Category Archives: Cell Biology

In a lab pushing the boundaries of biology, an embedded ethicist keeps scientists in check – STAT

T

he young scientists had a question. They were working with mouse embryos from which all living cells had been chemically dissolved away.

So far, so good, thought the bioethicist, as she listened to the presentation at a Harvard Medical School lab meeting.

The scientists were seeding the mouse scaffolds with human stem cells. Those cells were expected to turn into human liver cells and perhaps a mini human liver; and human kidney cells and perhaps mini human kidneys; andhumanheart and brain cells and

Wait.

Jeantine Lunshof insists she is not the ethics police. It says so on the door to her closet-sized office at Harvard. She doesnt find reasons to reflexively shut down experiments. She doesnt snoop around for deviations from ethical guidelines. But when scientists discuss their research in the twice-weekly lab meetings she attends, I will say, hmm, that raises some good questions, Lunshof said.

There is no shortage of good questions for Lunshof, who for the last three years has been embedded in the synthetic biology lab of George Church, the visionary whose projects include trying to resurrect the wooly mammoth and to write a human genome from scratch. Church is also famous for arguing that it is ethically acceptable to edit the genomes of human embryos if doing so will safely alleviate suffering, and for encouraging people to make their full genome sequence public, privacy be damned.

In the Church lab, Lunshof told STAT, you have incredibly interesting conversations.

George Church has a wild idea to upend evolution. Heres your guide

Rapid advances in genomics and stem cell biology are forcing researchers to regularly confront ethical quandaries that seem straight out of science fiction. The power to create organisms with cells, tissue, and even organs from different species,called a chimera, raises thornyquestions: What is the moral status of a primordial human brain nourished with a rudimentary heart and circulatory system, all inside a mouse scaffold? Can it feel pain? Should it not be created in the first place? Genome-editing presents otherchallenges: Where does therapy end and enhancement begin? Could genome-editing to prevent dwarfism, for example, go a little further and create a future NBA star? How should society balance competing values such as autonomy, like the freedom of parents to do everything they can for their children, and justice, as in not creating classes of genetic haves and have nots?

George is far ahead of everyone else in the kinds of experiments he undertakes, said John Aach, a senior scientist in Churchs lab who works closely with Lunshof. She performs a service in making them slow down to where the rest of the world is. Otherwise George might stumble. It doesnt take much to stumble and make a mess of things. Jeantine keeps things moving on the bioethics side as the science is moving ahead.

Lunshofs role is unusual if not unique. Genetics researchers will tap a bioethicist to join a grant or consult on a project, but it is rarely if ever the case that a genetics lab has a full-time bioethicist, said Brendan Parent, a bioethicist at New York University. He and others are unaware of any other such embeds. Instead, bioethicists and biologists tend to interact when they serve on committees convened by universities, scientific organizations, or government.

In contrast, Lunshof not only coauthors papers with Church and his colleagues, but also helps draft protocols for some of the cutting-edge science the lab conducts. By being present at the creation, she is able to flag ethical minefields before the lab finds itself bumbling acrossone.

She provides me with a comfort zone, Church said. I think much more about societal concerns that the labs research might raise. Shes here while were just starting to think about experiments, he added, and because of her we talk about [bioethics] earlier than most groups do. Jeantine is fearless in what she tackles.

The benefits of this collaboration extend beyond Church and his lab. Watching new biology emerge in real time has enabled Lunshof to develop much-needed new ways of thinking aboutbioethics, giving her field and the world outside the lab a fighting chance to keep up.

Its at the lab meetings every Monday and Thursday afternoon that Lunshof typically learns what might next land on her to-do list. The 50 or so scientists in attendance update Church on their research and others offer comments. The rows of chairs are generally all filled. Lunshof, in typically casual lab attire, rarely asks questions, instead taking notes and keeping track of who she needs to follow up with.

This week, researchers discussed plans to do cognitive testing on participants in a project centered on having their genomes sequenced. Lunshofs ears pricked up.

The combination of genetics and intelligence has long been a danger zone, largely because measurements of intelligence are imprecise and shaped by the dominant culture, as decades of debate about IQ tests have shown. The tests do not measure cognition, let alone intelligence, Lunshof said during the meeting, arguing for staying away from linking the genome to cognition or IQ. She urged the scientists to be more precise in describing what the tests measured: memory and mental processing speed. Correcting things later by saying, No, we are not measuring IQ, really were not, is very difficult, she said.

When I feel that something is a problem, I feel completely free to say, Dont go down that road, Lunshofsaid in an interview. She is not paid by Harvard. Born and raised in the Netherlands, sheis an assistant professor there, at University Medical Center Groningen, and she was awarded a Marie Curie fellowship to move to Boston and support her work in Churchs lab.

Audacious project plans to create human genomes from scratch

No one in the lab ever puts pressure on me to legitimize anything or to agree with what theyre doing, she said. I am always on the alert for things that could get into delicate areas.

Lunshofs collaboration with Church began in 2006. Itwas the start of the Personal Genome Project, an effort to sequence peoples full genomes and mine the data to link genetics to health. Church was causing consternation by proposing that people make their genome and their health history publicly available.

My first reaction was, this is totally crazy, Lunshof recalled. Anonymity and confidentiality were central to everything we do in biomedical ethics.

But then she thought, what if Church is right? He had argued that its impossible to guarantee that a DNA sample would remain anonymous. (Hewould beproved right in 2013.) So why not do away with that charade at the outset, and instead of making empty promises of anonymity, tell volunteers from the get-go that anyone could know who they were?

