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Curbing Cancer Cell Growth & Metastasis-on-a-Chip’ Models Cancer’s Spread

Posted in 3D Plotting Scaffolds, Anaerobic Glycolysis, BioIT: BioInformatics, NGS, Clinical & Translational, Pharmaceutical R&D Informatics, Clinical Genomics, Cancer Informatics, Biological Networks, BioPrinting in Regenerative Medicine, Cancer and Current Therapeutics, CANCER BIOLOGY & Innovations in Cancer Therapy, Cell Biology, Signaling & Cell Circuits, Clinical & Translational, Clinical Genomics, Drug Development using MultiOrgan Chip, MicroEngineering Cell-Tissue & Systems, Oxidative phosphorylation, Warburg effect, tagged 3D printing, Acute Leukemia, anti-tumor pharma, antibody-drug conjugates, ASP2215, Cancer - General, Chemotherapy, Clonal evolution, Drug discovery, FMS-like tyrosine kinase-3 (FLT3) inhibitors, Hypoxia-inducible factors, Immunotherapy, metastasis, monitoring, nanoparticle, organ on a chip, Philadelphia chromosome (BCR-ABL), pluripotency factors, Ponatinib, reporter, self-renewal, serine metabolism, tumorigenesis, Wolf Prize in Chemistry on March 19, 2016| Leave a Comment »

Curbing Cancer Cell Growth & Metastasis-on-a-Chip’ Models Cancer’s Spread

Curator: Larry H. Bernstein, MD, FCAP

 

New Approach to Curbing Cancer Cell Growth

http://www.technologynetworks.com/Metabolomics/news.aspx?ID=189342

Using a new approach, scientists at The Scripps Research Institute (TSRI) and collaborating institutions have discovered a novel drug candidate that could be used to treat certain types of breast cancer, lung cancer and melanoma.

The new study focused on serine, one of the 20 amino acids (protein building blocks) found in nature. Many types of cancer require synthesis of serine to sustain rapid, constant and unregulated growth. To find a drug candidate that interfered with this pathway, the team screened a large library of compounds from a variety of sources, searching for molecules that inhibited a specific enzyme known as 3-phosphoglycerate dehydrogenase (PHGDH), which is responsible for the first committed step in serine biosynthesis. “In addition to discovering an inhibitor that targets cancer metabolism, we also now have a tool to help answer interesting questions about serine metabolism,” said Luke L. Lairson, assistant professor of chemistry at TSRI and principal investigator of cell biology at the California Institute for Biomedical Research (CALIBR). Lairson was senior author of the study, published recently in the Proceedings of the National Academy of Sciences (PNAS), with Lewis Cantley of Weill Cornell Medical College and Costas Lyssiotis of the University of Michigan. Addicted to Serine Serine is necessary for nucleotide, protein and lipid biosynthesis in all cells. Cells use two main routes for acquiring serine: through import from the extracellular environment or through conversion of 3-phosphoglycerate (a glycolytic intermediate) by PHGDH. “Since the late 1950s, it has been known that cancer cells use the process of aerobic glycolysis to generate metabolites needed for proliferative growth,” said Lairson. This process can lead to an overproduction of serine. The genetic basis for this abundance had remained mysterious until recently, when it was demonstrated that some cancers acquire mutations that increased the expression of PHGDH; reducing PHGDH in these “serine-addicted” cancer cells also inhibited their growth. The labs of Lewis C. Cantley at Weill Cornell Medical College (in work published in Nature Genetics) and David Sabatini at the Whitehead Institute (in work published in Nature) suggested PHGDH as a potential drug target for cancer types that overexpress the enzyme. Lairson and colleagues hypothesized that a small molecule drug candidate that inhibited PHGDH could interfere with cancer metabolism and point the way to the development of an effective cancer therapeutic. Importantly, this drug candidate would be inactive against normal cells because they would be able to import enough serine to support ordinary growth. As Easy as 1-2-800,000 Lairson, in collaboration with colleagues including Cantley, Lyssiotis, Edouard Mullarky of Weill Cornell and Harvard Medical School and Natasha Lucki of CALIBR, screened through a library of 800,000 small molecules using a high-throughput in vitro enzyme assay to detect inhibition of PHGDH. The group identified 408 candidates and further narrowed this list down based on cell-type specific anti-proliferative activity and by eliminating those inhibitors that broadly targeted other dehydrogenases. With the successful identification of seven candidate inhibitors, the team sought to determine if these molecules could inhibit PHGDH in the complex cellular environment. To do so, the team used a mass spectrometry-based assay (test) to measure newly synthesized serine in a cell in the presence of the drug candidates. One of the seven small molecules tested, named CBR-5884, was able to specifically inhibit serine synthesis by 30 percent, suggesting that the molecule specifically targeted PHGDH. The group went on to show that CBR-5884 was able to inhibit cell proliferation of breast cancer and melanoma cells lines that overexpress PHGDH. As expected, CBR-5884 did not inhibit cancer cells that did not overexpress PHGDH, as they can import serine; however, when incubated in media lacking serine, the presence of CBR-5884 decreased growth in these cells. The group anticipates much optimization work before this drug candidate can become an effective therapeutic. In pursuit of this goal, the researchers plan to take a medicinal chemistry approach to improve potency and metabolic stability.

 

How Cancer Stem Cells Thrive When Oxygen Is Scarce

3/29/2016  Johns Hopkins University    http://www.biosciencetechnology.com/news/2016/03/how-cancer-stem-cells-thrive-when-oxygen-scarce

image: Shutterstock

Working with human breast cancer cells and mice, scientists at The Johns Hopkins University say new experiments explain how certain cancer stem cells thrive in low oxygen conditions. Proliferation of such cells, which tend to resist chemotherapy and help tumors spread, are considered a major roadblock to successful cancer treatment.

