Lifeboat Foundation: Safeguarding Humanity
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Category: biotech/medical – Page 2655

Traditional cancer research is well funded but ALT cancers are not. SENS Research is aiming to raise funds to address this vital gap in our scientific knowledge. Most scary thing of all is that some regular cancers that abuse telomerase can switch to this ALT method to keep growing when telomerase blocking therapies are used.

The paper I’ll point out today is a timely one, given that the SENS Research Foundation’s fundraiser for early stage work on a therapy for alternative lengthening of telomeres (ALT) cancers is nearing its close. There are still thousands of dollars left in the matching fund, so give it some thought if you haven’t yet donated. The search for ways to safely sabotage ALT is a useful, important line of research because blocking telomere lengthening is a path to a universal cancer therapy, those research groups presently working on it are all looking to achieve this goal by interfering in the activities of telomerase, cancers can switch from using telomerase to using ALT, and next to no-one is working on ways to suppress ALT mechanisms. It seems fairly clear based on the evidence to date that the universal cancer therapy that lies ahead, built by inhibiting telomere lengthening, must involve a blockade of both telomerase and ALT. The open access paper below reinforces this point, the authors investigating how exactly cancers switch from telomerase to ALT to maintain their dangerous growth.

Cancer research today has a grand strategy problem. There is only so much funding and only so many researchers, but hundreds of subtypes of cancer. Therapies tend to be highly specific to the peculiarities of one type of cancer or a small class of cancers, meaning that great expense and time leads to a treatment that is only applicable for a fraction of cancer patients, all too often a tiny fraction. Further, since tumors evolve at great speed, any one individual patient’s cancer may find its way out from under the hammer by changing its signature and mode of operation. All is not doom and gloom, however. Consider that the research community could build a therapy applicable to all cancers with little to no modification, where the cost of development would be no greater than any one of the highly specific therapies presently in use and under development. That therapy would be, of course, based on the blockade of telomere lengthening.

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Calico, a company focused on aging research and therapeutics, today announced that Daphne Koller, Ph.D., is joining the company as Chief Computing Officer. In this newly created position, Dr. Koller will lead the company’s computational biology efforts. She will build a team focused on developing powerful computational and machine learning tools for analyzing biological and medical data sets. She and her team will work closely with the biological scientists at Calico to design experiments and construct data sets that could provide a deeper understanding into the science of longevity and support the development of new interventions to extend healthy lifespan.

Calico will try to use machine learning to understand the complex biological processes involved in aging.

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The key to the researcher’s discovery is in the use of adenosine. This naturally occurring molecule can be injected into bone tissue to coax human pluripotent stem cells (which are capable of becoming any type of cell in the body), to regenerate. In the experiment, this method helped fix cranial bone defects in mice, without causing infections or tumors.

Pluripotent cells can become any type of cell (muscle, heart, skin or bone) through differentiation; but prompting the process and directing stem cell differentiation is very complicated and can be very expensive. The method has also been known to cause the development of teratomas (tumors that contain multiple tissues taken from various organs upon transplantation.).

But, by simply adding adenosine to human pluripotent stem cells, the research team managed to effectively and safely direct stem cell differentiation. Right now, the team is focused on understanding how this single molecule is signaling bone formation.

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When it comes to the billions of neurons in your brain, what you see at birth is what get—except in the hippocampus. Buried deep underneath the folds of the cerebral cortex, neural stem cells in the hippocampus continue to generate new neurons, inciting a struggle between new and old as the new attempts to gain a foothold in memory-forming center of the brain.

In a study published online in Neuron, Harvard Stem Cell Institute (HSCI) researchers at Massachusetts General Hospital and the Broad Institute of Harvard and MIT in collaboration with an international team of scientists found they could bias the competition in favor of the newly generated .

“The hippocampus allows us to form new memories of ‘what, when and where’ that help us navigate our lives,” said HSCI Principal Faculty member and the study’s corresponding author, Amar Sahay, PhD, “and neurogenesis—the generation of new neurons from stem cells—is critical for keeping similar memories separate.”