Lunshof had studied philosophy and Tibetan language and culture as an undergraduate, then had written a doctoral thesis on ethical issues in genomics. She also had earned a nursing degree, and worked at the Netherlands Cancer Institute in Amsterdam. In 2006, she stumbled on the PGP website and sent an email expressing her interest in it. Church replied within hours and their partnership was born.

Together, they developed a new form of patient consent for the Personal Genome Project. Called open consent, it was founded on principles new to the bioethics of genetic research. It tells participants they wont have privacy and confidentiality. Instead, consent is based on values such as reciprocity (scientists and volunteers interact as equals) and veracity. Lunshof is also a big believer in the ethical concept of citizenry, including allowing ones genetic data to be accessed by all qualified scientists tohelp advance medical progress and alleviate human suffering.

Because of advances in genetics and genomics, it made sense to abandon the traditional idea of medical confidentiality, Lunshof said, or at least not make it central.

That was a minority opinion. The National Institutes of Health, a main funder of Churchs lab, wasnt ready to embrace the idea of genetic privacy being violable, said Aach. It and the genetics community went in the other direction, saying we have to take steps to protect privacy, a huge and costly undertaking.

With the development of open consent, the Personal Genome Project took off, and now has more than 5,000 participants in the United States alone.

When I feel that something is a problem, I feel completely free to say, Dont go down that road.

Bioethicist Jeantine Lunshof

The ethics debate around genomics intensified with publication of a breakthrough 2012 paperon CRISPR, the revolutionary new genome-editing technology. After Church and his team got CRISPR to edit the genomes of human cells, later that year, they and others quickly faced two quandaries: Should CRISPR ever be used to enhance peoples genetic inheritance? Should it be used to edit the genomes of human eggs, sperm, or early embryos, producing changes that could be inherited by offspring and, maybe, generations of designer babies?

For many scientists and ethicists, the line-in-the-sand position on such germline editing and genetic enhancement has long been no. Lunshof had other ideas.

From the bioethics standpoint, she told STAT one afternoon at a Harvard Medical School cafe, it is not clear why altering genes [for enhancement] is by definition unethical. Some philosophers have consistently argued that there is a duty to at least consider genetic enhancement.

The CRISPR patent decision: Your six takeaways

In the real world, Prospective parents decide to use or not to use reproductive technologies, Lunshof argued, and that could one day include germline genome editing.

That reflects the balancing act she brings to the ethical puzzles she tries to unravel. Sometimes two core values are in conflict. In the case of germline editing and enhancement, parental autonomy (to make reproductive choices) might clash with the idea that all children are entitled to an equal start in the world. But the latter is honored in the breach more than the observance, Lunshof says, and so should not be allowed to trump parental autonomy.

Last week, a report from the National Academy of Sciences and the National Academy of Medicine opened the door to germline editing. It opposed enhancement, but called the line between enhancement and therapy blurry. Lunshof beat them to it: The criteria for what is therapy and what is enhancement are fluid, she wrote two years ago.

For all the passions that germline editing incites, its effects would be small: It requires in vitro fertilization, so few parents would use it (unless reproductive sex goes the way of flip phones). Other applications of CRISPR could be more consequential. One could alter ecosystems. Calledgene drive, it is a technology for editing the genomes of an organism in a way that causes the change to be inherited by every offspring, contrary to usual inheritance patterns.

As scientists in Churchs lab and elsewhereinvolved the public in conversations about testing gene drives in wild populations of mice or mosquitoes, Lunshof recently raised a novel bioethics question: If a bioneer community says yes to gene drive, it sets a precedent and could lead people in other places to allow it, too, she said. How much would this community be held morally accountable for genetic interventions elsewhere that go wrong?

The ethical minefield created by the possibility of seeding mouse embryo scaffolds with human stem cells, and possibly growing a functional, if mini, human brain, has been trickier to navigate. Youd grow human organs, Lunshof said. My question was, what if this worked?

There didnt seem to be any government or other rules against it. Scientists using stem cells from embryos are supposed to clear experiments with an Embryonic Stem Cell Research Oversight (ESCRO) Committee, which many research universities have established. But Churchs lab proposed to use stem cells produced by reverting adult cells back to an embryo-like state. And although there are rules against creating human chimeras, it wasnt clear whether this thing would be a chimera: It wouldnt be a single living entity, though it might have living human cells or even organs.It seemed there was no bureaucracy to stop the experiment.

Lunshof spent hours with the two scientists who were planning the experiment. She primes the lab to be sensitive to ethical issues even when they dont know what to be sensitive about, Aach said. She proposed asking the ESCRO committee. Church agreed. It decided that the experiment did not violate any known guideline but asked him to keep the committee informed as the experiments progressed.

As it happens, the experiments didnt work and the lab moved on smack into another ethical conundrum.

First human-pig chimeras created, sparking hopes for transplantable organs and debate

This time, postdoctoral fellow Eswar Iyer was using a process called micropatterning to create special surfaces on glass slides. Placed on them, human stem cells formed a precisely shaped little colonythat differentiated into one or another organ.

Iyer described this work at a 2015 lab meeting. Twophrases made Lunshof sit up: embryo-like features and generation of cerebral organoids.

