Updates
Later: we do have the placards. Very sensible placards. My wife approved.
Original Post
Olivia, our soccer-playing granddaughter is now taking driving lessons.
I will be driving to Walmart this a.m. -- actually biking to Walmart this a.m. -- to get one of those yellow "student driver" stickers.
This is one option:
Another option:
I'm looking for this one:
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The Medical Page
A reader sent me this story: how breast cancer spreads to other parts of the body.
Many of the questions asked below are, no doubt, answered in the research regarding these genes.
- an NR2F1 gene prevents pre-malignant breast cells from spreading to other parts of the body
- two immediate questions
- is the NR2F1 gene "generally" found in all men and women?
- is the NR2F1 gene "specific" for pre-malignant breast cells or "all/most/some" pre-malignant cells, regardless of origin?
- however, another gene, the HER2 gene suppresses the NR2F1 gene, allowing pre-malignant breast cells to spread to other parts of the body:
- again, the immediate questions:
- is the HER2 gene "generally" found in all men and women?
- is the HER2 gene "specific" to the NR2F1 gene? Most likely, yes.
After that, so many questions [later: a lot of these questions have been answered; from another non-medical news source].
- right now, it appears researchers are suggesting using the NR2F1-generated protein as a diagnostic tool, not a therapeutic tool. Why?
- that is easy to answer, but most likely the research will lead to using NR2F1-generated protein as both a diagnostic and a therapeutic tool, a two-fer, as it were.
- but if only used as a diagnostic tool, my conspiracy theory antennae are raised.
- how does either the NR2F1 gene or the HER2 gene mediate its action? Obviously through a protein but exactly how?
- what is the "go-between" protein coded for by the NR2F1 gene and what is the target site on the pre-malignant cell,
- because those are perhaps the two best things on which to focus
- develop a simple molecule that when ingested in pill form (or injected directly into the bloodstream) would have the same "lock-and-key" site for the protein mediated by the HER2 gene
- how "universal" is the pre-malignant breast cell "target" site ["lock-and-key"] with regard to other pre-malignant breast cells, or is unique only to the breast cell?
- "why" would the body "evolute" an NR2F1 gene? That question might be a bit easier to anser than the next question:
- "why" would the body "evolute" an HER2 gene?
- did genetic precursors to these two genes have other, more general, roles in human development millennials ago?
- how do we know this isn't fake news, like the Covid-19 vaccines?
Other links:
- News Medical Net, April 26, 2022: an explanation why a small but significant percentage of women with early-stage breast cancer never progress into an invasive breast tumor but instead die after their pre-malignant lesion reoccurs only in other organs. This explains why testing for a certain protein in all women after a certain age may be similar to testing for prostate-specific antigen (PSA) in men as a screening tool.
- Eurekalert, November 23, 2021: using the "newly-discovered protein" as a therapeutic modality.
- NCBI.NLM.NIH, online July 29, 2019.
- wiki entry: I didn't see NR2F1 mentioned at the wiki entry. I believe I read somewhere that NR2F1-breast cancer represents about 30% of all breast cancer. I have no idea if this is accurate; if that was old information; where this issue stands now. I'm also not sure why all the media interest all of a sudden in April, 2022; NR2F1 has been "around" for some time, although the HER2 news might be a new development.
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