The new research, suggesting that low-oxygen conditions spur growth through the same chain of biochemical events in both embryonic stem cells and breast cancer stem cells, could offer a path through that roadblock, the investigators say.

“There are still many questions left to answer but we now know that oxygen poor environments, like those often found in advanced human breast cancers serve as nurseries for the birth of cancer stem cells,” said Gregg Semenza, M.D., Ph.D., the C. Michael Armstrong Professor of Medicine and a member of the Johns Hopkins Kimmel Cancer Center. “That gives us a few more possible targets for drugs that diminish their threat in human cancer.”

A summary of the findings was published online March 21 in the Proceedings of the National Academy of Sciences.

“Aggressive cancers contain regions where the cancer cells are starved for oxygen and die off, yet patients with these tumors generally have the worst outcome. Our new findings tell us that low oxygen conditions actually encourage certain cancer stem cells to multiply through the same mechanism used by embryonic stem cells.”

All stem cells are immature cells known for their ability to multiply indefinitely and give rise to progenitor cells that mature into specific cell types that populate the body’s tissues during embryonic development. They also replenish tissues throughout the life of an organism. But stem cells found in tumors use those same attributes and twist them to maintain and enhance the survival of cancers.

Recent studies showed that low oxygen conditions increase levels of a family of proteins known as HIFs, or hypoxia-inducible factors, that turn on hundreds of genes, including one called NANOG that instructs cells to become stem cells.

Studies of embryonic stem cells revealed that NANOG protein levels can be lowered by a chemical process known as methylation, which involves putting a methyl group chemical tag on a protein’s messenger RNA (mRNA) precursor. Semenza said methylation leads to the destruction of NANOG’s mRNA so that no protein is made, which in turn causes the embryonic stem cells to abandon their stem cell state and mature into different cell types.

Zeroing in on NANOG, the scientists found that low oxygen conditions increased NANOG’s mRNA levels through the action of HIF proteins, which turned on the gene for ALKBH5, which decreased the methylation and subsequent destruction of NANOG’s mRNA. When they prevented the cells from making ALKBH5, NANOG levels and the number of cancer stem cells decreased. When the researchers manipulated the cell’s genetics to increase levels of ALKBH5 without exposing them to low oxygen, they found this also decreased methylation of NANOG mRNA and increased the numbers of breast cancer stem cells.

Finally, using live mice, the scientists injected 1,000 triple-negative breast cancer cells into their mammary fat pads, where the mouse version of breast cancer forms. Unaltered cells created tumors in all seven mice injected with such cells, but when cells missing ALKBH5 were used, they caused tumors in only 43 percent (six out of 14) of mice. “That confirmed for us that ALKBH5 helps preserve cancer stem cells and their tumor-forming abilities,” Semenza said.

How cancer stem cells thrive when oxygen is scarce    https://www.sciencedaily.com/releases/2016/03/160328100159.htm

The new research, suggesting that low-oxygen conditions spur growth through the same chain of biochemical events in both embryonic stem cells and breast cancer stem cells, could offer a path through that roadblock, the investigators say.

“There are still many questions left to answer but we now know that oxygen poor environments, like those often found in advanced human breast cancers serve as nurseries for the birth of cancer stem cells,” says Gregg Semenza, M.D., Ph.D., the C. Michael Armstrong Professor of Medicine and a member of the Johns Hopkins Kimmel Cancer Center.

Chuanzhao Zhang, Debangshu Samanta, Haiquan Lu, John W. Bullen, Huimin Zhang, Ivan Chen, Xiaoshun He, Gregg L. Semenza.
Hypoxia induces the breast cancer stem cell phenotype by HIF-dependent and ALKBH5-mediated m6A-demethylation of NANOG mRNA.
Proceedings of the National Academy of Sciences, 2016; 201602883     DOI: 10.1073/pnas.1602883113

Significance

Pluripotency factors, such as NANOG, play a critical role in the maintenance and specification of cancer stem cells, which are required for primary tumor formation and metastasis. In this study, we report that exposure of breast cancer cells to hypoxia (i.e., reduced O₂ availability), which is a critical feature of the tumor microenvironment, induces N⁶-methyladenosine (m⁶A) demethylation and stabilization of NANOG mRNA, thereby promoting the breast cancer stem cell (BCSC) phenotype. We show that inhibiting the expression of AlkB homolog 5 (ALKBH5), which demethylates m⁶A, or the hypoxia-inducible factors (HIFs) HIF-1α and HIF-2α, which activate ALKBH5 gene transcription in hypoxic breast cancer cells, is an effective strategy to decrease NANOG expression and target BCSCs in vivo.

N⁶-methyladenosine (m⁶A) modification of mRNA plays a role in regulating embryonic stem cell pluripotency. However, the physiological signals that determine the balance between methylation and demethylation have not been described, nor have studies addressed the role of m⁶A in cancer stem cells. We report that exposure of breast cancer cells to hypoxia stimulated hypoxia-inducible factor (HIF)-1α- and HIF-2α–dependent expression of AlkB homolog 5 (ALKBH5), an m⁶A demethylase, which demethylated NANOG mRNA, which encodes a pluripotency factor, at an m⁶A residue in the 3′-UTR. Increased NANOG mRNA and protein expression, and the breast cancer stem cell (BCSC) phenotype, were induced by hypoxia in an HIF- and ALKBH5-dependent manner. Insertion of the NANOG 3′-UTR into a luciferase reporter gene led to regulation of luciferase activity by O₂, HIFs, and ALKBH5, which was lost upon mutation of the methylated residue. ALKBH5 overexpression decreased NANOG mRNA methylation, increased NANOG levels, and increased the percentage of BCSCs, phenocopying the effect of hypoxia. Knockdown of ALKBH5 expression in MDA-MB-231 human breast cancer cells significantly reduced their capacity for tumor initiation as a result of reduced numbers of BCSCs. Thus, HIF-dependent ALKBH5 expression mediates enrichment of BCSCs in the hypoxic tumor microenvironment.

