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monica guzman

Miami
As seen in: Nature, British Pharmacological Society, Entrepreneur, The Seattle Times, Cascade PBS Ideas Festival, Podbean, Seattle PI, Letras Libres, AllSides
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Articles

Spatial remodeling of bone marrow architecture defines tissue-state signatures of disease activity and therapeutic response in myelodysplastic neoplasms

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By Aleksandra Kopacz, Jian Chai, Arvin E. Ruiz, Itzel Valencia, Jeanne Jiang, Fabio Socciarelli, Jiwoon Park, Christopher Mason, Ling Zhang, David A Sallman, Gail J. Roboz, Pinkal Desai, Justin Kaner, Joshua A. Fein, monica guzman, Mónica Guzmán, Neal I. Lindeman, Amy Chadburn, Madhu M. Ouseph, Paul Simonson, Julia T. Geyer, Giorgio G. Inghirami, Shahin Rafii, David Redmond, Sanjay Patel, Ryan Nachman, Caitlin Unkenholz
| Nature Verified
Abstract Myelodysplastic neoplasms (MDS) disrupt bone marrow hematopoiesis, yet clinical assessment relies largely on blast enumeration and qualitative morphology, which incompletely capture marrow architecture and disease state. We applied whole-slide multiplex immunofluorescence imaging with single-cell phenotyping to map bone marrow microarchitecture in MDS.
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The co-receptor Neuropilin-1 enhances proliferation in inv(16) acute myeloid leukemia via VEGF signaling - Leukemia

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By Roger Lazaro, Mayumi Sugita, Kai Hu, monica guzman
| Nature Verified
Abstract Oncogenic programs regulate the proliferation and maintenance of cancer stem cells, and can define pharmacologic dependencies. In acute myeloid leukemia (AML) with the chromosome inversion 16 (inv(16)), the fusion oncoprotein CBFβ::MYH11 regulates pathways associated with leukemia stem cell activity. Here we demonstrate that expression of Neuropilin-1 (NRP1) is regulated by the fusion oncoprotein, and promotes AML expansion.
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Glucocorticoids paradoxically promote steroid resistance in B cell acute lymphoblastic leukemia through CXCR4/PLC signaling - Nature Communications

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By Souleymane Abdoul-Azize, Céline Derambure, monica guzman
| Nature Verified
Abstract Glucocorticoid (GC) resistance in childhood relapsed B-cell acute lymphoblastic leukemia (B-ALL) represents an important challenge. Despite decades of clinical use, the mechanisms underlying resistance remain poorly understood. Here, we report that in B-ALL, GC paradoxically induce their own resistance by activating a phospholipase C (PLC)-mediated cell survival pathway through the chemokine receptor, CXCR4.
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