It was the de-cellularized mouse dilemma all over again, but with glass slides instead of mouse scaffolding, and, again, no rules seemed to apply. There are federal prohibitions against allowing an embryo to develop past the point where it forms a structure called a primitive streak, which happens on the 15th day after fertilization. At this point the embryo can no longer split (into twins) and is therefore widely regarded as a morally significant individual. But human cells or tissues developing on the micropatterned surfaces never form a primitive streak; only whole embryos do.

The question, Lunshof said, was, What is the threshold where a synthetic entity is enough of an embryo that the same moral questions must be considered?

That question loomed even larger with those cerebral organoids, primordial mini-brains that are even more realistic and much more embryo-like, Church said.

Cerebral organoids, too, fall through the cracks of the rules on embryo research, Lunshof said, but we know were doing things that involve the same ethical issues that inspired the rules, such as when human life begins, when something has a moral status, and whether since this is brain tissue the thing is sentient.

After the lab meeting, Iyer dropped by her office. The 10-minute visit he expected lasted two-and-a-half hours. Lunshof not only asked him to explain every detail of every slide he had shown. Their conversation also ranged into Western and Eastern philosophy (Iyer is a Hindu), especially views on when life begins. They agreed to keep talking.

Lunshof gave Church a rundown of the discussion, began looking for scholarly papers that might shed light on the ethically-uncharted territory, and figured out what rules are applicable. She also took the helm of a working group on the ethics of embryo-like entities.

One result is a paper to be published in eLife, an online biology journal. In it, Lunshof, Aach, Iyer, and Church propose that research limits for these entities be based as directly as possible on the generation of morally concerning features. (The entities are called SHEEFs: Synthetic Human Entities with Embryo-like Features.) For instance: How human are the cerebral organoids? Do they feel pain? How could youtell?

Just because the thing cannot develop into a baby is not a valid reason to green-light the experiments, Lunshof said. She believes that if human cells are highly organized and display functional interactivity as a blood supply in a cerebral organoid would then one must at least consider the possibility that the SHEEF has moral status.

Lunshof also initiated a discussion of SHEEFs with Harvards stem-cell oversight committee, which led to a meeting last November at Harvard Law School. There, Church explained that it is possible to get blood vessels to infuse cerebral organoids, which allows us to go to larger and larger organoids. So far, he said, we can see beautiful structures very similar to advanced cerebral [tissue]. There is essentially no limit to the technology, so we need to focus on the ethics and the humanity as guides to how far to take the science.

Which means Lunshof is unlikely to run out of good questions.

Sharon Begley can be reached at sharon.begley@statnews.com Follow Sharon on Twitter @sxbegle

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In a lab pushing the boundaries of biology, an embedded ethicist keeps scientists in check - STAT

Molecular biology: Fingerprinting cell identities – Science Daily

Every cell has its own individual molecular fingerprint, which is informative for its functions and regulatory states. Researchers from Ludwig-Maximilians-Universitaet (LMU) in Munich have now carried out a comprehensive comparison of methodologies that quantify RNAs of single cells.

The cell is the fundamental unit of all living organisms. Hence, in order to understand essential biological processes and the perturbations that give rise to disease, one must first dissect the functions of cells and the mechanisms that regulate them. Modern high-throughput protein and nucleic-acid sequencing techniques have become an indispensable component of this endeavor. In particular, single-cell RNA sequencing (scRNA-seq) permits one to determine the levels of RNA molecules -- the gene copies -- that are expressed in a given cell, and several versions of the methodology have been described in recent years. The spectrum of genes expressed in a given cell amounts to a molecular fingerprint, which yields a detailed picture of its current functional state. "For this reason, the technology has become an extraordinarily valuable tool, not only for basic research but also for the development of new approaches to treat diseases," says LMU biologist Wolfgang Enard. Enard and his team have now undertaken the first comprehensive comparative analysis of the various RNA sequencing techniques, with regard to their sensitivity, precision and cost efficiency. Their results appear in the leading journal Molecular Cell.

The purpose of scRNA-seq is to identify the relative amounts of the messenger RNA (mRNA) molecules present in the cells of interest. mRNAs are the blueprints that specify the structures of all the proteins made in the cell, and represent "transcribed" copies of the corresponding genetic information encoded in specific segments of the genomic DNA in the cell nucleus. In the cytoplasm surrounding the nucleus, the nucleotide sequences of mRNAs are "translated" into the amino-acid sequences of proteins by molecular machines called ribosomes. Thus a complete catalog of the mRNAs in a cell provides a comprehensive view of the proteins that it produces, and tells one what subset of the thousands of genes in the genome are active and how their activity is regulated. Furthermore, aberrant patterns of gene activity point to disturbances in gene expression and cell function, and reveal the presence of specific pathologies. The scRNA-seq procedure itself can be carried out using commercially available kits, but many researchers prefer to assemble the components required for their preferred formulations themselves.

In order to ascertain which of the methods currently in use is most effective and economical, Enard and his colleagues applied six different methods to mouse embryonal stem cells and compared the spectra of mRNAs detected by each of them. They then used this data to compute how much it costs for each method to reliably detect differently expressed genes between two cell types. "This comparison revealed that some of the commercial kits are ten times more expensive than the corresponding home-made versions," Enard says. However, the researchers point out that the choice of the optimal method largely depends on the conditions and demands of the individual experiment. "It does make a difference whether one wants to analyze the activity of hundreds of genes in thousands of individual cells, or thousands of genes in hundreds of cells," Enard says. "We were able to demonstrate which method is best for a given purpose, and we also obtained data that will be useful for the further development of the technology."