Specific Proteins Found to Jump Start Spread of Cancer Cells

http://www.genengnews.com/gen-news-highlights/specific-proteins-found-to-jump-start-spread-of-cancer-cells/81252417/

Metastatic breast cancer cells. [National Cancer Institute]
http://www.genengnews.com/Media/images/GENHighlight/thumb_Feb29_2016_NCI_MetastaticBreastCancerCells1797514764.jpg

Scientists at the University of California, San Diego School of Medicine and Moores Cancer Center, with colleagues in Spain and Germany, have discovered how elevated levels of particular proteins in cancer cells trigger hyperactivity in other proteins, fueling the growth and spread of a variety of cancers. Their study (“Prognostic Impact of Modulators of G Proteins in Circulating Tumor Cells from Patients with Metastatic Colorectal Cancer”) is published in Scientific Reports.

Specifically, the international team, led by senior author Pradipta Ghosh, M.D., associate professor at the University of California San Diego School of Medicine, found that increased levels of expression of some members of a protein family called guanine nucleotide exchange factors (GEFs) triggered unsuspected hyperactivation of G proteins and subsequent progression or metastasis of cancer.

The discovery suggests GEFs offer a new and more precise indicator of disease state and prognosis. “We found that elevated expression of each GEF is associated with a shorter, progression-free survival in patients with metastatic colorectal cancer,” said Dr. Ghosh. “The GEFs fared better as prognostic markers than two well-known markers of cancer progression, and the clustering of all GEFs together improved the predictive accuracy of each individual family member.”

In recent years, circulating tumor cells (CTCs), which are shed from primary tumors into the bloodstream and act as seeds for new tumors taking root in other parts of the body, have become a prognostic and predictive biomarker. The presence of CTCs is used to monitor the efficacy of therapies and detect early signs of metastasis.

But counting CTCs in the bloodstream has limited utility, said Dr. Ghosh. “Enumeration alone does not capture the particular characteristics of CTCs that are actually tumorigenic and most likely to cause additional malignancies.”

Numerous efforts are underway to improve the value and precision of CTC analysis. According to Dr. Ghosh the new findings are a step in that direction. First, GEFs activate trimeric G proteins, and second, G protein signaling is involved in CTCs. G proteins are ubiquitous and essential molecular switches involved in transmitting external signals from stimuli into cells’ interiors. They have been a subject of heightened scientific interest for many years.

Dr. Ghosh and colleagues found that elevated expression of nonreceptor GEFs activates Gαi proteins, fueling CTCs and ultimately impacting the disease course and survival of cancer patients.

“Our work shows the prognostic impact of elevated expression of individual and clustered GEFs on survival and the benefit of transcriptome analysis of G protein regulatory proteins in cancer biology,” said Dr. Ghosh. “The next step will be to carry this technology into the clinic where it can be applied directly to deciphering a patient’s state of cancer and how best to treat.”

Metastasis-on-a-Chip’ Models Cancer’s Spread

http://www.mdtmag.com/news/2016/03/metastasis-chip-models-cancers-spread?et_cid=5200644&et_rid=461755519

In the journal Biotechnology Bioengineering, the team reports on its “metastasis-on-a-chip” system believed to be one of the first laboratory models of cancer spreading from one 3D tissue to another.

The current version of the system models a colorectal tumor spreading from the colon to the liver, the most common site of metastasis. Skardal said future versions could include additional organs, such as the lung and bone marrow, which are also potential sites of metastasis. The team also plans to model other types of cancer, such as the deadly brain tumor glioblastoma

To create the system, researchers encapsulated human intestine and colorectal cancer cells inside a biocompatible gel-like material to make a mini-organ. A mini-liver composed of human liver cells was made in the same way. These organoids were placed in a “chip” system made up of a set of micro-channels and chambers etched into the chip’s surface to mimic a simplified version of the body’s circulatory system. The tumor cells were tagged with fluorescent molecules so their activity could be viewed under a microscope.

To test whether the system could model metastasis, the researchers first used highly aggressive cancer cells in the colon organoid. Under the microscope, they saw the tumor grow in the colon organoid until the cells broke free, entered the circulatory system and then invaded the liver tissue, where another tumor formed and grew. When a less aggressive form of colon cancer was used in the system, the tumor did not metastasize, but continued to grow in the colon.

To test the system’s potential for screening drugs, the team introduced Marimastat, a drug used to inhibit metastasis in human patients, into the system and found that it significantly prevented the migration of metastatic cells over a 10-day period. Likewise, the team also tested 5-fluorouracil, a common colorectal cancer drug, which reduced the metabolic activity of the tumor cells.

“We are currently exploring whether other established anti-cancer drugs have the same effects in the system as they do in patients,” said Skardal. “If this link can be validated and expanded, we believe the system can be used to screen drug candidates for patients as a tool in personalized medicine. If we can create the same model systems, only with tumor cells from an actual patient, then we believe we can use this platform to determine the best therapy for any individual patient.”

The scientists are currently working to refine their system. They plan to use 3D printing to create organoids more similar in function to natural organs. And they aim to make the process of metastasis more realistic. When cancer spreads in the human body, the tumor cells must break through blood vessels to enter the blood steam and reach other organs. The scientists plan to add a barrier of endothelial cells, the cells that line blood vessels, to the model.

This concept of modeling the body’s processes on a miniature level is made possible because of advances in micro-tissue engineering and micro-fluidics technologies. It is similar to advances in the electronics industry made possible by miniaturizing electronics on a chip.

