Sorry, folks. You can’t fully grasp the Odyssey by seeing a film version! You also can’t comprehend it by reading it in a book. You have to hear it sung by a bard in dactylic hexameter while in such an ecstatic state of drunkenness, you channel the Muse and add your own lines.
And thanks to all the Marchetti lab members who worked on this project over the years: Dr. Christine Pauken, Elizabeth Raby, Dr. Shelby R. Kenney, Vic Rhamos, and Ankita Schwarting.
New paper out now in Cancers:
"Comprehensive Longitudinal Linear Mixed Modeling of CTCs Illuminates the Role of Trop2, EpCAM, and CD45 in CTC Clustering and Metastasis"
https://t.co/6g2pQJIjBO
system activity such as tucatinib and trastuzumab deruxtecan. Thanks to biostatistician Dr. Huining Kang, medical oncologist Dr. Ursa Brown-Glaberman, and PI Dr. Dario Marchetti for their extraordinary work, insights, and support in this research. 11/11
system activity such as tucatinib and trastuzumab deruxtecan. Thanks to biostatistician Dr. Huining Kang, medical oncologist Dr. Ursa Brown-Glaberman, and PI Dr. Dario Marchetti for their extraordinary work, insights, and support in this research. 11/11
We conclude that Trop2 and EpCAM facilitate CTC clustering and that cluster size increases after brain metastasis in Her2+ (aggressive) but not HR+ (less aggressive) disease. HER2+ cancers will therefore benefit from early application of therapeutics with central nervous 10/
We futher found that in CTCs expressing Trop2, diagnosis with brain metastasis was associated with greater cluster size in the more aggressive breast cancer subtype, but not in the less aggressive subtype. 9/
metastatic diagnosis, cluster number, size, presence of immune cells in CTC clusters, and expression of EpCAM by CTCs all increased in the more aggressive subtype, but stayed relatively constant in the less aggressive subtype. 8/
We then performed longitudinal analysis via Linear Mixed Effects Model (LMM) to determine whether CTC clustering and presence differs after metastatic diagnosis between patients with aggressive (Her2+) and less aggressive (HR+) breast cancer subtypes. We found that after 7/
clustering during breast cancer progression. We first analyzed correlations among our biomarkers of CTC presence and clustering, and found that both Trop2 and EpCAM were highly predictive of cluster size and presence, as was presence of immune cells in CTC clusters. 6/
for classifying CTCs. EpCAM's only close molecular relative, Trop2, is often expressed by CTCs, and is a drug target for novel therapies. To interrogate Trop2 and EpCAM's actions in CTCs, we performed a large-scale longitudinal analysis to determine their effects on CTC 5/
EpCAM (epithelial cell adhesion molecule) is a cell surface protein that promotes cell-cell adhesion in healthy epithelia as well as cancerous tissues. While EpCAM is one of the main diagnostic markers of CTCs, not all CTCs express it, so it's imperative to expand criteria 4/
Regardless of subtype, metastasis spreads via circulating tumor cells (CTCs), which disseminate from the primary tumor through the vasculature to secondary sites where they enter dormancy and/or trigger distant metastasis. 3/
Breast cancer is the most frequently diagnosed cancer in the world, and results in an estimated 685,000 deaths every year, with this burden projected to increase substantially over the next two decades. Treatment remains challenging because breast cancers are so heterogeneous. 2/
New paper out now in Cancers:
"Comprehensive Longitudinal Linear Mixed Modeling of CTCs Illuminates the Role of Trop2, EpCAM, and CD45 in CTC Clustering and Metastasis"
https://t.co/6g2pQJIjBO
If you're able to simultaneously believe that "criticizing Islam isn't Islamophobia" and also that "criticizing Israel is anti-Semitism", you should take a long hard look at yourself...because you're really cool