The new findings are of particular interest in the field of genomics. For example, scRNA-seq is a fundamental prerequisite for the success of the effort to assemble a Human Cell Atlas -- one of the most ambitious international projects in genomics since the initial sequencing of the human genome. It aims to provide no less than a complete inventory of all the cell types and subtypes in the human body at all stages of development from embryo to adult on the basis of their patterns of gene activity. It is estimated that the total number of cells in the human body is on the order of 3.5 1013. Scientists expect that such an atlas would revolutionize our knowledge of human biology and our understanding of disease processes.

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Molecular biology: Fingerprinting cell identities - Science Daily

Protein once thought exclusive to neurons helps some cancers grow, spread, defy death – Medical Xpress

February 21, 2017 Dr. Ping-Hung Chen, Dr. Sandra Schmid, Dr. Marcel Mettlen and other research team members determined that aggressive cancer cells adapt nerve cell mechanisms to maintain or squelch signals needed to survive and grow. Credit: UT Southwestern

How we think and fall in love are controlled by lightning-fast electrochemical signals across synapses, the dynamic spaces between nerve cells. Until now, nobody knew that cancer cells can repurpose tools of neuronal communication to fuel aggressive tumor growth and spread.

UTSouthwestern Medical Center researchers report those findings in two recent studies, one in the Proceedings of the National Academy of Sciences (PNAS) and the second in Developmental Cell

"Many properties of aggressive cancer growth are driven by altered cell signaling," said Dr. Sandra Schmid, senior author of both papers and Chair of Cell Biology at UTSouthwestern. "We found that cancer cells are taking a page from the neuron's signaling playbook to maintain certain beneficial signals and to squelch signals that would harm the cancer cells."

The two studies find that dynamin1 (Dyn1) - a protein once thought to be present only in nerve cells of the brain and spinal cord - is also found in aggressive cancer cells. In nerve cells, or neurons, Dyn1 helps sustain neural transmission by causing rapid endocytosis - the uptake of signaling molecules and receptors into the cell - and their recycling back to the cell surface. These processes ensure that the neurons keep healthy supplies at the ready to refire in rapid succession and also help to amplify or suppress important nerve signals as necessary, Dr. Schmid explained.

"This role is what the cancer cells have figured out. Aggressive cancer cells have usurped the mechanisms that neurons use for the rapid uptake and recycling of neural transmitters. Instead of neural transmitters, the cancer cells use Dyn1 for rapid uptake and recycling of EGF (epidermal growth factor) receptors. Mutations in EGF receptors are drivers of breast and lung cancers," she said of the Developmental Cell study.

In order to thrive, cancer cells must multiply faster than nearby noncancerous cells. EGF receptors help them do that, she explained.

Cancer cell survival is another factor in disease progression. In the PNAS study, the Schmid lab found that aggressive cancer cells appear to have adapted neuronal mechanisms to thwart a key cancer-killing pathway triggered by activating "death receptors" (DRs) on cancer cells. Specifically, aggressive cancer cells appear to have adapted ways to selectively activate Dyn1 to suppress DR signaling that usually leads to cancer cell death.

"It is amazing that the aggressive cancers use a signaling pathway to increase the activity of EGF and also turn on Dyn1 pathways to suppress cancer death - so you have this vicious circle," said Dr. Schmid, who holds the Cecil H. Green Distinguished Chair in Cellular and Molecular Biology.

She stressed that less aggressive cancers respond to forms of chemotherapy that repress EGF signaling and/or die in response to the TRAIL-DR pathway. However, aggressive lung and breast cancer cells have adapted ways to commandeer the neuronal mechanisms identified in these studies.

The hope is that this research will someday lead to improved strategies to fight the most aggressive cancers, she said. Currently, her laboratory is conducting research to identify Dyn1 inhibitors as potential anticancer drugs using a 280,000-compound library in a shared facility at UTSouthwestern.

"Cancer is a disease of cell biology. To grow, spread, and survive, cancer cells modify normal cellular behavior to their advantage. They can't reinvent the underlying mechanisms, but can adapt them. In these studies, we find that some cancer cells repurpose tools that neurons use in order to get a competitive advantage over nearby normal cells," she said.

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Protein once thought exclusive to neurons helps some cancers grow, spread, defy death - Medical Xpress

Stanford-developed nanostraws sample a cell’s contents without damage – Stanford University News

Cells within our bodies divide and change over time, with thousands of chemical reactions occurring within each cell daily. This makes it difficult for scientists to understand whats happening inside. Now, tiny nanostraws developed by Stanford researchers offer a method of sampling cell contents without disrupting its natural processes.

Nicholas Melosh, associate professor of materials science and engineering, developed a new, non-destructive system for sampling cells with nanoscale straws. The system could help uncover mysteries about how cells function. (Image credit: L.A. Cicero)

A problem with the current method of cell sampling, called lysing, is that it ruptures the cell. Once the cell is destroyed, it cant be sampled from again. This new sampling system relies on tiny tubes 600 times smaller than a strand of hair that allow researchers to sample a single cell at a time. The nanostraws penetrate a cells outer membrane, without damaging it, and draw out proteins and genetic material from the cells salty interior.

Its like a blood draw for the cell, said Nicholas Melosh, an associate professor of materials science and engineering and senior author on a paper describing the work published recently in Proceedings of the National Academy of Sciences.

The nanostraw sampling technique, according to Melosh, will significantly impact our understanding of cell development and could lead to much safer and effective medical therapies because the technique allows for long term, non-destructive monitoring.

