Laura Menocal

ORCID: 0000-0002-2070-0106
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About
Contact & Profiles
Research Areas
  • Neuroscience and Neural Engineering
  • Photoreceptor and optogenetics research
  • Nicotinic Acetylcholine Receptors Study
  • Nanoplatforms for cancer theranostics
  • bioluminescence and chemiluminescence research
  • CAR-T cell therapy research
  • Advanced biosensing and bioanalysis techniques
  • 3D Printing in Biomedical Research
  • Immune Cell Function and Interaction
  • Molecular Communication and Nanonetworks
  • Physical Unclonable Functions (PUFs) and Hardware Security
  • T-cell and B-cell Immunology
  • Antimicrobial Peptides and Activities
  • Neuroscience and Neuropharmacology Research
  • Advanced Memory and Neural Computing
  • Vanadium and Halogenation Chemistry
  • Metal complexes synthesis and properties
  • Metal-Catalyzed Oxygenation Mechanisms
  • Cancer, Stress, Anesthesia, and Immune Response

Memorial Sloan Kettering Cancer Center
2019-2023

Cornell University
2023

Stony Brook University
2013

T cell receptor (TCR) signal strength is a key determinant of responses. We developed cancer mouse model in which tumor-specific CD8 cells (TST cells) encounter tumor antigens with varying TCR strength. High-signal-strength interactions caused TST to up-regulate inhibitory receptors (IRs), lose effector function, and establish dysfunction-associated molecular program. undergoing low-signal-strength also up-regulated IRs, including PD1, but retained cell-intrinsic functional state....

10.1084/jem.20201966 article EN cc-by-nc-sa The Journal of Experimental Medicine 2021-12-22

Abstract Oncogenes can initiate tumors only in certain cellular contexts, which is referred to as oncogenic competence. In melanoma, whether cells the microenvironment endow such competence remains unclear. Using a combination of zebrafish transgenesis coupled with human tissues, we demonstrate that GABAergic signaling between keratinocytes and melanocytes promotes melanoma initiation by BRAFV600E. GABA synthesized cells, then acts on GABA-A receptors keratinocytes. Electron microscopy...

10.1158/2159-8290.cd-23-0389 article EN cc-by-nc-nd Cancer Discovery 2023-08-09

We report the synthesis and characterisation of mixed-metal binuclear ruthenium(II)-vanadium(IV) complexes, which were used as potential photodynamic therapeutic agents for melanoma cell growth inhibition. The novel [Ru(pbt)2(phen2DTT)](PF6)2·1.5H2O 1 (where phen2DTT = 1,4-bis(1,10-phenanthrolin-5-ylsulfanyl)butane-2,3-diol pbt 2-(2'-pyridyl)benzothiazole) [Ru(pbt)2(tpphz)](PF6)2·3H2O 2 tpphz tetrapyrido[3,2-a:2',3'-c:3'',2''-h:2''',3'''-j]phenazine) synthesised characterised. Compound was...

10.1039/c3dt50547b article EN Dalton Transactions 2013-01-01

<p>Combined supplementary figures and figure legends. Supplementary Fig. 1: Switching requires direct contact between nascent melanoma cells keratinocytes in vivo. 2: vitro. 3: does not involve cell fusion cells. 4: Exosome-like vesicles are transferred from to keratinocytes. 5: GABAergic signaling is active skin 6: Melanoma express GAD1 produce GABA. 7: Disruption of GABA blocks melanoma/keratinocyte communication. 8: Specialized cell-cell junction signatures enriched 9: present near...

10.1158/2159-8290.27026102 preprint EN 2024-09-16

<p>Combined supplementary figures and figure legends. Supplementary Fig. 1: Switching requires direct contact between nascent melanoma cells keratinocytes in vivo. 2: vitro. 3: does not involve cell fusion cells. 4: Exosome-like vesicles are transferred from to keratinocytes. 5: GABAergic signaling is active skin 6: Melanoma express GAD1 produce GABA. 7: Disruption of GABA blocks melanoma/keratinocyte communication. 8: Specialized cell-cell junction signatures enriched 9: present near...

10.1158/2159-8290.27026102.v1 preprint EN 2024-09-16

<div>Abstract<p>Oncogenes can only initiate tumors in certain cellular contexts, which is referred to as oncogenic competence. In melanoma, whether cells the microenvironment endow such competence remains unclear. Using a combination of zebrafish transgenesis coupled with human tissues, we demonstrate that GABAergic signaling between keratinocytes and melanocytes promotes melanoma initiation by BRAFV600E. GABA synthesized cells, then acts on GABA-A receptors keratinocytes....

10.1158/2159-8290.c.6866738.v2 preprint EN 2024-09-16

<div>Abstract<p>Oncogenes can initiate tumors only in certain cellular contexts, which is referred to as oncogenic competence. In melanoma, whether cells the microenvironment endow such competence remains unclear. Using a combination of zebrafish transgenesis coupled with human tissues, we demonstrate that GABAergic signaling between keratinocytes and melanocytes promotes melanoma initiation by BRAF<sup>V600E</sup>. GABA synthesized cells, then acts on GABA-A...

10.1158/2159-8290.c.6866738.v1 preprint EN 2023-10-05

<div>Abstract<p>Oncogenes can only initiate tumors in certain cellular contexts, which is referred to as oncogenic competence. In melanoma, whether cells the microenvironment endow such competence remains unclear. Using a combination of zebrafish transgenesis coupled with human tissues, we demonstrate that GABAergic signaling between keratinocytes and melanocytes promotes melanoma initiation by BRAFV600E. GABA synthesized cells, then acts on GABA-A receptors keratinocytes....

10.1158/2159-8290.c.6866738 preprint EN 2023-10-05
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