We're hiring! Join our team at Einstein and put your computational imaging skills to work where it really matters: improving outcomes for cancer patients. Come join a multidisciplinary team in NYC that's pushing science from bench to bedside. ๐ฌ
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Huge congratulations to first author Mohd Nauman and all the co-authors and collaborators who made this story possible!
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@einsteinmededu.bsky.social
@monteeinsteinpath.bsky.social
Taken together, the data support a model where stemness sits at the top of a hierarchy, controlling at least two separable programs: a MenaINV-dependent extravasation module and a MenaINV-independent survival module, both needed for efficient lung colonization.
Later on, when these non-stem cells go on to form metastases, they acquire stemness!
Knocking out MenaINV in stem cells eliminates their ability to extravasate into lung tissue, but their survival advantage remains. Adding MenaINV to non-stem cells makes them suddenly become much more capable of crossing the endothelium.
A key player here is MenaINV, an invasive isoform of the actin regulator Mena that we and others have linked to tumor cell intravasation and extravasation. We show that cancer stem cells express more MenaINV, and that turns out to be central to their metastatic advantage.โ
Using a intravital imaging of a fluorescent reporter for stemness, we track individual stem cells in the living lung and find that they do not just show up more often, they are intrinsically better at both getting out of lung blood vessels and staying alive once they do.
Cancer stem cells (yellow) and non-stem cells (red) that have exited the blood vessels inside the live lung.
Super excited to share our latest work, now out as a preprint on bioRxiv! In this one, we ask a simple question with big implications: how do breast cancer stem cells gain such a huge edge during early lung metastasis?
www.biorxiv.org/content/10.6...
Great @cdi-einstein.bsky.social seminar by Jose Javier Bravo Cordero from @mountsinainyc.bsky.social covering ECM architecture, metabolism and neuroscience. Fantastic work! Thanks for visiting us!
Metastasis drives most #breastcancer deaths.
A new study led by Dr. Rachel Hazan of Einstein shows how the Wnt/ERK/CDK4/6 pathway fuels the growth of aggressive hybrid tumor cells. Blocking it slowed tumor growth and reduced aggressiveness.
In British J of Cancer tinyurl.com/5xpscst6
#metasasis
Great go see this finally come out! Exciting work! Congratulations!
Please join me in congratulating the newly minted Dr. Madeline Friedman DeLuca! She did a phenomenal job in her thesis defense today!
#ProudPI
@cdi-einstein.bsky.social @einsteinmededu.bsky.social @monteeinsteinpath.bsky.social
Was a really great talk!
Congratulations Neta! !ืืื ืืื
Got to hear the amazing Miriam Merad talk today. Fantastic work she's doing understanding how to better target tumor associated macrophages!
WR-JSHS? I heard that they are trying to get it back for next year.
What a fantastic day of science! Those were amazing projects!
Super excited to hear all the great student research at #WESEF (the second largest science fair in the country).
My list, just 7 of the nearly 800 projects being presented today, shows how students are helping to fight sickle cell disease, lung cancer, and inflammatory bowel disease.
Welcome!!!
Just finished reviewing grants for study section. Quick question for other reviewers. What do you read first when reviewing a grant? Coment on your favorite method and why.
1๏ธโฃ Abstract/Narrative
2๏ธโฃ๏ธ Specific Aims
3๏ธโฃ Research Strategy
4๏ธโฃ Biosketches
5๏ธโฃ Straight through like a book
๐ Show results
Oh my! So glad to see you're trying it out the protocol and fighting metastasis.
If you haven't, check out our JoVE video. We introduced a few new tools to make the surgery easier.
app.jove.com/v/62761/a-pe...
Good luck. Reach out if you have any questions! Looking forward to seeing your videos!
So excited to share the latest work from the amazing Serena Lucotti and the rest of the David Lyden Lab out now in Cell.
Super honored to have been able to help out in this great work!
news.weill.cornell.edu/news/2025/02...
www.cell.com/cell/abstrac...
For your favorite AI... Worked well in Perplexity.
My zip code is XXXXX. Look up who my senators are and who my representative in the house is and write separate letters to them urging them to oppose the NIH cuts to indirect costs. Talk about how it will be damaging to science and to the country.
Please write to your representatives in congress asking them to oppose the cuts in NIH funding. Whether you think that limiting overhead is good or bad, drastically cutting funding in such a short time span is destructive. If this stands, the negative impact on science will be felt for generations.
New work from @cdi-einstein.bsky.social member @dentenberg.bsky.social showing how in certain conditions chemotherapy may enhance mechanisms of dissemination. Important work. www.biorxiv.org/content/10.1...
Our findings point to another way in which tumor associated macrophages help cancer cells escape and spread. But our findings also suggest that microenvironment-based therapies, like blocking macrophage repolarization, may reduce the pro-metastatic side effects of NAC in breast cancer.
increase in macrophage-tumor cell NF-kB/ Notch1 signaling, which results in MenaINV induction. Blocking the Notch pathway during paclitaxel treatment stops this effect.
One way this happens is through the increase in MenaINV, a protein tumor cells use to get in and out of blood vessels in the breast and the lung. In this new work investigated what may cause this increase. We find that NAC causes a re-polarization of tumor-associated macrophages. This leads to an
Neoadjuvant chemotherapy (NAC) helps shrink tumors and extend the lives of many breast cancer patients. That is clear. However, a few years ago we and others discovered that in some cases, neoadjuvant paclitaxel may have an unwanted side effect where dissemination is inadvertently increased.