What we hope to do, using this technology, is to watch as these cells change over time and be able to infer how different environmental conditions and chemical cocktails influence their development to help optimize the therapy process, Melosh said.

If researchers can fully understand how a cell works, then they can develop treatments that will address those processes directly. For example, in the case of stem cells, researchers are uncovering ways of growing entire, patient-specific organs. The trick is, scientists dont really know how stem cells develop.

For stem cells, we know that they can turn into many other cell types, but we do not know the evolution how do they go from stem cells to, say, cardiac cells? There is always a mystery. This sampling technique will give us a clearer idea of how its done, said Yuhong Cao, a graduate student and first author on the paper.

The sampling technique could also inform cancer treatments and answer questions about why some cancer cells are resistant to chemotherapy while others are not.

With chemotherapy, there are always cells that are resistant, said Cao. If we can follow the intercellular mechanism of the surviving cells, we can know, genetically, its response to the drug.

The sampling platform on which the nanostraws are grown is tiny about the size of a gumball. Its called the Nanostraw Extraction (NEX) sampling system, and it was designed to mimic biology itself.

In our bodies, cells are connected by a system of gates through which they send each other nutrients and molecules, like rooms in a house connected by doorways. These intercellular gates, called gap junctions, are what inspired Melosh six years ago, when he was trying to determine a non-destructive way of delivering substances, like DNA or medicines, inside cells. The new NEX sampling system is the reverse, observing whats happening within rather than delivering something new.

Its a super exciting time for nanotechnology, Melosh said. Were really getting to a scale where what we can make controllably is the same size as biological systems.

Building the NEX sampling system took years to perfect. Not only did Melosh and his team need to ensure cell sampling with this method was possible, they needed to see that the samples were actually a reliable measure of the cell content, and that samples, when taken over time, remained consistent.

When the team compared their cell samples from the NEX with cell samples taken by breaking the cells open, they found that 90 percent of the samples were congruous. Meloshs team also found that when they sampled from a group of cells day after day, certain molecules that should be present at constant levels remained the same, indicating that their sampling accurately reflected the cells interior.

With help from collaborators Sergiu P. Pasca, assistant professor of psychiatry and behavioral sciences, and Joseph Wu, professor of radiology, Melosh and co-workers tested the NEX sampling method not only with generic cell lines, but also with human heart tissue and brain cells grown from stem cells. In each case, the nanostraw sampling reflected the same cellular contents as lysing the cells.

The goal of developing this technology, according to Melosh, was to make an impact in medical biology by providing a platform that any lab could build. Only a few labs across the globe, so far, are employing nanostraws in cellular research, but Melosh expects that number to grow dramatically.

We want as many people to use this technology as possible, he said. Were trying to help advance science and technology to benefit mankind.

Melosh is also a professor in the photon science directorate at SLAC National Accelerator Laboratory, a member of Stanford Bio-X, the Child Health Research Institute, the Stanford Neurosciences Institute, Stanford ChEM-H and the Precourt Institute for Energy. Wu is also the Simon H. Stertzer, MD, Professor; he is director of the Stanford Cardiovascular Institute and a member of Stanford Bio-X, the Child Health Research Institute, Stanford ChEM-H and the Stanford Cancer Institute. Pasca is also a member of Stanford Bio-X, the Child Health Research Institute, the Stanford Neurosciences Institute and Stanford ChEM-H.

The work was funded by the National Institute of Standards and Technology, the Knut and Alice Wallenberg Foundation, the National Institutes of Health, Stanford Bio-X, the Progenitor Cell Biology Consortium, the National Institute of Mental Health, an MQ Fellow award, the Donald E. and Delia B. Baxter Foundation and the Child Health Research Institute.

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Stanford-developed nanostraws sample a cell's contents without damage - Stanford University News

Cancer cells adapt nerve cell mechanisms to fuel aggressive tumor … – News-Medical.net

February 21, 2017 at 2:28 AM

How we think and fall in love are controlled by lightning-fast electrochemical signals across synapses, the dynamic spaces between nerve cells. Until now, nobody knew that cancer cells can repurpose tools of neuronal communication to fuel aggressive tumor growth and spread.

UT Southwestern Medical Center researchers report those findings in two recent studies, one in the Proceedings of the National Academy of Sciences (PNAS) and the second in Developmental Cell.

"Many properties of aggressive cancer growth are driven by altered cell signaling," said Dr. Sandra Schmid, senior author of both papers and Chair of Cell Biology at UT Southwestern. "We found that cancer cells are taking a page from the neuron's signaling playbook to maintain certain beneficial signals and to squelch signals that would harm the cancer cells."

The two studies find that dynamin1 (Dyn1) - a protein once thought to be present only in nerve cells of the brain and spinal cord - is also found in aggressive cancer cells. In nerve cells, or neurons, Dyn1 helps sustain neural transmission by causing rapid endocytosis - the uptake of signaling molecules and receptors into the cell - and their recycling back to the cell surface. These processes ensure that the neurons keep healthy supplies at the ready to refire in rapid succession and also help to amplify or suppress important nerve signals as necessary, Dr. Schmid explained.

"This role is what the cancer cells have figured out. Aggressive cancer cells have usurped the mechanisms that neurons use for the rapid uptake and recycling of neural transmitters. Instead of neural transmitters, the cancer cells use Dyn1 for rapid uptake and recycling of EGF (epidermal growth factor) receptors. Mutations in EGF receptors are drivers of breast and lung cancers," she said of the Developmental Cell study.