Scientists Synthesize Anti-Cancer Agent

Fri, 03/11/2016   Rice University
http://www.dddmag.com/news/2016/03/scientists-synthesize-anti-cancer-agent

A schematic shows a trioxacarcin C molecule, whose structure was revealed for the first time through a new process developed by the Rice lab of synthetic organic chemist K.C. Nicolaou. Trioxacarcins are found in bacteria but synthetic versions are needed to study them for their potential as medications. Trioxacarcins have anti-cancer properties. Source: Nicolaou Group/Rice University  http://www.dddmag.com/sites/dddmag.com/files/ddd1603_rice-anticancer.jpg

A team led by Rice University synthetic organic chemist K.C. Nicolaou has developed a new process for the synthesis of a series of potent anti-cancer agents originally found in bacteria.

The Nicolaou lab finds ways to replicate rare, naturally occurring compounds in larger amounts so they can be studied by biologists and clinicians as potential new medications. It also seeks to fine-tune the molecular structures of these compounds through analog design and synthesis to improve their disease-fighting properties and lessen their side effects.

Such is the case with their synthesis of trioxacarcins, reported this month in the Journal of the American Chemical Society.

“Not only does this synthesis render these valuable molecules readily available for biological investigation, but it also allows the previously unknown full structural elucidation of one of them,” Nicolaou said. “The newly developed synthetic technologies will allow us to construct variations for biological evaluation as part of a program to optimize their pharmacological profiles.”

At present, there are no drugs based on trioxacarcins, which damage DNA through a novel mechanism, Nicolaou said.

Trioxacarcins were discovered in the fermentation broth of the bacterial strain Streptomyces bottropensis. They disrupt the replication of cancer cells by binding and chemically modifying their genetic material.

“These molecules are endowed with powerful anti-tumor properties,” Nicolaou said. “They are not as potent as shishijimicin, which we also synthesized recently, but they are more powerful than taxol, the widely used anti-cancer drug. Our objective is to make it more powerful through fine-tuning its structure.”

He said his lab is working with a biotechnology partner to pair these cytotoxic compounds (called payloads) to cancer cell-targeting antibodies through chemical linkers. The process produces so-called antibody-drug conjugates as drugs to treat cancer patients. “It’s one of the latest frontiers in personalized targeting chemotherapies,” said Nicolaou, who earlier this year won the prestigious Wolf Prize in Chemistry.

Fluorescent Nanoparticle Tracks Cancer Treatment’s Effectiveness in Hours

Bevin Fletcher, Associate Editor    http://www.biosciencetechnology.com/news/2016/03/fluorescent-nanoparticle-tracks-cancer-treatments-effectiveness-hours

Using reporter nanoparticles loaded with either a chemotherapy or immunotherapy, researchers could distinguish between drug-sensitive and drug-resistant tumors in a pre-clinical model of prostate cancer. (Source: Brigham and Women’s Hospital)

Bioengineers at Brigham and Women’s Hospital have developed a new technique to help determine if chemotherapy is working in as few as eight hours after treatment. The new approach, which can also be used for monitoring the effectiveness of immunotherapy, has shown success in pre-clinical models.

The technology utilizes a nanoparticle, carrying anti-cancer drugs, that glows green when cancer cells begin dying. Researchers, using  the “reporter nanoparticles” that responds to a particular enzyme known as caspase, which is activated when cells die, were able to distinguish between a tumor that is drug-sensitive or drug-resistant much faster than conventional detection methods such as PET scans, CT and MRI.  The findings were published online March 28 in the Proceedings of the National Academy of Sciences.

“Using this approach, the cells light up the moment a cancer drug starts working,” co-corresponding author Shiladitya Sengupta, Ph.D., principal investigator in BWH’s Division of Bioengineering, said in a prepared statement.  “We can determine if a cancer therapy is effective within hours of treatment.  Our long-term goal is to find a way to monitor outcomes very early so that we don’t give a chemotherapy drug to patients who are not responding to it.”

Cancer killers send signal of success

Nanoparticles deliver drug, then give real-time feedback when tumor cells die   BY   SARAH SCHWARTZ

New lab-made nanoparticles deliver cancer drugs into tumors, then report their effects in real time by lighting up in response to proteins produced by dying cells. More light (right, green) indicates a tumor is responding to chemotherapy.

Tiny biochemical bundles carry chemotherapy drugs into tumors and light up when surrounding cancer cells start dying. Future iterations of these lab-made particles could allow doctors to monitor the effects of cancer treatment in real time, researchers report the week of March 28 in theProceedings of the National Academy of Sciences.

“This is the first system that allows you to read out whether your drug is working or not,” says study coauthor Shiladitya Sengupta, a bioengineer at Brigham and Women’s Hospital in Boston.

Each roughly 100-nanometer-wide particle consists of a drug and a fluorescent dye linked to a coiled molecular chain. Before the particles enter cells, the dye is tethered to a “quencher” molecule that prevents it from lighting up. When injected into the bloodstream of a mouse with cancer, the nanoparticles accumulate in tumor cells and release the drug, which activates a protein that tears a cancer cell apart. This cell-splitting protein not only kills the tumor cell, but also severs the link between the dye and the quencher, allowing the nanoparticles to glow under infrared light.

