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Cell Biology

Advanced prostate cancer treatment failure due to cell reprogramming – Medical Xpress

May 4, 2017 Micrograph showing prostatic acinar adenocarcinoma (the most common form of prostate cancer) Credit: Wikipedia

Columbia University Medical Center (CUMC) researchers have discovered a molecular mechanism that reprograms tumor cells in patients with advanced prostate cancer, reducing their response to anti-androgen therapy. The findings, based on a study in mice, could help to determine which patients should avoid anti-androgen therapy and identify new treatments for people with advanced prostate cancer.

The study was published online April14th in the journal Cancer Discovery.

Since androgens (male hormones) are known to drive prostate cancer, patients with recurrent or advanced disease are typically treated with anti-androgen medications. However, most patients fail treatment and develop an aggressive form of prostate cancer known as castration-resistant prostate cancer, or CRPC.

"It's been a mystery why some patients do not respond to anti-androgens, and why a subset of these patients actually get worse after treatment," said study co-leader Cory Abate-Shen, PhD, the Michael and Stella Chernow Professor of Urological Oncology and professor of urology, medicine, systems biology, and pathology and cell biology at CUMC. "Our findings show that in many of these patients, the tumor cells are reprogrammed so that they are no longer dependent on androgens."

To learn about the molecular mechanisms that drive resistance to anti-androgens, Drs. Abate-Shen and Michael Shen co-led a team to develop a strain of mice that lack two tumor-suppressor genes, Trp53 and Pten. These genes are both mutated in about 25 percent of patients with advanced prostate cancer. Mice that were treated with the anti-androgen drug abiraterone failed to respond and had accelerated tumor growthsimilar to some humans with advanced prostate cancer who do not respond to anti-androgen therapy.

"We found a number of genes that were overexpressed in mice with CRPC and also conserved in patients with the disease. Among the most interesting of these was SOX11, which regulates the development of the nervous system," said study co-leader Michael M. Shen, PhD, professor of medical sciences at CUMC.

Most localized, slow-growing prostate cancers are largely composed of epithelial cells, which are rich in androgen receptors that increase their susceptibility to anti-androgen therapy. In contrast, aggressive prostate cancers, particularly those that fail treatment, often contain many neuroendocrine-like cells, which lack androgen receptors and are therefore less responsive to anti-androgen therapy.

"This raised the question, where are the neuroendocrine-like cells in prostate tumors coming from?" said Dr. Abate-Shen. "While previous research hinted that epithelial tumor cells may be reprogrammed to become neuroendocrine-like cells, our study provides the first direct evidence that this reprogramming is actually occurring and that it is mediated, at least in part, by SOX11."

The researchers also demonstrated that SOX11 acts in a similar fashion in human prostate cancer cells.

"By giving anti-androgens to patients with CRPC, we are eliminating the cancer cells that need androgen to survive and enriching the tumor with the remaining neuroendocrine-like cells. The net effect is to create an even more aggressive tumor," said Dr. Shen.

The researchers also identified several "master regulators"genes that control SOX11 and other genes involved in prostate cancer reprogrammingthat might be targeted for new prostate cancer treatments.

"Based on our findings, genetic testing to identify SOX11 and the master regulators may be considered before embarking on anti-androgen therapy for patients with advanced prostate cancer," said Dr. Shen.

Explore further: Study uncovers an additional strategy for targeting treatment-resistant prostate cancer

More information: Min Zou et al, Transdifferentiation as a Mechanism of Treatment Resistance in a Mouse Model of Castration-resistant Prostate Cancer, Cancer Discovery (2017). DOI: 10.1158/2159-8290.CD-16-1174

Prostate cancer cells depend on signaling through the androgen receptor (AR) to grow and survive. Many anti-cancer therapies that target ARs are initially successful in patients, including a class of drugs known as CYP17A1 ...

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Prostate cancer is one of the most common cancers in men. Tumor growth is critically regulated by the androgen receptor, and treatment strategies to lower androgens, such as testosterone, are a mainstay of clinical treatment. ...

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Columbia University Medical Center (CUMC) researchers have discovered a molecular mechanism that reprograms tumor cells in patients with advanced prostate cancer, reducing their response to anti-androgen therapy. The findings, ...

