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Profil bibliographique

Ashley V. DiMarco

Informations fournies par OpenAlex. Research Africa ne déduit ni nationalité, ni poste, ni coordonnées personnelles.

53Publications signalées
362Citations signalées
2Affiliations récentes

Les institutions déclarées

Les domaines associés

Lung Cancer Treatments and MutationsCancer Immunotherapy and BiomarkersEpigenetics and DNA MethylationRNA modifications and cancerImmunotherapy and Immune Responses

Les publications récentes

Accès ouvert 2025 supplementary-materials OpenAlex

Supplementary Table S1 from RIT1M90I Is a Driver of Lung Adenocarcinoma Tumorigenesis and Resistance to Targeted Therapy

Ashley V. DiMarco, Mirunalini Ravichandran, Jeffrey Lau, Anthony Lima et autres

Supplementary Table S1: Assessment of immunohistochemistry staining intensity on lungs from RIT1 mice. Pathological findings are summarized for all tumors within each animal. Localization of CD3-positive T cells is described. IHC staining intensity is qualitatively scored as +++; strongly positive, +/-; mixed …

0 citations
Accès ouvert 2025 other OpenAlex

Data from RIT1M90I Is a Driver of Lung Adenocarcinoma Tumorigenesis and Resistance to Targeted Therapy

Ashley V. DiMarco, Mirunalini Ravichandran, Jeffrey Lau, Anthony Lima et autres

Abstract RIT1 is a RAS-family guanosine triphosphatase that is mutated in 2.4% and amplified in up to 14% of patients with lung adenocarcinoma. Yet the oncogenic potential of RIT1 in the lungs has not been fully established. Consequently, patients with RIT1 alterations …

1 citation
2025 article OpenAlex

RIT1M90I Is a Driver of Lung Adenocarcinoma Tumorigenesis and Resistance to Targeted Therapy

Ashley V. DiMarco, Mirunalini Ravichandran, Jeffrey Lau, Anthony Lima et autres

RIT1 is a RAS-family guanosine triphosphatase that is mutated in 2.4% and amplified in up to 14% of patients with lung adenocarcinoma. Yet the oncogenic potential of RIT1 in the lungs has not been fully established. Consequently, patients with RIT1 alterations are …

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0 citations Cancer Research
Accès ouvert 2025 other OpenAlex

Data from APOBEC3 Activity Promotes the Survival and Evolution of Drug-Tolerant Persister Cells during EGFR Inhibitor Resistance in Lung Cancer

Nina Marie G. Garcia, Jessica N. Becerra, Sharan Srinivasan, Brock J. McKinney et autres

Abstract APOBEC mutagenesis is one of the most common endogenous sources of mutations in human cancer and is a major source of genetic intratumor heterogeneity. High levels of APOBEC mutagenesis are associated with poor prognosis and aggressive disease across diverse cancers, but …

0 citations
Accès ouvert 2025 other OpenAlex

Figure 3 from APOBEC3 Activity Promotes the Survival and Evolution of Drug-Tolerant Persister Cells during EGFR Inhibitor Resistance in Lung Cancer

Nina Marie G. Garcia, Jessica N. Becerra, Sharan Srinivasan, Brock J. McKinney et autres

APOBEC3B expression alters the evolutionary trajectory of acquired resistance to EGFR inhibitors. A, Kinetics of evolution of gefitinib resistance in PC9 cells with or without A3B expression. B, Representative dose–response curves to gefitinib for sensitive and resistant A3B-off and A3B-on PC9 cells. …

0 citations
Accès ouvert 2025 other OpenAlex

Figure 2 from APOBEC3 Activity Promotes the Survival and Evolution of Drug-Tolerant Persister Cells during EGFR Inhibitor Resistance in Lung Cancer

Nina Marie G. Garcia, Jessica N. Becerra, Sharan Srinivasan, Brock J. McKinney et autres

Engineering an inducible system for APOBEC3B expression in PC9 cells. A, qRT-PCR analysis showing A3A and A3B expression in PC9 cells following treatment with gefitinib or osimertinib over the course of 14 days. Error bars represent SEM of three technical replicates. Veh, …

0 citations

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