Reporter nanoparticle that monitors its anticancer efficacy in real time

Ashish Kulkarni^a,^b,¹,Poornima Rao^a,^b,Siva Natarajan^a,^b,Aaron Goldman, et al.
http://www.pnas.org/content/early/2016/03/28/1603455113.abstract

The ability to identify responders and nonresponders very early during chemotherapy by direct visualization of the activity of the anticancer treatment and to switch, if necessary, to a regimen that is effective can have a significant effect on the outcome as well as quality of life. Current approaches to quantify response rely on imaging techniques that fail to detect very early responses. In the case of immunotherapy, the early anatomical readout is often discordant with the biological response. This study describes a self-reporting nanomedicine that not only delivers chemotherapy or immunotherapy to the tumor but also reports back on its efficacy in real time, thereby identifying responders and nonresponders early on

The ability to monitor the efficacy of an anticancer treatment in real time can have a critical effect on the outcome. Currently, clinical readouts of efficacy rely on indirect or anatomic measurements, which occur over prolonged time scales postchemotherapy or postimmunotherapy and may not be concordant with the actual effect. Here we describe the biology-inspired engineering of a simple 2-in-1 reporter nanoparticle that not only delivers a cytotoxic or an immunotherapy payload to the tumor but also reports back on the efficacy in real time. The reporter nanoparticles are engineered from a novel two-staged stimuli-responsive polymeric material with an optimal ratio of an enzyme-cleavable drug or immunotherapy (effector elements) and a drug function-activatable reporter element. The spatiotemporally constrained delivery of the effector and the reporter elements in a single nanoparticle produces maximum signal enhancement due to the availability of the reporter element in the same cell as the drug, thereby effectively capturing the temporal apoptosis process. Using chemotherapy-sensitive and chemotherapy-resistant tumors in vivo, we show that the reporter nanoparticles can provide a real-time noninvasive readout of tumor response to chemotherapy. The reporter nanoparticle can also monitor the efficacy of immune checkpoint inhibition in melanoma. The self-reporting capability, for the first time to our knowledge, captures an anticancer nanoparticle in action in vivo.

 

Cancer Treatment’s New Direction  
Genetic testing helps oncologists target tumors and tailor treatments
http://www.wsj.com/articles/cancer-treatments-new-direction-1459193085

Evan Johnson had battled a cold for weeks, endured occasional nosebleeds and felt so fatigued he struggled to finish his workouts at the gym. But it was the unexplained bruises and chest pain that ultimately sent the then 23-year-old senior at the University of North Dakota to the Mayo Clinic. There a genetic test revealed a particularly aggressive form of acute myeloid leukemia. That was two years ago.

The harrowing roller-coaster that followed for Mr. Johnson and his family highlights new directions oncologists are taking with genetic testing to find and attack cancer. Tumors can evolve to resist treatments, and doctors are beginning to turn such setbacks into possible advantages by identifying new targets to attack as the tumors change.

His course involved a failed stem cell transplant, a half-dozen different drug regimens, four relapses and life-threatening side effects related to his treatment.

Nine months in, his leukemia had evolved to develop a surprising new mutation. The change meant the cancer escaped one treatment, but the new anomaly provided doctors with a fresh target, one susceptible to drugs approved for other cancers. Doctors adjusted Mr. Johnson’s treatment accordingly, knocked out the disease and paved the way for a second, more successful stem cell transplant. He has now been free of leukemia for a year.

Now patients with advanced cancer who are treated at major centers can expect to have their tumors sequenced, in hopes of finding a match in a growing medicine chest of drugs that precisely target mutations that drive cancer’s growth. When they work, such matches can have a dramatic effect on tumors. But these “precision medicines” aren’t cures. They are often foiled when tumors evolve, pushing doctors to take the next step to identify new mutations in hopes of attacking them with an effective treatment.

Dr. Kasi and his Mayo colleagues—Naseema Gangat, a hematologist, and Shahrukh Hashmi, a transplant specialist—are among the authors of an account of Mr. Johnson’s case published in January in the journal Leukemia Research Reports.

Before qualifying for a transplant, a patient’s blasts need to be under 5%.

To get under 5%, he started on a standard chemotherapy regimen and almost immediately, things went south. His blast cells plummeted, but “the chemo just wiped out my immune system,”

Then as mysteriously as it began, a serious mycotic throat infection stopped. But Mr. Johnson couldn’t tolerate the chemo, and his blast cells were on the rise. A two-drug combination that included the liver cancer drug Nexavar, which targets the FLT3 mutation, knocked back the blast cells. But the stem cell transplant in May, which came from one of his brothers, failed to take, and he relapsed after 67 days, around late July.

He was put into a clinical trial of an experimental AML drug being developed by Astellas Pharma of Japan. He started to regain weight. In November 2014, doctors spotted the initial signs in blood tests that Mr. Johnson’s cancer was evolving to acquire a new mutation. By late January, he relapsed again , but there was a Philadelphia chromosome mutation,  a well-known genetic alteration associated with chronic myeloid leukemia. It also is a target of the blockbuster cancer drug Gleevec and several other medicines.

Clonal evolution of AML on novel FMS-like tyrosine kinase-3 (FLT3) inhibitor therapy with evolving actionable targets

Naseema Gangat, Mark R. Litzow, Mrinal M. Patnaik, Shahrukh K. Hashmi, Naseema Gangat

Leukemia Research Reports  Volume 5, 2016, Pages 7–10       doi:10.1016/j.lrr.2016.01.002

Highlights

•   The article reports on a case of AML that underwent clonal evolution.

•   We report on novel acquisition of the Philadelphia t(9;22) translocation in AML.

•   Next generation sequencing maybe helpful in these refractory/relapse cases.

•   Novel FLT3-inhibitor targeted therapies are another option in patients with AML.

•   Personalizing cancer treatment based on evolving targets is a viable option.

For acute myeloid leukemia (AML), identification of activating mutations in the FMS-like tyrosine kinase-3 (FLT3) has led to the development of several FLT3-inhibitors. Here we present clinical and next generation sequencing data at the time of progression of a patient on a novel FLT3-inhibitor clinical trial (ASP2215) to show that employing therapeutic interventions with these novel targeted therapies can lead to consequences secondary to selective pressure and clonal evolution of cancer. We describe novel findings alongside data on treatment directed towards actionable aberrations acquired during the process. (Clinical Trial: NCT02014558; registered at: 〈https://clinicaltrials.gov/ct2/show/NCT02014558〉)

The development of kinase inhibitors for the treatment of leukemia has revolutionized the care of these patients. Since the introduction of imatinib for the treatment of chronic myeloid leukemia, multiple other tyrosine kinase inhibitors (TKIs) have become available[1]. Additionally, for acute myeloid leukemia (AML), identification of activating mutations in the FMS-like tyrosine kinase-3 (FLT3) has led to the development of several FLT3-inhibitors [2], [3], [4] and [5]. The article herein reports a unique case of AML that underwent clonal evolution while on a novel FLT3-inhibitor clinical trial.