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Advanced prostate cancer treatment failure due to cell reprogramming - Medical Xpress

Cell Biology

UCD’s Jodi Nunnari elected to National Academy of Sciences – Davis Enterprise

Professor Jodi Nunnari, chair of the department of molecular and cellular biology in the College of Biological Sciences at UC Davis, has been elected as a member of the National Academy of Sciences.

Nunnari studies mitochondria, tiny structures that provide energy to living cells and that are implicated in a wide range of diseases, including heart disease, stroke and inherited conditions.

Jodi Nunnari. Courtesy photo

Beginning as a postdoctoral researcher, Jodi has made discoveries that have transformed her field and helped demystify the genesis of a broad range of diseases, said Ralph Hexter, interim chancellor of UCD.

Her pioneering work is a prime example of our universitys commitment to fundamental research to improve the human condition. I could not be happier to see her receive this much-deserved recognition.

Nunnaris lab studies the behavior of mitochondria which have their own DNA, separate from the cell nucleus inside cells. Her work looks at the mechanisms through which mitochondria divide and fuse together, and at how mitochondrial DNA is organized and transmitted.

Nunnari is among 84 new members and 21 foreign associates elected to the academy this year. She is one of 27 current or retired UCD faculty who are members or foreign associates of the academy.

Election to the National Academies of Sciences is among the highest honors a scientist can receive in recognition of their distinguished scholarly contributions, said Mark Winey, dean of the College of Biological Sciences.

Jodis election is very well deserved for her groundbreaking work on mitochondria. As powerhouses of the cell, mitochondrial failure is linked to a variety of inherited diseases, as well as neurological disorders and aging.

Nunnari earned her bachelors degree from the College of Wooster in Ohio and her doctorate, in pharmacology, from Vanderbilt University. She carried out her postdoctoral research in the laboratory of Peter Walter at UC San Francisco, where she discovered that mitochondria form a dynamic network with the cell. This concept has led her to fundamental insights into how mitochondria grow, divide and function.

The National Academy of Sciences is a private, nonprofit institution that was established under a congressional charter signed by President Abraham Lincoln in 1863. Together with the National Academy of Engineering and the National Academy of Medicine, it provides advice on science, engineering, and health policy to the federal government and other organizations.

UC Davis News

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UCD's Jodi Nunnari elected to National Academy of Sciences - Davis Enterprise

Cell Biology

Starvation leads to ‘cell death’ which isn’t good for the body – Hindustan Times

Cell death, caused due to lack of glucose in which cells die in an unexpected manner, follows a process similar to what we would expect from an immune response, a new study found.

Are you one of those who starve yourselves for losing weight? You might want to think that again. According to a new study, researchers have characterized the cell death process due to starvation, in which the endoplasmic reticulum plays a leading role.

The study got published in journal Molecular and Cellular Biology.

Usually, programmed cell death -- also called apoptosis -- follows a biochemical pathway related to the permeabilization of mitochondria; However, we observed that in cases of cell death due to lack of glucose, cells die in an unexpected way, following a process similar to what we would expect from an immune response, stated Dr. Cristina Muoz-Pinedo, studys lead author.

The study finds that in cell-death-related treatments such as chemotherapy, the mitochondrial pathway is activated. Instead, when starved, cells activate the so-called death receptors on their membrane, which are normally used by the lymphocytes of the immune system to attack and destroy infected cells.

Starving yourself to losing weight may not be the bet options, the study found.

The researchers have been able to relate the activation of these membrane receptors to the endoplasmic reticulum, a cellular organelle involved in protein synthesis and lipid metabolism, as well as intracellular transport.

Feeling the stress produced by the lack of nutrients, the reticulum send an alarm signal that triggers the appearance of death receptors in the membrane, said Dr Muoz-Pinedo.

According to our in vitro results, we assume that this is how the tumour cells located in the centre of a tumour -- the so-called necrotic core -- die, because there are never enough nutrients in those areas. On the other hand, in ischemia, besides the lack of oxygen there is also cell death due to lack of glucose, so this process could also be related to the activity of the endoplasmic reticulum at a biochemical level, added the IDIBELL researcher.

