About

Christopher S Chen is an Associate Professor in the Division of Humanities at UC Santa Cruz, affiliated with the Literature Department, Critical Race and Ethnic Studies, Creative Writing Program, Porter College, and Oakes College. His areas of expertise include 20th- and 21st-century African American literature, Asian American literature, modern and contemporary US poetry and poetics, comparative ethnic literary studies, racial capitalism, and theories of comparative racialization. His research interests focus on contemporary avant-gardes and experimental writing, as well as the intersections of race, ethnicity, and literature within American cultural contexts.

Research topics

• Medicine
• Biology
• Neuroscience
• Gerontology
• History
• Archaeology
• Psychology

Selected publications

• Oncogenic Alterations in PI3K Signaling Emulated Optogenetically Recapitulate Some Phenotypic Changes in Mammary Epithelia

  ACS Synthetic Biology · 2026-01-19

  articleOpen accessSenior authorCorresponding

  Cancer is known to be a disease of altered cellular signaling; however, the relationship between mutation-specific changes to signal transduction and the phenotypic consequences produced remains poorly understood. Here, we investigate two common breast cancer driver mutations, the PIK3CAH1047R mutation and the ErbB2 amplification, both of which activate the PI3K-Akt pathway but paradoxically drive distinct cellular outcomes. Indeed, in nontransformed mammary epithelial cells, PI3KH1047R expression induced features of epithelial–mesenchymal transition (EMT), while ErbB2amp cells exhibited a hyperproliferative phenotype. Characterization of PI3K axis signaling revealed that ErbB2amp cells display prolonged, stimulus-dependent PI3K activation, whereas PI3KH1047R cells show constitutive, ligand-independent signaling. To test whether these distinct dynamics contribute to the phenotypic responses, we employed an iLID-based optogenetic system that enables precise, tunable control of endogenous PI3K activity. Using this tool to mimic the mutation-specific dynamics in MCF10A mammary epithelial cells, we found that PI3K signaling patterns alone were sufficient to reproduce key features of the PIK3CA H1047R-associated EMT phenotype but not the ErbB2-associated proliferative phenotype. These findings suggest that the temporal encoding of pathway activity, not merely its magnitude, can drive some phenotypic changes in oncogenic progression, explain how distinct mutations within a common signaling pathway can produce divergent cellular phenotypes, and provide a workflow for interrogating the functional consequences of changes in signaling dynamics.

  PublisherOA PDFDOI

• Bmp9 regulates Notch signaling and the temporal dynamics of angiogenesis via Lunatic Fringe

  Developmental Cell · 2026-02-05

  articleOpen access

  Sprouting angiogenesis and blood vessel stabilization require precise coordination between endothelial cells (ECs) and pericytes. Bone Morphogenic Protein 9 (Bmp9), whose signaling through activin receptor-like kinase 1 (Alk1) is dysregulated in several diseases, was thought to regulate these processes by independently activating Notch target genes in an additive fashion with canonical Notch signaling. Here, through predictive computational modeling validated in mice, zebrafish, and human cell lines, we uncover that Bmp9 enhances Notch activity synergistically by upregulating Lunatic Fringe (Lfng) in ECs. Specifically, Bmp9-induced Lfng enhances Notch receptor activation, most strongly when Delta-like ligand 4 (Dll4) is also present. This Lfng regulation alters vessel branching by modulating the timing of EC phenotype selection and rearrangement during angiogenesis. Lfng also contributes to pericyte-driven vessel stabilization by mediating Jagged1 upregulation in Bmp9-stimulated ECs. In summary, Bmp9-upregulated Lfng enhances Dll4-Notch1 signaling in ECs and Jag1-Notch3 activation in pericytes, shaping angiogenic sprouting and stabilization outcomes.

  PublisherDOI

• A 16-to-256QAM G-Band Subharmonic Phase-Modulating Transmitter for Beyond-5G Communications

  2026-02-15

  article

  This paper presents a highly integrated G-band digital transmitter for beyond-5G communications featuring: 1) a subharmonic phase-modulating architecture with timeinvariant phase tripling, 2) a GS/s segmented 9-bit digital-to-phase converter (DTPC) with a sub-degree rms error, and 3) a carrier-saturating and multiplying chain for direct QAM synthesis. It achieves <tex xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">$51.2 \text{Gbps} / 16 \text{QAM}, 24 \text{Gbps} / 64 \text{QAM}$</tex>, and 8Gbps/256QAM with −2 dBm peak output power while consuming <tex xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">$280-\text{to}-350 \text{mW}$</tex> DC power.