Our work herein presents clinical and next generation sequencing data at the time of progression to illustrate these important concepts stemming from Darwinian evolution [6]. We describe novel findings alongside data on treatment directed towards actionable aberrations acquired during the process.

Our work focuses on a 23-year-old male who presented with 3 months history of fatigue and easy bruising, a white blood count of 22.0×10⁹/L with 51% circulating blasts, hemoglobin 7.6 g/dL, and a platelet count of 43×10⁹/L. A bone marrow biopsy confirmed a diagnosis of AML. Initial cytogenetic studies identified trisomy 8 in all the twenty metaphases examined. Mutational analysis revealed an internal tandem duplication of the FLT3 gene (FLT3-ITD).

He received standard induction chemotherapy (7+3) with cytarabine (ARA-C; 100 mg/m²for 7 days) and daunorubicin (DNM; 60 mg/m² for 3 days). His induction chemotherapy was complicated by severe palatine and uvular necrosis of indeterminate etiology (possible mucormycosis).

Bone marrow biopsy at day 28 demonstrated persistent disease with 10% bone marrow blasts (Fig. 1). Due to his complicated clinical course and the presence of a FLT3-ITD, salvage therapy with 5-azacitidine (5-AZA) and sorafenib (SFN) was instituted. Table 1.
The highlighted therapies were employed in this particular case at various time points as shown in Fig. 1.

http://ars.els-cdn.com/content/image/1-s2.0-S221304891530025X-gr1.jpg

References

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   • 

 

 

 

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3-D Printing confirms physical model of brain folds

Posted in 3D Printing for Medical Application, Biopolymer Blend Open Porous, tagged 3D printing, brain, Brain folds, cortex, MRI on February 1, 2016| Leave a Comment »

3D Printing Confirms Physical Model of Brain Folds

Reporter: Irina Robu, PhD

Highly folded brains are not present in most animals but only in some primates, dolphins, elephants and pigs. However, not a lot is understood of how the brain folds. Researchers at Harvard John A. Paulson School of Engineering and Applied Sciences collaborating with scientists in Finland and France have shown that while many molecular processes are important in determining cellular events,what ultimately causes the brain to fold in a simple mechanical instability associated with buckling.  Understanding how the brain folds is important because it can unlock the inner workings of the brain and unravel brain-related disorders.

The number, size, shape and position of neuronal cells during brain growth all lead to the expansion of the gray matter,relative to the underlying white matter. This puts the cortex under compression, leading to a mechanical instability that causes it to crease locally. Growth differential between the brain’s outer cortex and the soft tissue underneath explains the variations in the folding patterns, the relative size of the brain, and the relative expansion of the cortex.

A gel model of a fetal brain after being immersed in liquid solvent. The resulting compression led to the formation of folds similar in size and shape to real brains. Credit: Mahadevan Lab/Harvard SEAS

Based on this, the team collaborated with neuroanatomists and radiologists in France and tested the theory using data from human fetuses. The team made a three-dimensional, gel model of a smooth fetal brain based on MRI images. The model’s surface was coated with a thin layer of elastomer gel, as an analog of the cortex. To mimic cortical expansion, the gel brain was immersed in a solvent that is absorbed by the outer layer causing it to swell relative to the deeper regions. Within minutes of being immersed in liquid solvent, the resulting compression led to the formation of folds similar in size and shape to real brains.

The research shows that if part of the brain does not grow properly or the geometry is disrupted,  the major folds are not in the right place causing a dysfunction in the brain.

Source

http://phys.org/news/2016-02-d-physical-brain.html

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Huge advance in burn surgery

Posted in 3D Printing for Medical Application, tagged 3D Modeling, 3D printing, 3D Scanning, Design, Industry Insights, Medical & Dental, News, North America, research, science on November 20, 2015| Leave a Comment »

Huge advance in burn surgery

Curator: Larry H. Bernstein, MD, FCAP

 

 

26-Hour Face Transplant Made Possible with 3D Printing

By Tyler Koslow On Thu, Nov 19, 2015

One fateful night back in 2001, a former volunteer firefighter from Mississippi named Patrick Hardison bravely entered a burning home seeking to rescue anyone who might be stuck inside. When the burning house collapsed upon Hardison, he was left with critical injuries that completely disfigured his facial features, leaving him complete unrecognizable even to his own wife and children. This horrific accident forced Hardison onto the operating table over 70 times, where traditional surgical operations were only adding to the mental and physical strain he had been undergoing since the fire had left him disfigured.

 

It wasn’t until Dr. Eduardo D. Rodriguez, a plastic surgeon at NYU’s Langone Medical Center, came up with a plan to give Hardison a full face transplant. The plan involved finding a ‘donor’ who matched in hair color, skin color, blood type, and who also has a similar skeletal structure to Hardinson. Once the selected donor was found, Rodriguez and his staff utilized 3D Systems’ Virtual Surgical Planning (VSP) technology, which allows for adequate surgical preparation by offering cutting guides over an actual 3D scan of the bone structure of both the patient and the donor.

 

 

VSP Technology

VSP technology is able to create these surgical templates by using medical scan data, which are transformed into 3D models and, in some cases, are even 3D printed for a visual aid. 3D Systems’ Medical Modeling team actually assisted in the printing of these templates, using a biocompatible 3D printing material that is easily sterilized, and can, therefore, be safely utilized within the confines of an operating room.