In order to thrive, cancer cells must multiply faster than nearby noncancerous cells. EGF receptors help them do that, she explained.

Cancer cell survival is another factor in disease progression. In the PNAS study, the Schmid lab found that aggressive cancer cells appear to have adapted neuronal mechanisms to thwart a key cancer-killing pathway triggered by activating "death receptors" (DRs) on cancer cells. Specifically, aggressive cancer cells appear to have adapted ways to selectively activate Dyn1 to suppress DR signaling that usually leads to cancer cell death.

"It is amazing that the aggressive cancers use a signaling pathway to increase the activity of EGF and also turn on Dyn1 pathways to suppress cancer death - so you have this vicious circle," said Dr. Schmid, who holds the Cecil H. Green Distinguished Chair in Cellular and Molecular Biology.

She stressed that less aggressive cancers respond to forms of chemotherapy that repress EGF signaling and/or die in response to the TRAIL-DR pathway. However, aggressive lung and breast cancer cells have adapted ways to commandeer the neuronal mechanisms identified in these studies.

The hope is that this research will someday lead to improved strategies to fight the most aggressive cancers, she said. Currently, her laboratory is conducting research to identify Dyn1 inhibitors as potential anticancer drugs using a 280,000-compound library in a shared facility at UT Southwestern.

"Cancer is a disease of cell biology. To grow, spread, and survive, cancer cells modify normal cellular behavior to their advantage. They can't reinvent the underlying mechanisms, but can adapt them. In these studies, we find that some cancer cells repurpose tools that neurons use in order to get a competitive advantage over nearby normal cells," she said.

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Cancer cells adapt nerve cell mechanisms to fuel aggressive tumor ... - News-Medical.net

Deep learning predicts hematopoietic stem cell development – Phys.Org

February 21, 2017 What are they going to be? Hematopoietic stem cells under the microscope: New methods are helping the Helmholtz scientists to predict how they will develop. Credit: Helmholtz Zentrum Mnchen

Autonomous driving, automatic speech recognition, and the game Go: Deep Learning is generating more and more public awareness. Scientists at the Helmholtz Zentrum Mnchen and their partners at ETH Zurich and the Technical University of Munich (TUM) have now used it to determine the development of hematopoietic stem cells in advance. In 'Nature Methods' they describe how their software predicts the future cell type based on microscopy images.

Today, cell biology is no longer limited to static states but also attempts to understand the dynamic development of cell populations. One example is the generation of different types of blood cells from their precursors, the hematopoietic stem cells. "A hematopoietic stem cell's decision to become a certain cell type cannot be observed. At this time, it is only possible to verify the decision retrospectively with cell surface markers," explains Dr. Carsten Marr, head of the Quantitative Single Cell Dynamics Research Group at the Helmholtz Zentrum Mnchen's Institute of Computational Biology (ICB).

He and his team have now developed an algorithm that can predict the decision in advance. So-called Deep Learning is the key. "Deep Neural Networks play a major role in our method," says Marr. "Our algorithm classifies light microscopic images and videos of individual cells by comparing these data with past experience from the development of such cells. In this way, the algorithm 'learns' how certain cells behave."

Three generations earlier than standard methods

Specifically, the researchers examined hematopoietic stem cells that were filmed under the microscope in the lab of Timm Schroeder at ETH Zurich. Using the information on appearance and speed, the software was able to 'memorize' the corresponding behaviour patterns and then make its prediction. "Compared to conventional methods, such as fluorescent antibodies against certain surface proteins, we know how the cells will decide three cell generations earlier," reports ICB scientist Dr. Felix Buggenthin, joint first author of the study together with Dr. Florian Bttner.

But what is the benefit of this look into the future? As study leader Marr explains, "Since we now know which cells will develop in which way, we can isolate them earlier than before and examine how they differ at a molecular level. We want to use this information to understand how the choices are made for particular developmental traits."

In the future, the focus will expand beyond hematopoietic stem cells. "We are using Deep Learning for very different problems with sufficiently large data records," explains Prof. Dr. Dr. Fabian Theis, ICB director and holder of the Mathematical Modelling of Biological Systems Chair at the TUM, who led the study together with Carsten Marr. "For example, we use very similar algorithms to analyse disease-associated patterns in the genome and identify biomarkers in clinical cell screens."

Explore further: Enough is enoughstem cell factor Nanog knows when to slow down

More information: Buggenthin, F. et al. (2017): Prospective identification of hematopoietic lineage choice by deep learning. Nature Methods, DOI: 10.1038/nmeth.4182

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Deep learning predicts hematopoietic stem cell development - Phys.Org

Lab opens doors for an undergrad experience – Harvard Gazette

For most college freshmen, working in a lab typically means following the step-by-step instructions of class assignments with the goal of performing a specific experiment to produce a predetermined result.

But a handful of Harvard freshmen got the chance to experience real lab work by exploring how altering genes in yeast affected the cells functions.

Created by postdoctoral fellow James Martenson and Vlad Denic, a professor of molecular and cellular biology, the Wintersession class was designed to give undergraduates an up-close-and-personal view of the research that takes place in Harvard labs, and the opportunities they have to take part.

Students often arent aware these opportunities exist, so we think of this as a gateway for freshmen interested in doing research, Martenson said. But we also wanted to emphasize some of the critical thinking skills we use every day as scientists, but which may not be emphasized as much in more traditional coursework.

Over the course of the multiday class, each student worked with genetically altered strains of yeast to perform a series of three experiments.

