Today is the anniversary of the prostate surgery that removed both that organ and the cancer it contained that I first mentioned here in Surgery as a fresh start. A year after the surgery and ten months after I wrote that entry, what I said then--“that thing was killing me, both literally and figuratively and I'm much better off without it”--still holds true. My perspective on the my treatment and its outcome has, if anything, become firmer.
To mark the occasion, I present all the cancer research from KPBS and campuses on the campaign trail I’ve included in Overnight News Digests since the last two times I’ve mentioned the topic of cancer, Quitting smoking in the New Year and Health research and outreach from KPBS and campuses on the campaign trail.
Following my policy of “if it moves, it leads,” here is the one video, which comes from KPBS: Task Force Recommends New Lung Cancer Screening Guidelines.
The U.S. Preventative Services Task Force said lung cancer screening for many chain-smokers and former smokers should be done with a CT scan instead of an X-ray.I’ll have more to say about smoking in another entry. For now, follow over the jump for the rest of the stories about cancer research.
Virginia Commonwealth University: VCU researchers show experimental drug could enhance the effectiveness of existing multiple myeloma and myeloid leukemia therapies
By John Wallace
Tuesday, Feb. 18, 2014
A pre-clinical study led by Virginia Commonwealth UniversityMassey Cancer Center and Department of Internal Medicine researchers suggests that an experimental drug known as dinaciclib could improve the effectiveness of certain multiple myeloma and myeloid leukemia therapies.Michigan Tech: A Better Way to Purify Peptide-Based Drugs
The study, recently published in the journal Molecular Cancer Therapeutics, showed that dinaciclib disrupted a cell survival mechanism known as the unfolded protein response (UPR). Without the UPR, multiple myeloma and myeloid leukemia cells were unable to combat damage caused by some anti-cancer agents.
By Marcia Goodrich
Last Modified 4:50 PM, February 14, 2014
Peptides are an intriguing class of drugs. They are made of amino acids, just as humans are, and because of their intimate relationship with our own biological molecules, they have the potential to fight some of the most intractable diseases, including cancer.UCSB: Global Regulator of mRNA Editing Found
But they can be difficult and expensive to make. A year’s worth of the anti-HIV peptide drug enfuvirtide costs $25,000. Now a chemist at Michigan Technological University has overcome an important hurdle in the manufacturing process by developing a quicker, simpler purification method. As a bonus, his technique also works on DNA.
The new technology separates perfect peptides from those that do not make the grade, says Shiyue Fang. During production, amino acids attach to each other in chains to form the desired peptide, but some of the chains are never completed. To separate these truncated peptides, Fang’s team adds a polymerizable group of atoms to the mix.
Protein controls editing, expanding the information content of DNA
By Scott LaFee
February 06, 2014
An international team of researchers, led by scientists from the University of California, San Diego School of Medicine and Indiana University, have identified a protein that broadly regulates how genetic information transcribed from DNA to messenger RNA (mRNA) is processed and ultimately translated into the myriad of proteins necessary for life.UCSD: Split Decision: Stem Cell Signal Linked With Cancer Growth
The findings, published today in the journal Cell Reports, help explain how a relatively limited number of genes can provide versatile instructions for making thousands of different messenger RNAs and proteins used by cells in species ranging from sea anemones to humans. In clinical terms, the research might also help researchers parse the underlying genetic mechanisms of diverse diseases, perhaps revealing new therapeutic targets.
“Problems with RNA editing show up in many human diseases, including those of neurodegeneration, cancer and blood disorders,” said Gene Yeo, PhD, assistant professor in the Department of Cellular and Molecular Medicine at UC San Diego. “This is the first time that a single protein has been identified that broadly regulates RNA editing. There are probably hundreds more. Our approach provides a method to screen for them and opens up new ways to study human biology and disease.”