  PublisherDOI

• The Effect of Mechanical Loading on Sprouting Angiogenesis from Engineered Macro‐vessel Model (Small Methods 4/2026)

  Small Methods · 2026-02-01

  article

  Front Cover In article number 2500850, Levenberg and co-workers developed a novel stretchable macro-vessel model embedded in collagen, subjected to distinct mechanical loading profiles to study sprouting angiogenesis. Finite-element-analysis maps strain distributions, revealing that lateral stretch enhances sprouting and alignment, while longitudinal stretch inhibits it. The study offers a predictive, controllable platform to guide vascular architecture using external mechanical cues.

  PublisherDOI

• Sphingosine-1-phosphate cross-talks to Notch via a S1PR1-Dll4-MPDZ complex to regulate endothelial barrier function

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-05-21

  articleSenior author

  Sphingosine-1-phosphate (S1P), a key bioactive component of high-density lipoproteins (HDL), is instrumental in mediating cardiovascular benefits of HDL, largely by enhancing endothelial barrier integrity. Here, we discovered that S1P induces Notch1 activation, and this Notch activation is required to enhance Rac1 activity and adherens junction assembly, which in turn stimulates endothelial barrier integrity. S1P rapidly activates Notch1 by stimulating the G-coupled protein receptor, S1P Receptor 1 (S1PR1) to drive internalization of the Notch ligand Delta-like protein 4 (Dll4). Notably, this internalization of Dll4 and subsequent activation of Notch does not involve traditional G-protein signaling; instead, S1P-bound S1PR1 forms a complex with Dll4 via the scaffolding protein MPDZ, and the undergoes co-endocytosis. Importantly, the loss or inhibition of Notch, Dll4, S1PR1, or MPDZ results in barrier defects. These findings elucidate a novel S1PR1-Dll4-MPDZ-Notch1 signaling axis that coordinates S1P and Notch signaling to regulate of endothelial cell signaling and barrier function.

  PublisherDOI

• Empagliflozin enhances metabolic efficiency and improves left ventricular hypertrophy in a hypertrophic cardiomyopathy mouse model

  European Heart Journal · 2025-04-30 · 9 citations

  articleOpen access

  BACKGROUND AND AIMS: Hypertrophic cardiomyopathy (HCM) is a genetic cardiac disorder characterized by left ventricular hypertrophy (LVH), diastolic dysfunction, and impaired metabolic efficiency. This study investigates the therapeutic potential of the sodium-glucose cotransporter 2 inhibitor (SGLT2i) empagliflozin (EMPA) in ameliorating these pathological features in a mouse model carrying the myosin R403Q mutation. METHODS: Male mice harbouring the R403Q mutation were treated with EMPA for 16 weeks. Multi-nuclear magnetic resonance spectroscopy (31P, 13C, and 23Na MRS), echocardiography, transcriptomic, proteomic, and phosphoproteomic profiling were utilized to assess metabolic, structural, and functional changes. RESULTS: Empagliflozin facilitated the coupling of glycolysis with glucose oxidation and normalized elevated intracellular sodium levels. Treatment resulted in a significant reduction in LVH and myocardial fibrosis as evidenced by echocardiography and histopathology. These structural improvements correlated with enhancements in mitochondrial adenosine triphosphate (ATP) synthesis, fatty acid oxidation, and branched-chain amino acid catabolism. Furthermore, EMPA improved left ventricular diastolic function and contractile reserve, underscored by improved ATP production and reduced energy cost of contraction. Notably, these benefits were linked to down-regulation of the mammalian target of rapamycin signalling pathway and normalization of myocardial substrate metabolic fluxes. CONCLUSIONS: Empagliflozin significantly mitigates structural and metabolic dysfunctions in a mouse model of HCM, underscoring its potential as a therapeutic agent for managing this condition. These findings suggest broader applicability of SGLT2i in cardiovascular diseases, including those due to myocardial-specific mutations, warranting further clinical investigation.

  PublisherDOI

• Acoramidis Has a Beneficial Effect Compared With Placebo on Change From Baseline in NAC ATTR Stage at Month 30 in Patients With ATTR-CM: Results From the ATTRibute-CM Study

  Journal of Nuclear Cardiology · 2025-08-01

  article
  PublisherDOI

• A 71-86GHz 1024QAM Direct-Carrier Phase-Modulating Transmitter with Digital-to-Phase Converters and Constant-Envelope Phasors

  2025-06-15

  article

  This paper presents a $71-86 \mathrm{GHz}$ 1024QAM Direct-Carrier Phase-Modulating Transmitter (DCPM-TX), solely by using 9-bit digital-to-phase converters based on digitally-controlled artificial dielectric (DiCAD) transmission lines, and constant-envelope phasor combiners. The prototype DCPM-TX delivers 20Gbps at 1024QAM and 25Gbps at 256QAM across $71-86 \mathrm{GHz}$ with peak $P_{\text {out }}$ over 16dBm while consuming 340mW DC power and $0.675 \mathrm{~mm}^{2}$ core Si area.

