist, cosmologist and astrobiologist at Arizona State University, where he is a Regents’ Professor, talked about the varied topics during a 15-minute interview Dec. 21.

Time travel was the first topic raised by Goldstein, and Davies replied: “People want to know, can it really be done? And, the answer is, well, maybe.” He explained that using Einstein’s theory, “we know how to travel in the future … just move. You can only go forward in time … this way.”

Davies didn’t want to give too much away on the radio show about time travel, since it is the topic of the annual Sci-fi meets Sci-Fact lecture at ASU. Davies, who is director of the BEYOND Center for Fundamental Concepts in Science, will deliver the lecture at 7 p.m., Jan. 31, in Neeb Hall on ASU’s Tempe campus.

However, he shared with Goldstein, “with something like a wormhole in space, it might be possible to go back in time.”

Other topics covered during the interview were one-way missions to Mars, the importance of continuing to search for extraterrestrial intelligence (SETI) and the importance of imagination to a scientist.

Davies also discussed his current research on cancer, as director of one of the 12 federally funded physical-science oncology centers looking at cancer research through fresh eyes … those of a physicist, rather than a biologist or chemist.

The interview is on the KJZZ website at http://kjzz.org/content/1112/beyond-science-fiction
Article source:
KJZZ “Here and Now”

Article:
http://kjzz.org/content/1112/beyond-science-fiction

Editor’s Note: Links are included for informational purposes only. Due to varying editorial policies, news publications may remove or change a link for archival purposes at any time without notice.

Rodger P McEver, M.D. Oklahoma Medical Research Foundation – ‘Force-regulated Adhesion of Leukocytes to Vascular Surfaces’

Monday, January 9th, 2012

Speaker: Rodger P McEver, M.D. is Chair, Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation. He studies how circulating blood cells attach to blood vessel surfaces at sites of tissue injury or infection.

Location: Biodesign Auditorium

Web Cast: View Web Cast

Date & Time: TBA, 2012 12:00 p.m.

Title: Force-regulated Adhesion of Leukocytes to Vascular Surfaces

Abstract: During inflammation, flowing leukocytes tether to and roll on activated endothelial cells, then decelerate and arrest before they emigrate into the underlying tissues. Interactions of selectins with glycosylated ligands mediate leukocyte rolling, a prerequisite for integrin-mediated deceleration and arrest. Counterintuitively, rolling requires a minimal flow rate, or shear threshold. As flow drops below this threshold, rolling becomes more rapid and irregular until the cells detach. Shear stress applies force to bonds between selectins and their ligands, which affects their lifetimes. As flow increases from suboptimal levels, force first prolongs bond lifetimes (catch bonds) until they reach a maximal level. Further increases in force shorten bond lifetimes (slip bonds). Catch bonds between selectins and ligands enable flow-enhanced adhesion of leukocytes to vascular surfaces and may prevent inappropriate agglutination of circulating cells. Recent data indicate that the mechanical environment of blood flow influences the functions of other adhesion receptors on leukocytes and platelets during infection or tissue injury. Mechanical forces might also regulate migration of tumor cells in extravascular tissues and metastasis of tumor cells through the blood stream.

Thank you and if you have questions please contact Amanda Wilber! And don’t forget, coffee will be served!

Amanda Wilber, Center for the Convergence of Physical Science and Cancer Biology

Arizona State University | P.O. Box 871504 | Tempe, AZ 85287

480.965.3860 | Fax: 480.965.6362
email hidden; JavaScript is required