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Starvation leads to 'cell death' which isn't good for the body - Hindustan Times

Anatomy

Grey's Anatomy Season 13, Episode 22 Recap: "Leave It Inside" – Refinery29

Except, of course, when Walter returns to the hospital later in the episode, and Minnick isnt there, Kerev isnt exactly looking for permission to save a life. Walter can no longer see because of the pressure from his tumor, and Kerev and Edwards team up to lie to not only the parents but the hospital. They put into his file the drugs that they would have given him if he was seizing, book an Emergency Room, and allow Dr. Amelia Shepherd to operate even though they know they dont have permission.

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Grey's Anatomy Season 13, Episode 22 Recap: "Leave It Inside" - Refinery29

Anatomy

Grey’s Anatomy recap: ‘Leave It Inside’ – EW.com (blog)

The tumor diagram is down, guys. I repeat: The tumor diagram is DOWN.

Meredith has actually removed the giant tumor from the wall of her bedroom and left it outside Amelias room. Its a new era inGreys Anatomy, but to be fair, when youre courting a new man, I think weve all had that moment when weve said, Its hard to look at my dead ex-husbands tumor art while Im trying to cultivate intimacy. You know what Im saying? Of course you do.

This week is all about the tumors: the awkward obstacles that we exist with and are hurt by. Its the way we live with the tumors. How Maggie awkwardly handles Meredith and Riggs. How Meredith fights the pain of losing Derek. How Bailey handles church and state when Minnickcalls out that Warren isnt a risk taker. And then, you know, actual tumors. Lets just hop in.

Thick Skin and A Tumor Heart

DeLuca and April end up together with a poor girl whose sexcapade turns into a free fall down two flights of stairs when she mistakes the front door for the bathroom. But the thing is, shes just stopping in for a broken arm, even though she has a gigantic heart tumor that would even make Erica Hahn show emotion.

But Holly is feelingvery calmabout all of this. Shes crushing the bedroom game while the tumor allows her to, and you have to respect how excited she is to get back in the saddle. Her words, not mine. Seriously. As Meredith continues to evaluate her, her evening companion shows up, and she tells Meredith to just say shes dead. I mean, girl has anagenda. But so does Maggie. She thinks she might have a way to work around Hollys tumor, and after enough persuasion, Maggie convinces her. This could be bad, yall. Maggie still needs to get beaten down by Seattles disastrous ways.

When they get in, that tumor is way bigger than even Maggie realized. It doesnt look so good for our girl. This tumor its invaded into her esophagus. Maybe even her spine.Everyones ready to close, and this is a room of women who once took a tumor right out of Geena Davis noggin. These ladiesknow tumors. Maggie isnt ready to give up, but its just too much, and Maggie has to explain to Holly that she wasnt able to remove the tumor. Hollys a great sport and says that the tumor is part of her, and shes learned to live with that.

But You Gotta Have Faith, Faith, Faith

Minnick doesnt do so great with that separation either, by the way. Right after throwing Warren under the medical bus, she runs off to Arizona to proposition some after-shift activities. Naked activities. This woman and her pivots, yall. (OR Board Note: Does Minnickremind you at all of a female Mark Sloan? Just consider it.)Theyre interrupted by a young boy who has stumbled into the hospital, parent-free.

Alex steps in to chat with the boy, who lives with a woman named Charlotte on a farm. Whileconsidering what to do next, he begins seizing. After finding his parents, Stephanie reveals that he has quite a sizable tumor on his brain. But when the surgeons offer surgery, his parents say that Liam will not be having surgery because thats not Gods will. If he heals, hell heal on his own.

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Grey's Anatomy recap: 'Leave It Inside' - EW.com (blog)

Cell Biology

New study uses 10x Genomics’ Single Cell 3′ Solution to unravel stem cell self-renewal mechanism – News-Medical.net

May 4, 2017

10x Genomics, a company focused on enabling the mastery of biology by accelerating genomic discovery, today announced publication of an article in the journal Nature of a collaborative research study with researchers at the Stanford University School of Medicine. The article entitled, "Non-equivalence of Wnt and R-spondin ligands during Lgr5+ intestinal stem-cell self-renewal," utilizes the 10x Genomics' Single Cell 3' Solution for single-cell RNA-seq (scRNA-seq) to unravel the priming and self-renewal mechanisms of intestinal stem cells (ISCs).

