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Appearing on "The Katie Phang Show" early Saturday morning, former federal prosecutor Glenn Kirschner served a warning to House Minority Leader Kevin McCarthy (R-CA) that he will be in a world of hurt if he defies a House Jan 6th committee subpoena, an action which could, in turn, set him up for multiple criminal charges.
McCarthy, who is desperately hoping to take over as House speaker after the midterms election had his lawyer send a letter to the committee this week telling them he will not comply and claiming the subpoenas it has issued are not constitutional -- a claim that has already been shot down by federal judges.
Speaking with former prosecutor Phang, Kirschner claimed the committee really has no choice but to refer the California Republican to the Justice Department for criminal prosecution.
"It seems hardly surprising that McCarthy will say he will likely defy the subpoena from the January 6th committee. Should the committee and will the committee, refer him to the DOJ for criminal prosecution?" host Phang prompted.
"How can the committee not refer him to a criminal prosecution?" Kirschner shot back. "You cannot investigate crimes, including crimes by high government officials, if people just thumb their nose at lawfully-issued subpoenas. Make no mistake about it, courts have ruled over and over again that the committee was lawfully constituted, accordingly, and it is lawfully exercising its power."
"As a matter of principle, the January 6th committee must refer Kevin McCarthy for criminal contempt of Congress if he chooses to turn up his nose to the subpoena," he continued. "Someone better tell Kevin McCarthy to buckle up buttercup, there are a whole lot of crimes that you will be committing if you continue to conceal the misconduct of Donald Trump from the January 6th committee, and by extension, the American people."
"You are not just making the crime of contempt of Congress, you are potentially committing a crime of accessory after the fact and a misrepresentation of a felony," he elaborated. "These are in Title 18 of the criminal code. I have the ugly big blue book of crimes; if you cover up the crimes of another, and those crimes are quote, 'recognizable in the eyes of the United States,' you are committing a criminal offense."
"McCarthy, potentially, has a whole lot of trouble coming his way if he continues to conceal the crimes of Donald Trump," he added.
Watch below or at this link.
MSNBC 05 28 2022 07 30 25 youtu.be
(Reuters) - Russian President Vladimir Putin told the leaders of France and Germany in a phone call on Saturday that Russia was willing to discuss ways to make it possible for Ukraine to resume shipments of grain from Black Sea ports, the Kremlin said. Russia and Ukraine account for nearly a third of global wheat supplies, while Russia is also a key global fertilizer exporter and Ukraine is a major exporter of corn and sunflower oil. "For its part, Russia is ready to help find options for the unhindered export of grain, including the export of Ukrainian grain from Black Sea ports," the Kremlin...
Genetic mutations can be benign or cancerous – a new method to differentiate between them could lead to better treatments
Most of the roughly 40 trillion cells of your body have nearly identical copies of your genome – the DNA inherited from your parents, containing instructions for everything from converting food to energy to fighting off infections. Healthy cells become cancerous through harmful mutations in the genome. If a cell’s genome is damaged by ultraviolet light, for example, it can result in mutations that tell the cell to grow uncontrollably and form a tumor.
Identifying the genetic changes that cause healthy cells to become malignant can help doctors select therapies that specifically target the tumor. For example, about 25% of breast cancers are HER2-positive, meaning the cells in this type of tumor have mutations that cause them to produce more of a protein called HER2 that helps them grow. Treatments that specifically target HER2 have dramatically increased survival rates for this type of breast cancer.
Scientists can now readily read cell DNA to identify mutations. The challenge is that the human genome is massive, and mutations are a normal part of evolution. The human genome is long enough to fill a 1.2 million-page book, and any two people can have about 3 million genetic differences. Finding one cancer-driving mutation in a tumor is like finding a needle in a stack of needles.
I am a computer scientist who explores large and complex genetic data sets to answer fundamental questions about biology and disease. My research team and I recently published a study using DNA from thousands of healthy people to help identify disease-causing mutations by using the principle of natural selection.
While genetic mutations are an everyday part of life, some can lead to cancer.
Using big data to find cancerous mutations
When determining what type of cancer mutation a patient has, the gold standard is to compare two samples from the patient: one from the tumor and one from healthy tissue (typically blood). Since both samples came from the same person, most of their DNA is identical; focusing only the genetic regions that differ from each other drastically narrows the location of a possible cancer-causing mutation.
The problem is that healthy tissue isn’t always collected from patients, for reasons ranging from clinical costs to narrow research protocols.
One way to get around this is to look at massive public DNA databases. Since cancer-driving mutations are detrimental to survival, natural selection tends to eliminate them over time in successive generations. Of all the mutations in a tumor, the ones that occur less frequently in a given population are more likely to be harmful than changes that are shared by many people. By counting how often a mutation occurs in these databases, researchers can distinguish between genetic changes that are common and likely benign and those that are rare and potentially cancerous.
One cancer-driving mutation can lead to a cascade of other mutations that lead to uncontrollable cell division.
Given the power of this approach, there has been a recent surge of projects to collect and share the DNA sequences from hundreds to thousands of individuals. These projects include the 1000 Genomes Project, Simons Genome Diversity Project, GnomAD and All of Us. There will likely be many more in the future.
Estimating how likely a mutation causes disease by how frequently it appears in a genome is common for small genetic changes called single-nucleotide variants (SNVs). SNVs affect just one position in the 3 billion neuclotide human genome. It could, for example, switch one thymine T to a cytosine C.
Most researchers and clinical pathologists use a catalog of variants that have been detected across thousands of samples. If an SNV identified in a tumor is not listed in the catalog, we can assume that it’s rare and possibly drives cancer. This works well for SNVs because detection of these mutations is usually accurate, with few false negatives.
However, this process breaks down for genetic changes across longer strands of DNA called structural variants (SVs). SVs are more complex because they include the addition, removal, inversion or duplication of sequences. Compared to much simpler SNVs, SVs have higher error rates in detection. False negatives are relatively frequent, resulting in incomplete catalogs that make comparing mutations against them difficult. Finding a tumor SV that isn’t listed in a catalog could mean that it’s rare and a cancer-driving candidate, or that it was missed when the catalog was created.
Focusing on verification
My colleagues and I solved these problems by moving from a process focused on detection to one that focuses on verification. Detection is difficult – it requires processing complex data to determine if there is enough evidence to support the existence of a mutation. On the other hand, verification limits decision-making just to whether or not the evidence at hand supports the existence of a specific event. Instead of looking for a needle in a stack of needles, we are now simply considering whether the needle we have is the one we want.
Our method leverages this strategy by searching through raw data from thousands of DNA samples for any evidence supporting specific SV. In addition to the efficiency benefits of only looking at the data flanking the target variant, if there is no such evidence, we can confidently conclude that the target variant is rare and potentially disease-causing.
Using our method, we scanned the SVs identified in prior cancer studies and found that thousands of SVs previously associated with cancers also appear in normal healthy samples. This indicates that these variants are more likely to be benign, inherited sequences rather than disease-causing ones.
All of Us is a research program from the National Institutes of Health with the aim of making medicine more tailored to individual needs.
Most importantly, our method performed just as well as the traditional strategy that requires both tumor and healthy samples, opening the door to reducing the cost and increasing the accessibility of high-quality cancer mutation analysis.
My team and I are exploring expanding our searches to include large collections of tumors from different types of cancers such as breast and lung. Determining which organ a tumor originated from is critical to prognosis and treatment because it can indicate whether the cancer has metastasized or not. Because most tumors have specific mutational signatures, recovering evidence of an SV within a specific tumor sample could help identify the patient’s tumor type and lead to faster treatment.