 

 

 

Using the careful surgical plan the Rodriguez and his team prepared on 3D Systems’ VSP technology, Hardinson received an extremely successful surgery and suddenly had all of the features of a human face again for the first time in years. Although the intensive surgery took Rodriguez and over 100 other individuals who assisted in the operation a whopping 26 hours to complete, the surgery would have likely been impossible to even plan without the preparation help offered by 3D Systems and their Virtual Surgical Planning technology. Now, thanks to Dr. Rodriguez, 3D Systems’ Medical Modeling team, and the rest of the NYU’s Langone Medical Center staff, Patrick Hardison can finally smile at the world, once again.

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Real Time Coverage and eProceedings of The 15th Annual EmTech MIT – MIT Media Lab: Top 10 Breakthrough Technologies & 2015 Innovators Under 35, 11/2 – 11/4/2015

Posted in Innovations, Intellectual Property, Interviews with Scientific Leaders, Investment in Technological Breakthrough, tagged 3D printing, drones, nuclear energy, robotics on November 5, 2015| Leave a Comment »

Real Time Coverage and eProceedings of The 15th Annual EmTech MIT – MIT Media Lab: Top 10 Breakthrough Technologies & 2015 Innovators Under 35, 11/2 – 11/4/2015

Curator: Aviva Lev-Ari, PhD, RN

Article ID #194: Real Time Coverage and eProceedings of The 15th Annual EmTech MIT – MIT Media Lab: Top 10 Breakthrough Technologies & 2015 Innovators Under 35, 11/2 – 11/4/2015. Published on 11/5/2015

WordCloud Image Produced by Adam Tubman

LIVE 11/2/2015 9AM @The 15th Annual EmTech MIT – MIT Media Lab: Top 10 Breakthrough Technologies & 2015 Innovators Under 35

http://pharmaceuticalintelligence.com/2015/11/02/live-1122015-9am-the-15th-annual-emtech-mit-mit-media-lab-top-10-breakthrough-technologies-2015-innovators-under-35/

LIVE 11/2/2015 10:15AM @The 15th Annual EmTech MIT – MIT Media Lab: Top 10 Breakthrough Technologies & 2015 Innovators Under 35

Augmented Knowledge

Rethinking Urban Infrastructure

Technology Spotlight: Cities

Driving Future of Mobility

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LIVE 11/2/2015 1:30PM @The 15th Annual EmTech MIT – MIT Media Lab: Top 10 Breakthrough Technologies & 2015 Innovators Under 35

Data Transparency Online

http://pharmaceuticalintelligence.com/2015/11/02/live-1122015-130pm-the-15th-annual-emtech-mit-mit-media-lab-top-10-breakthrough-technologies-2015-innovators-under-35/

Young Innovators:

« RNAi, CRISPR and Gene Expression Diagnostic Revelations »

LIVE 11/2/2015 2PM @The 15th Annual EmTech MIT – MIT Media Lab: Top 10 Breakthrough Technologies & 2015 Innovators Under 35

Infinite Energy

Big Data and Corporate Responsibility

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Global Entrepreneurship

Technology Spotlight: Big Data

Better Living Through Data

Lemelson-MIT Prize Honors

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Privacy and Security in the Digital Age

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Drones at Work

Italy: Advanced Manufacturing

Technology Spotlight: Materials

Young Innovator:

« Targeted immunotherapy DNA Replication »

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Robots Among Us

Breaking the Code for Better Health

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Start Making More Sense – Analog Devices

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Virtual Reality

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Disrupting Entrepreneurship: 3D Printing

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Progress towards 3D Bioprinting of blood supply: steps towards production of functional blood vessels presage production of other viable body part replacements

Posted in 3D Printing for Medical Application, Artificial Vascular Structures, Cardiovascular and Vascular Systems, tagged 3D bioprinting, 3D PRINTERS, 3D printing, ASIA on November 5, 2015| Leave a Comment »

Progress towards 3D Bioprinting of blood supply: steps towards production of functional blood vessels presage production of other viable body part replacements

Curator and Author: Justin Pearlman MD PhD

3D printing of human tissue requires a blood supply to support tissues that are more than a few millimeters thick. In recognition of the importance of achieving bioprinting with functioning vasculature, a Chinese company has committed to building a BioPrinter and BioInk (cell precursors and support) focused on vasculogenesis suitable for human implants. Meanwhile, researchers in the United States and in Australia have succeeded in printing vascular trees, for example, a branching vascular-like structure that supported blood circulation when grafted to a rat. The vascular pathways are printed within surrounding structures as a dissolvable substance (e.g., sugar) subesquently removed. Remaining steps include establishing adequacy of tissue perfusion and sustainable viability of the vessel integrity and function as well as survival of the surrounding tissue. Adult humans maintain abilities to remodel blood vessels (vasculogenesis, arteriogenesis, angiogenesis) so it may suffice to provide printed blood conduits and precursor cells and/or stimulants as a bridge and scaffold to vasculature development plus tissue perfusion in vivo, if they can meet the milestones of adequacy of biosafety, support of blood circulation, tissue perfusion, sustainability, as well as adaptation with promotion of growth and remodelling as needed.

SOURCE

http://3dprintingindustry.com/2015/11/02/researchers-successfully-implant-artificial-blood-vessels-made-with-3d-printing/?utm_source=3D+Printing+Industry+Update&utm_medium=email&utm_campaign=eaca83c47f-RSS_EMAIL_CAMPAIGN&utm_term=0_695d5c73dc-eaca83c47f-64568677

Revotek Unveils First Commercial Blood Vessel Bioprinter

BY MICHAEL MOLITCH-HOU ON MON, OCTOBER 26, 2015 · 3D PRINTERS,3D PRINTING, ASIA, BIOPRINTING 1 COMMENT

There may be another machine to add to our list of top 10 bioprinters on the market, or in development.  And this one could prove to be more important than all of the rest, as Revotek, the Chinese company behind the technology, claims that their new bioprinter is capable of 3D print blood vessels, a missing key ingredient to more complex 3D printed tissues.

