Alex Estrada
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Alex Estrada has a total of 13 co-authors. Here are the top co-authors by number of shared publications:
- Angelo Michael De Marzo
Sidney Kimmel Comprehensive Cancer Center Johns Hopkins University, School of Medicine Baltimore MD USA
14 shared publications - Apurv Rege
Department of Biological Sciences, University of Maryland Baltimore County, Baltimore, Maryland
14 shared publications - Carolina Gomes-Alexandre
Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland
14 shared publications - Charles J. Bieberich
Department of Biological Sciences, University of Maryland Baltimore County, Baltimore, Maryland
14 shared publications - Danielle Cannady
Department of Biological Sciences, University of Maryland Baltimore County, Baltimore, Maryland
14 shared publications - Gretchen Hubbard
Caris Life Sciences, Phoenix, Arizona
14 shared publications
Latest Publications
- Open Access
- 2 January 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table 4 from Combined MYC Activation and PTEN Loss Drives Molecular Features of Aggressive Preinvasive Lesions in Mouse Prostate
Differential expression analysis of BMPC PIN samples compared to FVB, and GSEA.
- 2 January 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table 4 from Combined MYC Activation and PTEN Loss Drives Molecular Features of Aggressive Preinvasive Lesions in Mouse Prostate
Differential expression analysis of BMPC PIN samples compared to FVB, and GSEA.
- Open Access
- 2 January 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table 1 from Combined MYC Activation and PTEN Loss Drives Molecular Features of Aggressive Preinvasive Lesions in Mouse Prostate
PCA loading values for PC1 and PC2, and GSEA for top genes.
- 2 January 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table 1 from Combined MYC Activation and PTEN Loss Drives Molecular Features of Aggressive Preinvasive Lesions in Mouse Prostate
PCA loading values for PC1 and PC2, and GSEA for top genes.
- Open Access
- 2 January 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure 1 from Combined MYC Activation and PTEN Loss Drives Molecular Features of Aggressive Preinvasive Lesions in Mouse Prostate
Volcano plots for PTEN-Null PIN, MYC-PIN, and BMPC-PIN compared to their respective wild-type lobes with differentially expressed genes (yellow), CCP score genes (labeled), and genes in proliferation associated GO-BP pathways (blue) mitotic spindle organization (A), cell division (B), chromosome segregation (C), DNA replication (D), G2/M transition mitotic cytokinesis (E), and cell cycle (F). (G) Volcano plots depicting the top PC1 genes that drove enrichment of the proliferation associated GO-BP pathways in A-F (blue).
- 2 January 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure 1 from Combined MYC Activation and PTEN Loss Drives Molecular Features of Aggressive Preinvasive Lesions in Mouse Prostate
Volcano plots for PTEN-Null PIN, MYC-PIN, and BMPC-PIN compared to their respective wild-type lobes with differentially expressed genes (yellow), CCP score genes (labeled), and genes in proliferation associated GO-BP pathways (blue) mitotic spindle organization (A), cell division (B), chromosome segregation (C), DNA replication (D), G2/M transition mitotic cytokinesis (E), and cell cycle (F). (G) Volcano plots depicting the top PC1 genes that drove enrichment of the proliferation associated GO-BP pathways in A-F (blue).
- Open Access
- 2 January 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table 3 from Combined MYC Activation and PTEN Loss Drives Molecular Features of Aggressive Preinvasive Lesions in Mouse Prostate
Differential expression analysis of PTEN-Null PIN samples compared to FVB, and GSEA.
- 2 January 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table 3 from Combined MYC Activation and PTEN Loss Drives Molecular Features of Aggressive Preinvasive Lesions in Mouse Prostate
Differential expression analysis of PTEN-Null PIN samples compared to FVB, and GSEA.
- Open Access
- 2 January 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure 4 from Combined MYC Activation and PTEN Loss Drives Molecular Features of Aggressive Preinvasive Lesions in Mouse Prostate
IHC staining for RPS2 in wild-type FVB, PTEN-Null PIN, MYCPIN,and BMPC-PIN, and antibody validation. A-B) PIN lesions with PTEN loss have decreased epithelial RPS2 compared to wild-type luminal epithelial cells. C-D) Higher power view of A and B. E-H) PIN lesions with MYC overexpression (MYC PIN [E-F] and BMPC PIN) have increased RPS2 staining, with the strongest staining observed in BMPC PIN [G-H]. I) Western blot from prostate cancer cell lines shows RPS2 antibody specificity by western blot analysis by showing a single band at the predicted molecular weight (37 kDa). Beta-Actin was used as a loading control.