  PublisherDOI

• Abstract 4363872: Acoramidis Improved Clinical Outcomes, Function, Quality of Life and NT-proBNP in Patients With Transthyretin Amyloid Cardiomyopathy Regardless of Atrial Fibrillation Status at Baseline

  Circulation · 2025-11-03

  article

  Background: Atrial fibrillation (AF) significantly impacts quality of life (QoL) and is often observed in patients with transthyretin amyloid cardiomyopathy (ATTR-CM). Acoramidis achieves near-complete (≥90%) transthyretin (TTR) stabilization and is approved in the USA, the UK, Europe and Japan for the treatment of ATTR-CM in adults. In the phase 3 ATTRibute-CM study (NCT03860935), acoramidis treatment significantly reduced the time to all-cause mortality (ACM) or first cardiovascular-related hospitalization (CVH) at Month 30, and resulted in improved 6-minute walk distance (6MWD), Kansas City Cardiomyopathy Questionnaire-Overall Summary (KCCQ-OS) scores and N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels relative to placebo. The clinical efficacy of acoramidis has not yet been reported in patients with ATTR-CM and with an AF or atrial flutter (AFL) diagnosis at baseline. Research Question: How does acoramidis treatment affect ACM or first CVH, 6MWD, KCCQ-OS scores, and NT-proBNP levels at Month 30 in participants with ATTR-CM with or without AF/AFL diagnosis at baseline? Methods: The ATTRibute-CM study design has been previously published. This post hoc analysis included participants in the modified intention-to-treat population (N=611) grouped by AF/AFL diagnosis at baseline (defined as recorded AF medical history or the presence of AF or AFL on an ECG at enrollment). The rate of ACM or first CVH at Month 30 was compared between groups using a stratified Cox proportional hazards model. Changes from baseline to Month 30 in 6MWD, KCCQ-OS scores and NT-proBNP levels were summarized descriptively. Results: Overall, 62.8% (384/611) of participants had an AF/AFL diagnosis at baseline (acoramidis: 255/409, placebo: 129/202). These participants had lower mean 6MWD and KCCQ-OS scores and higher median NT-proBNP levels than those without AF/AFL diagnosis at baseline. Treatment with acoramidis reduced ACM or first CVH, slowed the decline in 6MWD and KCCQ-OS scores and blunted the rise in NT-proBNP compared with placebo, regardless of AF/AFL diagnosis at baseline ( Table ). Conclusions: Acoramidis improved clinical outcomes (ACM, CVH), functional status, QoL and NT-proBNP levels relative to placebo in participants with ATTR-CM, regardless of AF/AFL diagnosis at baseline.

  PublisherDOI

• Engineering a heparin-mimetic biomaterial to promote tissue vascularization

  Communications Biology · 2025-11-14 · 2 citations

  articleOpen accessSenior author

  A major challenge in tissue engineering involves the development of synthetic biomaterials that effectively induce and maintain functional vascularization of engineered tissue constructs post implantation. While conjugating heparin to a dextran hydrogel developed a pro-angiogenic scaffold that led to substantial endothelial multicellular assembly in vitro and enhanced host vessel invasion in vivo, the inherent anti-coagulant bioactivities of native heparin elicited substantial local bleeding upon implantation. To decouple the pro-angiogenic effects from the anti-coagulant activity, we developed a synthetic, heparin-mimetic material by introducing sulfate adducts to the dextran backbone. These heparin-mimetic hydrogels bound and immobilized growth factors, enhanced angiogenic signaling, and promoted both in vitro vascular network formation in 3D and in vivo tissue microvascularization to a similar extent as heparin conjugated hydrogels, but without inducing local bleeding at implantation sites. This development of a fully synthetic, highly tunable angiogenic biomaterial provides a new material system to engineer functional vascularized tissues. Synthetic heparin-mimetic hydrogels immobilize angiogenic growth factors to promote tissue vascularization, providing salient properties of heparin-containing materials in promoting angiogenesis without the associated risk of bleeding.

  PublisherOA PDFDOI

Frequent coauthors

• Joshua C. Brumberg

  Queens College, CUNY

  38 shared

• John Kalambogias

  Burke Foundation

  6 shared

• Yi Zuo

  Sichuan University

  6 shared

• Titus Son

  Queens College, CUNY

  3 shared

• Anthony Gilmore

  3 shared

• Cindy S.‐Y. Lin

  University of Sydney

  3 shared

• Safraz Khan

  Queens College, CUNY

  3 shared

• Racheli Wercberger

  University of California, San Francisco

  3 shared