The renewal and differentiation of Lgr5+ ISCs is critical to the continuous regeneration of the epithelial lining of the gut, which enables us to absorb nutrients and provides a barrier to protect us from the external environment. Disruptions in this process can lead to or worsen human intestinal disorders such as inflammatory bowel disease (IBD), gastrointestinal cancer and Celiac disease.

This carefully regulated process occurs within a stem-cell niche called the intestinal crypt, and depends on Wnt signaling, which can be turned up by Wnt and R-spondin (RSPO) ligands. The authors sought to identify the unique functional roles of Wnt and RSPO ligands for regulating Lgr5+ ISCs and the relative contributions of both ligands to in vivo Wnt signaling and stem-cell biology.

The authors were able to show using in vivo experiments that Wnt and RSPO are not redundant signals. RSPO was shown to expand stem cell number. Although Wnt was needed to maintain Lgr5+ ISCs in the presence of RSPO, Wnt was not sufficient to induce additional numbers of Lgr5+ ISCs above a certain threshold, demonstrating that RSPO, and not Wnt, establishes the set point for Lgr5+ ISC number. The authors performed single-cell RNA-seq to definitively show that the signaling contributions of Wnt and RSPO elicited distinct effects on ISCs, by fully characterizing the expression profile for each unique cellular subtype on a cell-by-cell basis upon perturbation of those signals in vivo.

By characterizing gene expression from 13,102 single cells, Yan and colleagues were able to show that Lgr5- control cells represented differentiated cell types of the small intestinal lineages, including Paneth, goblet, enteroendocrine, enterocyte, pre-enterocyte, and tuft cells. The Lgr5+ cells consisted of three cellular sub-populations, corresponding to cycling stem cells, non-cycling stem cells, and transit amplifying cells. The authors were able to further show that these three distinct sub-populations of Lgr5+ cells were each uniquely affected by perturbations in Wnt and RSPO signaling, conclusively demonstrating that Wnts are priming factors that enable stem cells to be competent by expressing RSPO receptors on their cell surface, whereas RSPOs are actual self-renewal factors that expand stem cell number.

"Single-cell analysis provided conclusive evidence for the unique roles of Wnt and RSPO signaling to their respective function, either co-operatively priming Lgr5+ cells for competency, or for RSPO-mediated self-renewal," said Grace Zheng, Ph.D., research scientist at 10x Genomics. "This powerfully illustrates the utility of single-cell RNA-seq to monitor discrete stem-cell states and their dynamic perturbation. To do this with any other technology would have been extremely cumbersome, if not impossible."

"We are very excited about this result, and it opens up the possibility that analogous multi-tiered regulation by priming and self-renewal factors may be a generalized property of stem cells across other organ systems, either through Wnt and RSPO or functionally equivalent stem-cell niche components," said Ben Hindson, Ph.D., president, co-founder, and chief scientific officer of 10x Genomics. "This could have wide-reaching implications for stem-cell research and potentially yield new insight towards therapeutic applications in the future."

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New study uses 10x Genomics' Single Cell 3' Solution to unravel stem cell self-renewal mechanism - News-Medical.net

Anatomy

Anatomy of a Price Gouging Case – JD Supra (press release)

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Anatomy of a Price Gouging Case - JD Supra (press release)

Neuroscience

Facebook Explores Neuroscience For Next Typing Revolution – MediaFile

Facebook announced last week that it is researching and developing a neural interface that would allow people to type using their brains instead of their fingers. Users could type 100 words per minute with a silent speech system, enabling paralysis patients to communicate more efficiently with the world around them.

The neural interface system would not broadcast a users every thought onto the platform. Rather, it would work with the users thought process by sharing or typing only what he or she commands it to.

Facebooks 10-year game plan, published on its newsroom blog, outlining new technologies they want to create for the future of the platform.

