Lifeboat Foundation

Chemotherapy works off of a basic premise: kill all rapidly-growing cells in an effort to wipe out tumor cells. The tactic, while generally effective, has quite a few off-target casualties, including cells that produce hair and cells that line the stomach.

Scientists have tried to skirt the problem by creating missile-like drugs that zero in on cancer cells specifically, sparing healthy cells.

These missile-like drugs, known as antibody-drug conjugates (ADCs), have been in the works for decades, but only in recent years have they made it to clinical trials, Kimberly Tsui, a genetics graduate student, told me.

Today, thanks to remarkable advances in antiretroviral drugs, most people with the human immunodeficiency virus (HIV) can expect to live an almost normal lifespan. But that means staying on medications for life. If those are stopped, HIV comes roaring back in just weeks. Finding a permanent cure for HIV infection, where the virus is completely and permanently eliminated from the body, has proven much tougher. So, I’m encouraged by recent work that shows it may be possible to eliminate HIV in a mouse model, and perhaps—with continued progress—someday we will actually cure HIV in humans.

This innovative approach relies on a one-two punch: drugs and genetic editing. First, HIV-infected mice received an experimental, long-acting form of antiretroviral therapy (ART) that suppresses viral replication. This step cleared the active HIV infection. But more was needed because HIV can “hide” by inserting its DNA into its host’s chromosomes—lying dormant until conditions are right for viral replication. To get at this infectious reservoir, researchers infused the mice with a gene-editing system designed to snip out any HIV DNA still lurking in the genomes of their spleen, bone marrow, lymph nodes, and other cells. The result? Researchers detected no signs of HIV in more than one-third of mice that received the combination treatment.

The new study in Nature Communications is the product of a collaboration between the NIH-funded labs of Howard Gendelman, University of Nebraska Medical Center, Omaha, and Kamel Khalili, Temple University, Philadelphia [1]. A virologist by training, Khalili years ago realized that HIV’s ability to integrate into the genomes of its host’s cells meant that the disease couldn’t be thought of only as a typical viral infection. It had a genetic component too, suggesting that an HIV cure might require a genetic answer.

An international group of scientists studied the effects of 17 lifespan-extending interventions on gene activity in mice and discovered genetic biomarkers of longevity. The results of their study were published in the journal Cell Metabolism.

Nowadays, dozens of interventions are known that extend the lifespan of various living organisms ranging from yeast to mammals. They include chemical compounds (e.g. rapamycin), genetic interventions (e.g. mutations associated with disruption of growth hormone synthesis), and diets (e.g. caloric restriction). Some targets of these interventions have been discovered. However, there is still no clear understanding of the systemic molecular mechanisms leading to lifespan extension.

A group of scientists from Skoltech, Moscow State University and Harvard University decided to fill this gap and identify crucial molecular processes associated with longevity. To do so, they looked at the effects of various lifespan-extending interventions on the activity of genes in a mouse, a commonly used model organism closely related to humans.

Scientists have identified a class of drugs that may have potential to treat a rare and deadly form of brain cancer that affects young children.

The research team, led by Ranjit Bindra, MD, PhD, and colleagues at the Yale Cancer Center, also included co-senior authors Charles Brenner, PhD, professor and DEO of biochemistry at the University of Iowa Carver College of Medicine, and Michael E. Berens, PhD, from the Translational Genomics Research Institute in Phoenix.

The findings, published Aug. 22 in Nature Communications, focus on Diffuse Intrinsic Pontine Glioma (DIPG), a rare, incurable cancer that affects the brainstem in children under age 10. Previous work had identified mutations in a gene called PPM1D as a cause of this cancer.

First it was human embryos. Now scientists are trying to develop another way to modify human DNA that can be passed on to future generations, NPR has learned.

Reproductive biologists at Weill Cornell Medicine in New York City are attempting to use the powerful gene-editing technique called CRISPR to alter genes in human sperm. NPR got exclusive access to watch the controversial experiments underway.

The research is aimed at finding new ways to prevent disorders caused by genetic mutations that are passed down from men — including some forms of male infertility. The team is starting with a gene that can increase the risk for breast, ovarian, prostate and other cancers.

The ability to edit genes in living organisms offers the opportunity to treat a plethora of inherited diseases. However, many types of gene-editing tools are unable to target critical areas of DNA, and creating such a technology has been difficult as living tissue contains diverse types of cells.

Now, Salk Institute researchers have developed a new tool—dubbed SATI—to edit the mouse genome, enabling the team to target a broad range of mutations and cell types. The new genome-editing technology, described in Cell Research on August 23, 2019, could be expanded for use in a broad range of gene mutation conditions such as Huntington’s disease and the rare premature aging syndrome, progeria.

“This study has shown that SATI is a powerful tool for genome editing,” says Juan Carlos Izpisua Belmonte, a professor in Salk’s Gene Expression Laboratory and senior author of the paper. “It could prove instrumental in developing effective strategies for target-gene replacement of many different types of mutations, and opens the door for using genome-editing tools to possibly cure a broad range of genetic diseases.”

The street performer was only 10 years old. He put knives through his arms and walked on hot embers. By 14 he was dead. Someone dared him to jump from a roof. He did it, knowing it wouldn’t hurt.

The case of the Pakistani boy with a rare genetic disorder was described in 2006. He could feel warmth and cold and the texture of objects. But he never felt pain.

Now scientists have paired the discovery with the gene-editing tool CRISPR, in what they say is a step toward a gene therapy that could block severe pain caused by diabetes, cancer, or car accidents without the addictive effects of opioids.

Both recent new Kindle books (will be paperbacks also in time) concern the two streams of this project. Primal Eye 1979–2019 outlines circuit designs and hard considerations and outlines MVT Posthuman Psychology. The other Kindle book — ZENET Game of Immortality — details some of the gaming and soft matters.

Everybody isn’t going to live forever even given new genetic techniques and improved medicines. When you reach a terminal state beyond medical science, the only options seem cryogenic preservation, actual death, or Artificial-Death. PRIMAL EYE 40 years on (1979 to 2019) includes Conscious Circuits, Artifical-Death and Posthuman Psychology.

Experts at Weill Cornell Medicine in New York are using gene editing tool CRISPR to alter a string of human genetic code which is known to increase the risk of developing some cancers.