- 2 January 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure 4 from Combined MYC Activation and PTEN Loss Drives Molecular Features of Aggressive Preinvasive Lesions in Mouse Prostate
IHC staining for RPS2 in wild-type FVB, PTEN-Null PIN, MYCPIN,and BMPC-PIN, and antibody validation. A-B) PIN lesions with PTEN loss have decreased epithelial RPS2 compared to wild-type luminal epithelial cells. C-D) Higher power view of A and B. E-H) PIN lesions with MYC overexpression (MYC PIN [E-F] and BMPC PIN) have increased RPS2 staining, with the strongest staining observed in BMPC PIN [G-H]. I) Western blot from prostate cancer cell lines shows RPS2 antibody specificity by western blot analysis by showing a single band at the predicted molecular weight (37 kDa). Beta-Actin was used as a loading control.
- Open Access
- 2 January 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure 5 from Combined MYC Activation and PTEN Loss Drives Molecular Features of Aggressive Preinvasive Lesions in Mouse Prostate
Gene expression across five translation-related pathways for Pten-Null PIN samples is comparable to or less than wild-type samples, and expression increases in MYC-PIN and BMPC-PIN, with expression of some genes increasing even higher in primary and metastatic samples.
- 2 January 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure 5 from Combined MYC Activation and PTEN Loss Drives Molecular Features of Aggressive Preinvasive Lesions in Mouse Prostate
Gene expression across five translation-related pathways for Pten-Null PIN samples is comparable to or less than wild-type samples, and expression increases in MYC-PIN and BMPC-PIN, with expression of some genes increasing even higher in primary and metastatic samples.
- Open Access
- 2 January 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table 5 from Combined MYC Activation and PTEN Loss Drives Molecular Features of Aggressive Preinvasive Lesions in Mouse Prostate
Intersectionality of pathways identified as significantly activated or repressed by GSEA from each PIN group compared to its FVB counterpart.
- 2 January 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table 5 from Combined MYC Activation and PTEN Loss Drives Molecular Features of Aggressive Preinvasive Lesions in Mouse Prostate
Intersectionality of pathways identified as significantly activated or repressed by GSEA from each PIN group compared to its FVB counterpart.
- Open Access
- 2 January 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure 3 from Combined MYC Activation and PTEN Loss Drives Molecular Features of Aggressive Preinvasive Lesions in Mouse Prostate
Wild-type FVB, MYC-PIN, PTEN-Null PIN, BMPC-PIN, and BMPC primary tissue stained with H&E, and IHC staining for PTEN and phospho-AKT. Positive phospho-AKT staining in the epithelium of FVB and PIN samples is concordant with negative staining for PTEN. All tumor cells stain positively for phospho-AKT and negatively for PTEN.
- 2 January 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure 3 from Combined MYC Activation and PTEN Loss Drives Molecular Features of Aggressive Preinvasive Lesions in Mouse Prostate
Wild-type FVB, MYC-PIN, PTEN-Null PIN, BMPC-PIN, and BMPC primary tissue stained with H&E, and IHC staining for PTEN and phospho-AKT. Positive phospho-AKT staining in the epithelium of FVB and PIN samples is concordant with negative staining for PTEN. All tumor cells stain positively for phospho-AKT and negatively for PTEN.
- Open Access
- 2 January 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure 7 from Combined MYC Activation and PTEN Loss Drives Molecular Features of Aggressive Preinvasive Lesions in Mouse Prostate
Barcode plots for Hallmark MYC V1 and Hallmark MYC V2 in MYC-PIN (A) and BMPC-PIN (B) generate similar enrichment scores.
- 2 January 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure 7 from Combined MYC Activation and PTEN Loss Drives Molecular Features of Aggressive Preinvasive Lesions in Mouse Prostate
Barcode plots for Hallmark MYC V1 and Hallmark MYC V2 in MYC-PIN (A) and BMPC-PIN (B) generate similar enrichment scores.
- Open Access
- 2 January 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table 2 from Combined MYC Activation and PTEN Loss Drives Molecular Features of Aggressive Preinvasive Lesions in Mouse Prostate
Differential expression analysis of MYC PIN samples compared to FVB, and GSEA. Leading edge genes from GSEA using 'Dang MYC Bound' gene set for MYC PIN, BMPC PIN, and BMPC Primary samples compared with FVB samples.
- 2 January 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table 2 from Combined MYC Activation and PTEN Loss Drives Molecular Features of Aggressive Preinvasive Lesions in Mouse Prostate
Differential expression analysis of MYC PIN samples compared to FVB, and GSEA. Leading edge genes from GSEA using 'Dang MYC Bound' gene set for MYC PIN, BMPC PIN, and BMPC Primary samples compared with FVB samples.