We chose yeast because its a classic model organism in biology, Martenson said. A lot of very important work has been done in yeast. In fact, much of what we know about basic cell biology weve learned from yeast.

Using their various strains, he said, students performed a series of experiments aimed at testing how genetic changes altered organelle function.

A critical part of cell biology, organelles are essentially compartments inside cells, and include everything from mitochondria which act as the cells power plants to nuclei, which contain genetic material.

One key question in cell biology is how organelle quality is maintained, because many organelles house toxic chemical environments, Martenson explained. You also need a way to ensure the organelles are healthy, and if they do get sick, they need to be identified and eliminated before they cause a problem for the rest of the cell.

To probe questions of organelle health, Martenson is focusing on an organelle called the peroxisome and students did the same.

We started with a list of genes we had reason to believe were important for peroxisome function and quality control, but which were uncharacterized, he said. We thought it would be interesting for students to be involved in something that were actually interested in studying, so their work could yield interesting results that could inform our research.

For the students who took part, the experience was invaluable.

I didnt have a lot of lab experience, and I felt this class was a good way to expose myself to it, said Dylan Rice. I feel like Ive learned a lot, and Ive really enjoyed it so far.

Though she had already worked in another lab, Irla Belli said the relaxed atmosphere of the class helped her learn that making mistakes is often a key part of research.

You learn a lot from them, she said. In this four-day span, Ive learned more than from all the labs I had in class. This has solidified my desire to pursue the Ph.D. part of an M.D./Ph.D, and even though its very serious science, its relaxing.

For Amanda DiMartini, the class was a chance for an in-depth look at a field shes considering as a concentration.

I did some research in high school, but it was relatively simple, she said. Im interested in concentrating in some area of biology and this was a chance to see if I want to continue doing research throughout college. I feel like, in this class, were learning to think scientifically, and to think critically, and how to do research at a higher level. I dont regret [this class] at all.

By Colleen Walsh, Harvard Staff Writer | February 16, 2017

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Lab opens doors for an undergrad experience - Harvard Gazette

Vitamins and aminoacids regulate stem cell biology – Phys.Org

February 16, 2017 Credit: National Research Council of Italy

An International Reserach Team coordinated by Igb-Cnr has discovered a key role of vitamins and amino acids in pluripotent stem cells. The research is published in Stem Cell Reports, and may provide new insights in cancer biology and regenerative medicine

Vitamins and amino acids play a key role in the regulation of epigenetic modifications involved in the progression of diseases such as cancer. The research may have future implications in cancer biology. The study was published in Stem Cell Reports.

"We found that two metabolites, vitamin C and the amino acid L-Proline, are important players in the control of stem cell behaviour. This study shows that pluripotent embryonic stem cells present in the earliest phases of development are pushed toward a more immature 'naive' state by vitamin C, while they are forced to acquire a 'primed' state in the presence of L-Proline. Thus, vitamin C and L-Proline exert opposite effects on embryonic stem cells, and this correlates with their ability to modify DNA (DNA methylation) without altering the sequence, but instead, the regulation of gene expression," explained researcher Gabriella Minchiotti.

Stem cells possess the unique ability to self-renew and differentiate into other cell types, which makes them extremely interesting in medical and biological research. "Embryonic stem cells are the most 'potent' (defined as pluripotent), meaning that they can give rise to all cell types of an organism, such as cardiomyocytes, neurons, bones, etc. Like normal stem cells, cancer stem cells can also self-renew and differentiate, and are believed to be responsible for tumor growth and therapy resistance."

This study provides an important contribution to the understanding of how metabolites regulate pluripotency and shape the epigenome in embryonic stem cells, which have been largely unexplored and recently gained great interest. This knowledge not only enhances our understanding of the biology of normal stem cells but may offer novel insights into cancer stem cell biology, identifying novel potential therapeutic targets.

Explore further: Gene "bookmarking" regulates the fate of stem cells

More information: Stem Cell Reports, dx.doi.org/10.1016/j.stemcr.2016.11.011

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George Klein (19252016) – Nature.com

Gunnar Ask

George Klein, with his wife, Eva, discovered foundational phenomena in cancer research. He showed that normal cells carry genes, now known as tumour suppressors, that prevent cancer. He also worked out how the immune system comes to recognize and eliminate cancer cells.

Klein, who died on 10 December at the age of 91, had a youth filled with daring and peril. From a HungarianJewish family, he escaped being sent to a Nazi labour camp and from Russian patrols during the Second World War. He began medical studies in Budapest at the end of the war. In 1947, against all odds, a well-connected colleague arranged for Klein and a few other students to visit universities in Sweden. He was offered a place in the laboratory of the renowned cell biologist Torbjrn Caspersson at the Karolinska Institute.

Klein risked a return to communist Hungary to marry Eva, a fellow medical student he had known for mere weeks, and brought her back with him. The necessary documents typically took months to assemble, but he and Eva acquired them over a single workday using persuasion, pluck and bribes. They completed their PhDs at the Karolinska and maintained research groups there until about a month before George's death.

In 1957, a chair was created for him in tumour biology, a research field that he had helped to establish. The department of tumour biology that ensued was international and influential. Most of today's leading cancer researchers who are over 50 have had some interaction with George and his department. Seven secretaries wrangled his large correspondence. He invented social media before the technology existed.