In the video below, you’ll see the blood vessel printer working two nozzles alternatively to 3D print biocompatible tissues in the shape of a blood vessel.  It is claimed that the system is capable of creating a 10-cm tube in just two minutes.  The material is then placed into a culture of stem cells, growth factors, and nutrients, where Revotek says that it can differentiate the cells necessary to create a functioning blood vessel, keeping the stem cells active the whole time.

Kang Yujian, chief scientist at Revotek, explains, “The core of the printer is the BioBrick, in which there are stem cells. Given certain environment and conditions, it [the stem cell] can, according to our requirements, differentiate into the cells we need.” Dai Kerong, an academic at the Chinese Academy of Engineering, adds, “The achievement is not just about printing one blood vessel, but finding the method of sustaining vascular cells and other active substances. The method is useful in blood vessel printing, and in the printings of livers, kidneys and other organs.”

There are numerous cases of researchers and businesses working to 3D print blood vessels, which would be necessary to bring blood flow to cells being cultivated into complex organ tissues. Researchers at Harvard were able to print blood vessels in February of 2014; the Wake Forest Institute for Regenerative Medicine (WFIRM) is working towards the same goal; and the Fraunhofer Institute has its ArtiVasc3D project.  The implication here is that Revotek has fully completed its system, paving the way for commercial and research use.

China’s Sichuan Revotek Announces Creation of Stem Cell Bio-Ink Technology, 3D Bio-Printer, Software

BY BRIDGET BUTLER MILLSAPS · OCTOBER 26, 2015

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With both China as an up-and-coming player in the 3D printing industry and bioprinting as the biggest new process on the horizon, it’s no surprise that the two have come together, culminating in what could offer to serve as one of the most significant breakthroughs yet.

According to biotechnological company Sichuan Revotek Co., Ltd based in Chengdu, Sichuan Province, they are responsible for becoming the first producer of 3D printed blood vessels.

While the concepts of bioprinting are clear in terms of using 3D printers to facilitate the fabrication of live tissue and cellular structures with the goal being to stretch that toward organs, what has been truly challenging up until now is finding the tools and materials that can handle the job. From the software to the hardware and the actual ink, these are the areas those in research and development have reported lacking.

Now, Sichuan Revotek reports that not only do they know how to bioprint the blood vessels, but they have a comprehensive plan for doing so. They claim to have produced a full package to consist of stem cell bio-ink technology, a 3D bio-printer, and even a cloud computing platform.

“The creative breakthrough in the 3D blood vessel bio-printing means we have mastered the stem cell-based 3D bio-printing technology,” said Yang Keng, chairman of Sichuan Languang Development Co, Ltd.

This research and development program was headed up by James Kang. An expert in the area, he explains a little bit of basic information about blood vessels, as in essence they are an intricate and crucial part of bioprinting because they are the vehicles by which important nutrients travel to organs; thus, if scientists are hoping to produce 3D printed organs soon, they will need to be able to create these ‘indispensable elements’ for fabricating organs. Having the correct tools in place to make these elements overcomes a giant hurdle as so much of the problem is in producing the tissue gently so as not to damage or kill it all together.

“We have successfully realised the blood vessel regeneration by relying on the 3D bio-printer, the biosynsphere technology and the data model based on cloud computing,” Kang said.

The bio-ink that Kang and his company have developed is called Biosynsphere, and it is meant to offer patient-specific bioprinting for stem cells. This should add to the continued progress and eventual goal of many scientists hoping to be 3D printing organs in the near future.

The building of a foundation toward 3D printing organs is very important in that scientists could transform the traditional process of offering patients organ transplants. It’s possible that the days of long waiting lists and issues with organ rejection would be eliminated as 3D printing would offer immediate results with patient specific tissue. Being able to create the artificial network required with blood vessels is one more huge advance for the medical industry toward the eventual fabrication of organs.

What will this new ink eventually lead to?  Let’s hear your thoughts in the 3D Printing Stem Cells forumthread on 3DPB.com.

[Source: NDTV]

Researchers successfully 3D print blood vessels, a ‘game changer’ for artificial organs

ERIC BLATTBERG JULY 1, 2014 7:18 AM

TAGS: 3D PRINTING, BIO-PRINTING

Above: An illustration of the inside of a blood vessel.

Image Credit: Mopic / Shutterstock

Hundreds of thousands of people die annually because the demand for organs far exceeds the donor supply. Artificial organs could save those lives — and scientists just made a huge breakthrough in the field by “bio-printing” artificial vascular networks.

Researchers from the University of Sydney, MIT, Harvard, and Stanford have successfully bio-printed blood vessels, offering 3D-printed organs access to nutrients, oxygen, and waste-disposal routes, according to a study published Monday.

“While recreating little parts of tissues in the lab is something that we have already been able to do, the possibility of printing three-dimensional tissues with functional blood capillaries in the blink of an eye is a game changer,” said Dr. Luiz Bertassoni, the study’s lead author and a University of Sydney researcher.

To 3D print vascular networks, the researchers fabricated fine, interconnected fibers with an advanced bioprinter. Then they coated those fibers with human endothelial cells — these sit between circulating blood and vessel walls in the interior of blood vessels — and subsequently applied a protein-based material. They hardened the whole structure with light, then delicately removed the fibers, leaving behind a complex network of hollow cell material. After a week, those cells organized themselves into stable capillaries.

Cells inside the bioprinted vascular networks survived, differentiated, and proliferated at better rates than cells that received no nutrient supply.

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