By Scott LaFee
February 03, 2014
Researchers at the University of California, San Diego School of Medicine have identified a protein critical to hematopoietic stem cell function and blood formation. The finding has potential as a new target for treating leukemia because cancer stem cells rely upon the same protein to regulate and sustain their growth.University of Alabama at Birmingham: New ‘living document’ provides real-time Hepatitis C treatment guidance
Hematopoietic stem cells give rise to all other blood cells. Writing in the February 2, 2014 advance online issue of Nature Genetics, principal investigator Tannishtha Reya, PhD, professor in the Department of Pharmacology, and colleagues found that a protein called Lis1 fundamentally regulates asymmetric division of hematopoietic stem cells, assuring that the stem cells correctly differentiate to provide an adequate, sustained supply of new blood cells.
Asymmetric division occurs when a stem cell divides into two daughter cells of unequal inheritance: One daughter differentiates into a permanently specialized cell type while the other remains undifferentiated and capable of further divisions.
Written by Nicole Wyatt
February 06, 2014
When treatment guidelines for a particular disease emerge, they are often published in a peer-reviewed medical journal, which can take up to three years. One University of Alabama at Birmingham infectious diseases expert recently helped develop new Hepatitis C virus (HCV) guidelines that can be updated and published as new data emerge and new therapies are approved.Georgia Tech: In Vitro Innovation: Testing Nanomedicine With Blood Cells On A Microchip
HCV — which affects more than 3 million people in the United States and is the leading cause of cirrhosis and liver cancer, according to the Centers for Disease Control and Prevention — last saw guidelines released in 2011.
Posted February 4, 2014 | Atlanta, GA
Designing nanomedicine to combat diseases is a hot area of scientific research, primarily for treating cancer, but very little is known in the context of atherosclerotic disease. Scientists have engineered a microchip coated with blood vessel cells to learn more about the conditions under which nanoparticles accumulate in the plaque-filled arteries of patients with atherosclerosis, the underlying cause of myocardial infarction and stroke.UCSD: How DNA Damage Affects Golgi - The Cell's Shipping Department
In the research, microchips were coated with a thin layer of endothelial cells, which make up the interior surface of blood vessels. In healthy blood vessels, endothelial cells act as a barrier to keep foreign objects out of the bloodstream. But at sites prone to atherosclerosis, the endothelial barrier breaks down, allowing things to move in and out of arteries that shouldn’t.
In a new study, nanoparticles were able to cross the endothelial cell layer on the microchip under conditions that mimic the permeable layer in atherosclerosis. The results on the microfluidic device correlated well with nanoparticle accumulation in the arteries of an animal model with atherosclerosis, demonstrating the device’s capability to help screen nanoparticles and optimize their design.
By Debra Kain
January 30, 2014
In studying the impact of DNA damage on the Golgi, a research team from the University of California, San Diego School of Medicine and the Ludwig Institute for Cancer Research have discovered a novel pathway activated by DNA damage, with important consequences for the body's cellular response to chemotherapy.University of Alabama Birmingham: Interdisciplinary UAB researchers collaborate to establish new imaging method
Standard cancer treatments, including many chemotherapy drugs and radiation therapy, act on cells by causing DNA damage. In many cancer cells, DNA damage turns on signaling pathways that lead to cell death - the basis of the use of these treatments for cancer.
A better understanding of the signaling pathways that are activated in cells in response to DNA damage, and the influence they exert to determine the fate of the cell to live or die, ultimately could lead to more effective use of these DNA damaging agents to treat cancer.
By Jim Bakken
January 28, 2014
An interdisciplinary collaboration at the University of Alabama at Birmingham recently established a research method that has expanded the institution’s already robust capacity for discovery, addressing a need that will aid in critical initiatives addressing a variety of diseases including cancer, chronic inflammatory autoimmune diseases and age-related degenerative diseases.UCSD: Putting a Brake on Tumor Spread
The matrix-assisted laser desorption/ionization imaging mass spectrometry, or MALDI-IMS, method is a powerful tool for investigating the distribution of molecules within biological systems through the direct analysis of thin tissue sections.
Biomedical research is typically aimed at answering the fundamental questions of how, when, where and why important biological processes occur in the body and determining their relevance to human disease.