A seminal paper published in 1960 (G. Klein et al. Cancer Res. 20, 15611572; 1960) dissected the essential basis of modern tumour immunology. Before it, researchers thought that all cancers carried a common antigen that the immune system could recognize. The Kleins and their colleagues used a chemical carcinogen to induce tumours in mice, surgically removed these and immunized the animals with irradiated cells from their own tumours. Next, the group inoculated mice with viable cancer cells and demonstrated that the immune system would only reject cancerous cells if they came from the original tumour.

This clarified the field: the immune system could recognize and reject cancers, in a way that was specific to each individual. A year later, Klein's team wrote a paper showing the other side of the coin (H. O. Sjgren et al. Cancer Res. 21, 329337; 1961). Tumours caused by the mouse polyomavirus do indeed share a common antigen. This paved the way for the general observation that tumours caused by or carrying viruses share common antigens that the immune system can target.

The Kleins' experimental success rested on two cornerstones. One was the establishment of a large colony of inbred mouse strains essential for tumour transplantation studies. After an early sabbatical at the Fox Chase Cancer Center in Philadelphia, George brought back 200 inbred mice on the return flight to found the colony.

The other was that the Kleins were among the first to apply concepts of population dynamics to cancer cells. This approach led to the demonstration of genes for tumour suppression (with their colleague at the Karolinska Francis Wiener and cell biologist Henry Harris) in the 1970s, at a time when it was not even clear that cancer had a genetic basis. This anticipated the modern view of cancer as resulting from the Darwinian evolution of cancer cells. Consecutive mutations in multiple genes increased the ability of wayward cells to survive, proliferate and evade checks against their growth.

Other seminal contributions included the prediction that translocations between chromosomes could activate oncogenes and the discovery of the Epstein-Barr virus nuclear proteins, which are crucial in the viral transformation of normal cells to a cancerous state. Their team (with Rolf Kiessling, then a graduate student at the Karolinska) also discovered, in 1975, natural killer cells, which can eliminate both cancerous and infected cells.

George showed an unusually high intellectual presence that mesmerized younger researchers. The tumour-biology department broke the boundaries of classic disciplines: it integrated genetics and mouse studies with cell biology, immunology and the study of infectious agents.

George also published books on the humanities, philosophy and popular science. Topics ranged from the Holocaust, atheism and religion to mysteries in cell biology and personal portraits of his heroes in science, music, poetry and literature. He was a leading public intellectual, often on Swedish television and in newspapers. His last book, Resistance (Albert Bonniers Frlag, 2015; published in Swedish), won the prestigious Gerard Bonnier prize for the best essay collection of that year. It deals with resistance to extremism and to cancer. Throughout his life, George was preoccupied with the thin borders between evil and good, and health and disease.

He was an admired lecturer for general and scientific audiences. His preferred format was conversation with an interesting opponent. There was a time when most major international cancer conferences concluded with his creative remarks. Many are those who can witness how much they were affected by bouncing ideas and results around with George.

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Mutant Maize Offers Key to Understanding Plant Growth – UCR Today (press release)

Live cell time-lapse imaging of maize mutant provides crucial details for UC Riverside researchers

By Sean Nealon on February 13, 2017

From left, normal and mutant maize plants.

RIVERSIDE, Calif. (www.ucr.edu) How plant cells divide and how that contributes to plant growth has been one of the longstanding unsolved mysteries of cell biology. Two conflicting ideas have fueled the mystery.

The first idea is that cells divide merely to fill space in plant tissue, and therefore the orientation of the division is unimportant to growth. In other words, the contribution of individual cell behavior to overall growth isnt very important.

The second idea is that individual cells are the basic unit of life and their individual programs eventually build an organism. In other words, each new cell created contributes to proper patterning of the tissue. In this case, the orientation of each cells division is critical for how the plant tissue is patterned and also impacts growth.

New findings by a University of California, Riverside-led team of researchers, lend support to the second idea, that the orientation of cell division is critical for overall plant growth. The work was just published in the journal Proceedings of the National Academy of Sciences.

The researchers, led by Carolyn Rasmussen, an assistant professor of plant cell biology at UC Riverside and Pablo Martinez, a graduate student working in Rasmussens lab, together with Anding Luo and Anne Sylvester at University of Wyoming, were working with a maize mutant, called tangled1, with known defects in growth and division plane orientation of cells. Division plane orientation refers to the positioning of new cell walls during division.

Scanning electron micrographs of maize epidermal cells. Left is the mutant variety. Right is the wild variety.

They used time-lapse live cell imaging that represented hundreds of hours of maize, (commonly called corn in the United States), cells dividing. The time-lapse of imaging allowed them to characterize a previously unknown delay during cell division stages in the maize mutant. This study clarified the relationship between growth, timely division progression and proper division plane orientation.

This study suggests that delays during division do not necessarily cause growth defects, but that improper placement of new cell walls together with delays during division causes growth defects. Therefore, division plane orientation is a critical but potentially indirect factor for growth.

The findings might have long-term implications for increasing agricultural production. For example, during the Green Revolution of the mid-20th century, researchers developed short-stature, or dwarf, wheat and rice varieties that led to higher yields and are credited with saving over a billion people from starvation. Understanding the molecular mechanisms of plant growth might contribute in the long-term to developing more suitable short-stature maize varieties.

The paper is called Proper division plane orientation and mitotic progression together allow normal growth of maize.

Archived under: Science/Technology, Carolyn Rasmussen, College of Natural and Agricultural Sciences, Department of Botany and Plant Sciences, Pablo Martinez, press release

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Mutant Maize Offers Key to Understanding Plant Growth - UCR Today (press release)