This is about decoding those words youve already decided to share by sending them to the speech center of your brain, a Facebook newsroom blog post about its F8 2017 future of technology event said. We want to do this with non-invasive, wearable sensors that can be manufactured at scale.

The neuroscience behind this technological advancement has existed for over 10 years now, Dr. Henry Mahncke, the CEO of Posit Science, said in an interview with MediaFile.

Dr. Mahncke, who holds a Ph.D. in neuroscience from University of California San Francisco (UCSF), studies and creates software based brain training programs. These training programs test for brain plasticity, the brains ability to change itself at any age or any condition.

The brain is not fixed like a computer chip; it is constantly rebuilding and reorganizing itself, Dr. Mahncke said. When you learn to play piano, you are literally rewiring your brain. Everything you do or learn causes those changes.

A 3D brain scan from Posit Sciences Brain Image Gallery, depicting a brains connections and pathways between neurons.

Dr. Mahncke explained that Facebooks project does not want to open up a users skull to implant some sort of device, but would instead use a device to read his or her thoughts with a sensor. This kind of technology uses Near Infrared light (NIR) and a sensitive camera to focus on a specific part of the brain to detect activity. According to Dr. Mahncke, the camera would make strong guesses on what you were thinking by penetrating your skull with a particular wavelength of light.

I think weve entered a time where a lot of basic research of neuroscience is being realized, Dr. Mahncke said. Now its not just in a research setting, there are real world applications for it. We are entering a really fun and exciting age of applied neuroscience.

Dr. Mahncke also said that social media is here to stay, and believes we will create many more ways to share information in social media in the years to come. He added that the future of science and media are linked, but said it was hard to predict which will win and advance faster. He is excited to see the results, when or if Facebook lets this technology loose to the market.

One thing that interests me about these technologies [is that] there is a brain training component of them. A person is going to need to learn to control their brain activity in order for the camera to read them accurately. You will end up teaching yourself to organize your brain activity so the machine can read them most accurately. Its another way we have begun to adapt how we think to make it easier for the machines around us to work with us.

Facebook has been slowly moving from functioning as just a social media website to functioning as a technology company as its impact and innovation grows. Its innovations now have weight and legitimacy akin to Apple Inc. and other major technology influencers. With this potential technology, the way we communicate could change drastically in unforeseen ways. To Dr. Mahncke, what Facebook has begun to do is a neat next step in human cultural evolution in parallel with technological development.

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Facebook Explores Neuroscience For Next Typing Revolution - MediaFile

Neuroscience

Foreign Specialists at Neuroscience Workshop – Financial Tribune

A two-week international workshop on neuroscience opened in Tehran on April 29 sponsored jointly the International Brain Research Organization and Tarbiat Modarres University and Shahid Beheshti University of Medical Sciences. Specialists and experts from the US, Britain, Germany, Switzerland and Iran as well as students from regional countries are attending. Similar workshops have been held in the past by the Tarbiat Modarres and Shahid Beheshti universities and the Institute for Research in Fundamental Sciences in cooperation with international experts. This year, however, the event is more specialized and deals with newer realms of the science. Besides, fewer applicants have been admitted and the duration is longer so that participants would have in-depth and qualitative learning about the latest advancement in the field, said Yaqoub Fathollahi, research deputy at Tarbiat Modarres University, IRNA reported. In recent years, PhD and post PhD students as well as young faculty members from China, Turkey, India, Pakistan and Indonesia have shown interest in the event. Over 100 researchers registered for the current workshop but only 14 from Iran and regional countries were accepted, said the official. This years event is focusing on the effectiveness of research projects and their role in the development of neurosciences in the region. The workshop will close on May 12. IBRO is the global federation of neuroscience organizations that aims to promote and support neuroscience training, teaching, collaborative research and advocacy around the world. More than 80 international, national and regional scientific organizations constitute IBROs Governing Council, which together with the five IBRO Regional Committees, addresses the needs and advances the work of individual scientists and research communities. IBROs mission is to develop, support, coordinate and promote scientific research in fields related to the brain; promote international collaboration and sharing of scientific information on brain research throughout the world; provide for and assist in education and dissemination of information relating to brain research. Most advanced workshops of the IBRO in Asia have so far been hosted by Japan, China and South Korea.