By Scott LaFee
January 23, 2014
A team of scientists, led by principal investigator David D. Schlaepfer, PhD, a professor in the Department of Reproductive Medicine at the University of California, San Diego School of Medicine, has found that a protein involved in promoting tumor growth and survival is also activated in surrounding blood vessels, enabling cancer cells to spread into the bloodstream.Temple University: Tumor-suppressing genes might play important role in obesity, diabetes and cancer
The findings are published in this week’s online issue of The Journal of Cell Biology.
Blood vessels are tightly lined with endothelial cells, which form a permeability barrier to circulating cells and molecules. “Our studies show that pharmacological or genetic inhibition of the endothelial protein focal adhesion kinase, or FAK, prevents tumor spread by enhancing the vessel barrier function.”
January 17, 2014
The function of two tumor-suppressing genes could play a vital role in helping to control obesity and other diseases such as diabetes, heart disease and cancer, according to researchers in the Sbarro Institute for Cancer Research and Molecular Medicine at Temple.University of Iowa: Protein links liver cancer with obesity, alcoholism, and hepatitis
The researchers published their findings, “Silencing of RB1 and RB2/p130 during adipogenesis of bone marrow stromal cells results in dysregulated differentiation,” in the Feb. 1, 2014, issue of the journal Cell Cycle.
“We found that these two genes of the retinoblastoma family, Rb1 and Rb2/p130, are key proteins in regulating the formation and function of fat tissue in the body,” said Antonio Giordano, director of the Sbarro Institute and one of the paper’s lead authors. “If these proteins are not functioning properly, they are unable to control the formation of fat tissue in the body, so you have a continuous formation of fat tissue.”
Protein once thought to protect against cancer
By: Jennifer Brown
2013.12.30 | 07:00 AM
Obesity, alcoholism, and chronic hepatitis all increase the risk of getting liver cancer, which is the third leading cause of cancer death worldwide. Obesity in particular is driving a significant increase in liver cancer in the United States. These three health problems also increase cellular stress in the liver, but until now it has not been clear if there is a direct biological link between cellular stress and the development of liver cancer.Texas A&M: There’s something in the saliva
In a new study, University of Iowa researchers have identified an unexpected molecular link between liver cancer, cellular stress, and these health problems that increase the risk of developing this cancer.
The study, published Dec. 19 in the journal PLOS Genetics, shows that a protein called CHOP, which had previously been thought to generally protect against cancer, actually promotes liver cancer in mice and may do the same in humans.
by Jennifer Fuentes
January 23, 2014
As new oral cancer diagnoses rose to more than 41,000 in 2013, and demand for early detection continues to increase, research from Texas A&M University Baylor College of Dentistry’s diagnostic sciences department could introduce an oral cancer saliva test in the future while reducing the test’s risk of false positive results.University of Virginia: Children’s Cancer Test May Produce False Positives, U.Va. Researchers Find
All it takes is a test tube and a bit of saliva.
January 23, 2014
A test used to detect a type of cancer in children may produce false positives because it is based on a faulty assumption, researchers at the University of Virginia School of Medicine have determined.UCSD: Keeping Stem Cells Pluripotent
The test works by detecting a gene fusion thought to be unique to a rare form of cancer known as alveolar rhabdomyosarcoma. But the new U.Va. research shows that the fusion actually occurs during normal cellular development as well. The fusion of genes lasts only a brief time during normal development, but a diagnostic test could potentially detect it and indicate the presence of cancer where there is none, the researchers believe.
“Cancer does express this fusion. But it’s not totally unique now. It’s not black and white now. It’s shades of gray,” said researcher Hui Li of the School of Medicine’s Department of Pathology and the U.Va. Cancer Center. “In normal development, it’s only briefly expressed, so if we can understand the normal process a little better and know when exactly in development you see this, maybe we can develop a better assay to rule out this particular potential for false positives.”