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Amazing research on how PTSD can be pass down to the survivor’s offspring due to trauma altering the traumatic victim’s DNA Sequence.

Philadelphia, PA, September 1, 2016 – The children of traumatized people have long been known to be at increased risk for posttraumatic stress disorder (PTSD), and mood and anxiety disorders. However, according to Rachel Yehuda from the James J. Peters Veterans Affairs Medical Center at the Icahn School of Medicine at Mount Sinai who led a new study in Biological Psychiatry, there are very few opportunities to examine biologic alterations in the context of a watershed trauma in exposed people and their adult children born after the event.

One of the most intensively studied groups in this regard are the children of survivors of the Nazi concentration camps. From the work of Yehuda and others, there has been growing evidence that concentration camp survivors and their children might show changes in the epigenetic regulation of genes.

Epigenetic processes alter the expression of a gene without producing changes in the DNA sequence. DNA methylation is one of these epigenetic modifications, which regulates genome function through processes that add or remove a methyl group to a specific site in DNA, potentially affecting gene transcription.

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I remember 4 years ago at a CIO Life Sciences Conference in AZ when one of the leaders over a research lab mention the desire to finally enable patients to share their entire DNA sequence on a thumb drive with their doctor in order to be treated properly as well as have insights on the patient’s future risks. However, limitations such as HIPAA was brought up in the discussion. Personally, with how we’re advancing things like synthetic biology which includes DNA data storage, cell circuitry, electronic tattoos, etc. thumb drive maybe too outdated.

The circle that is personalized medicine consists of more than just doctor, patient, and patient data. Other elements are in the loop, such as EHR systems that incorporate gene-drug information and updated clinical guidelines.

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Very interesting and extremely interesting as we do more work on synthetic DNA as well.

Epigenetics isn’t limited to studying marks on chromatin; it can also put chromatin on a hair trigger, bringing spring-loaded action to its bead-on-a-string structures, exposing disease processes to transcriptional crossfire.

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Chromatin proteins have expanded the mammalian synthetic biology toolbox by enabling control of active and silenced states at endogenous genes. Others have reported synthetic proteins that bind DNA and regulate genes by altering chromatin marks, such as histone modifications. Previously we reported the first synthetic transcriptional activator, the “Polycomb-based transcription factor” (PcTF), that reads histone modifications through a protein-protein interaction between the PCD motif and trimethylated lysine 27 of histone H3 (H3K27me3). Here, we describe the genome-wide behavior of PcTF. Transcriptome and chromatin profiling revealed PcTF-sensitive promoter regions marked by proximal PcTF and distal H3K27me3 binding. These results illuminate a mechanism in which PcTF interactions bridge epigenetic marks with the transcription initiation complex. In three cancer-derived human cell lines tested here, many PcTF-sensitive genes encode developmental regulators and tumor suppressors. Thus, PcTF represents a powerful new fusion-protein-based method for cancer research and treatment where silencing marks are translated into direct gene activation.

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Cancer thrives when mutated cells undergo frequent division. Most anti-cancer drugs work by inserting themselves in between the DNA base pairs that encode our genetic information. This process is known as intercalation, and it can result in subtle changes to the DNA molecule’s geometric shape or tertiary structure. These structural changes interfere with the DNA’s transcription and a cell’s replication process, ultimately resulting in cell death.

While intercalating agents used in chemotherapy drugs are highly effective in fighting cancer, they also may kill important cells in the body and lead to other complications such as heart failure. Therefore, researchers are always searching for faster, cheaper and more accurate tools to aid in the design of next-generation anti-cancer drugs with reduced side effects.

A paper published in ACS Nano, one of the top nanotechnology journals in the world, explores this topic. “Modeling and Analysis of Intercalant Effects on Circular DNA Conformation,” (LINK TO http://pubs.acs.org/doi/abs/10.1021/acsnano.6b04876) focuses on the effect of the intercalating agent ethidium bromide (a mimic for many chemotherapy drugs) on the tertiary structure of DNA.

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