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Foreign Specialists at Neuroscience Workshop - Financial Tribune

Neuroscience

Why are lawyers using brain damage as a criminal defense? The science doesn’t support it – Los Angeles Times

When his criminal trial begins next week, attorneys for Andres Andy Avalos, a Florida man charged with murdering his wife, a neighbor and a local pastor, will mount an insanity defense on behalf of their client because, as they announced last summer, a PET scan revealed that Avalos has a severely abnormal brain. In March, shortly after an Israeli American teenager was arrested on suspicion that he made bomb threats against Jewish institutions in the U.S. and abroad, his lawyer declared that the teenager had a brain tumor that might have affected his behavior. Both cases are part of a growing movement in which attorneys use brain damage in service of a legal defense.

To support such claims in court, lawyers are turning to neuroscience. The defense brings in hired guns to testify that brain scans can identify areas of dysfunction linked to antisocial behavior, poor decision-making and lack of impulse control. The prosecution calls their own expert witnesses to argue that what a scientist might observe in brain scans shows nothing about that persons state of mind or past actions.

The truth is that even the most sophisticated brain scans cannot show direct correlations between brain dysfunction and specific criminal behavior, nor can they prove whether someone is legally insane. What neuroscience can show is that a persons decision to commit a crime or to do anything in life for that matter is triggered by a series of chemical and electrical interactions in the brain. It can also show approximately where those interactions are occurring.

Consider the case of Charles Whitman, who killed 14 people from a perch atop the Texas Tower at the University of Austin in 1966. (He killed his wife and mother the night before.) In a note he left before going on his killing rampage, Whitman wrote of having severe headaches and suggested that an autopsy might reveal a physical anomaly.

He had a brain tumor, it turned out, the size of a pecan. It was nestled between the thalamus, which relays sensory and motor information and regulates sleep, and the amygdala, which is associated with emotional regulation and behavior. Many of Whitmans family members and friends wanted to believe the tumor was responsible for triggering his actions. Yet a doctor reported that he didnt think the tumor was related to Whitmans psychiatric complaints or headaches, and certainly not to his homicidal rampage.

Texas Gov. John Connally called a state commission to review Whitmans case. In its final report, the commission allowed that the tumor conceivably could have contributed to his inability to control his emotions and actions, but said that it could not establish that the tumor actually caused the killings.

The tumor, then, didnt change Whitmans standing. As long as a person understands the difference between right and wrong and can appreciate the nature and consequences of his or her actions, he or she cannot be found legally insane. Whitmans crimes took care, planning and forethought. It would have been impossible to prove that the tumor qualified him as legally insane.

Its not yet clear if the lawyer representing the Israeli American suspect will submit evidence of his brain tumor in court, but it is clear that the teens actions required forethought and premeditation. He used Tor, a type of software that allows users to hide their computers identifying IP address. He also disguised his voice, an indication that he knew what he was doing and that there would be consequences if he was caught.

Though decades of research tell us that brain damage can alter peoples behavior and impair their ability to make sound judgments and rational decisions, in the legal realm, thats not enough for a successful criminal defense. There is, however, one limited area in which neuroscience can be applied appropriately and responsibly in the courtroom: sentencing.

Our judicial system has long recognized that people who suffer from psychiatric or mental illnesses should not be treated in the same way as their mentally healthy counterparts. Medical diagnoses of psychiatric conditions or cognitive impairment are considered mitigating circumstances that raise the possibility of alternatives to harsher punishments. Neuroscientific evidence can be used to support such diagnoses.

Although the legal system should recognize the value of neuroscience, it must also understand its limitations and guard against its abuse. When neuroscience is applied responsibly, it can mean treatment instead of incarceration, life instead of the death penalty.

Kevin Davis is a Chicago-based journalist and author of The Brain Defense: Murder in Manhattan and the Dawn of Neuroscience in Americas Courtrooms.

Follow the Opinion section on Twitter @latimesopinion or Facebook

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Why are lawyers using brain damage as a criminal defense? The science doesn't support it - Los Angeles Times