By blocking key signal, researchers maintain embryonic stem cells in vital, undifferentiated state
By Scott LaFee
January 13, 2014
While the ability of human embryonic stem cells (hESCs) to become any type of mature cell, from neuron to heart to skin and bone, is indisputably crucial to human development, no less important is the mechanism needed to maintain hESCs in their pluripotent state until such change is required.University of Arkansas: Physicists Quantify Temperature Changes in Metal Nanowires
In a paper published in this week’s Online Early Edition of PNAS, researchers from the University of California, San Diego School of Medicine identify a key gene receptor and signaling pathway essential to doing just that – maintaining hESCs in an undifferentiated state.
The finding sheds new light upon the fundamental biology of hESCs – with their huge potential as a diverse therapeutic tool – but also suggests a new target for attacking cancer stem cells, which likely rely upon the same receptor and pathway to help spur their rampant, unwanted growth.
Findings in field that affects cancer treatment, solar energy
Friday, January 17, 2014
FAYETTEVILLE, Ark. — Using the interaction between light and charge fluctuations in metal nanostuctures called plasmons, a University of Arkansas physicist and his collaborators have demonstrated the capability of measuring temperature changes in very small 3-D regions of space.University of Georgia: New aspirin-based prodrug may prevent damage caused by chemotherapy
Plasmons can be thought of as waves of electrons in a metal surface, said Joseph B. Herzog, visiting assistant professor of physics, who co-authored a paper detailing the findings that was published Jan. 1 by the journal Nano Letters, a publication of the American Chemical Society.
The paper, titled “Thermoplasmonics: Quantifying Plasmonic Heating in Single Nanowires, was co-written by Rice University researchers Mark W. Knight and Douglas Natelson.
January 9, 2014
Athens, Ga. - Researchers at the University of Georgia have developed a new prodrug that promises to reduce many of the negative side effects caused by cisplatin, a commonly prescribed chemotherapy treatment.UCSD: The Mouse That ROR’ed
Cisplatin may be used to treat a variety of cancers, but it is most commonly prescribed for cancer of the bladder, ovaries, cervix, testicles and lung. It is an effective drug, but it often causes severe and irreversible damage to a patient's kidneys, hearing and sense of balance.
UGA researchers combined cisplatin with aspirin in a new single prodrug formulation they call Platin-A, which prevents these negative side effects by reducing inflammation. They reported their findings recently in Angewandte Chemie, a journal published by the German Chemical Society.
ROR1 oncogene combines with another to accelerate, worsen blood cancer
By Scott LaFee
January 02, 2014
Researchers at the University of California, San Diego School of Medicine report that an oncogene dubbed ROR1, found on chronic lymphocytic leukemia (CLL) B cells but not normal adult tissues, acts as an accelerant when combined with another oncogene, resulting in a faster-developing, more aggressive form of CLL in mice.UCSD: How Cells Remodel After UV Radiation
The findings, published in the Dec. 30, 2013 Online Early Edition of PNAS, suggest ROR1 could be an important therapeutic target for patients with CLL, the most common form of blood cancer. Prevalence of CLL in the United States is high: 1 in 20 people over the age of 40 could have apparently pre-cancerous CLL-like cells in their blood. These people may develop actual CLL at a rate of about 1 percent per year. More than 15,000 new cases of CLL are diagnosed each year in the United States. Roughly 4,400 patients with CLL die annually.
Researchers map cell's complex genetic interactions to fix damaged DNA
By Scott LaFee
December 19, 2013
Researchers at the University of California, San Diego School of Medicine, with colleagues in The Netherlands and United Kingdom, have produced the first map detailing the network of genetic interactions underlying the cellular response to ultraviolet (UV) radiation.As you can see, the past two-and-a-half months have produced a bumper crop of research on cancer causes, detection, and treatment. As a beneficiary of such efforts, I say “carry on!” May I be around to mark the second anniversary of remaining cancer-free and celebrate another year of research.
The researchers say their study establishes a new method and resource for exploring in greater detail how cells are damaged by UV radiation and how they repair themselves. UV damage is one route to malignancy, especially in skin cancer, and understanding the underlying repair pathways will better help scientists to understand what goes wrong in such cancers.
The findings will be published in the December 26, 2013 issue of Cell Reports.