Benedito A. Carneiro
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View article: Table 3 from BrUOG360: A Phase Ib/II Study of Copanlisib in Combination with Rucaparib in Patients with Metastatic Castration-Resistant Prostate Cancer (mCRPC)
Table 3 from BrUOG360: A Phase Ib/II Study of Copanlisib in Combination with Rucaparib in Patients with Metastatic Castration-Resistant Prostate Cancer (mCRPC) Open
TRAEs.
View article: Figure 2 from BrUOG360: A Phase Ib/II Study of Copanlisib in Combination with Rucaparib in Patients with Metastatic Castration-Resistant Prostate Cancer (mCRPC)
Figure 2 from BrUOG360: A Phase Ib/II Study of Copanlisib in Combination with Rucaparib in Patients with Metastatic Castration-Resistant Prostate Cancer (mCRPC) Open
Swimmer plot showing treatment duration on study for all patients. Genomic alterations in the homologous recombination DNA repair and PI3K/AKT/mTOR pathways are noted for each patient.
View article: Supplementary Table S1 from BrUOG360: A Phase Ib/II Study of Copanlisib in Combination with Rucaparib in Patients with Metastatic Castration-Resistant Prostate Cancer (mCRPC)
Supplementary Table S1 from BrUOG360: A Phase Ib/II Study of Copanlisib in Combination with Rucaparib in Patients with Metastatic Castration-Resistant Prostate Cancer (mCRPC) Open
Supplementary Table S1. Dose-escalation Schema
View article: Figure 1 from BrUOG360: A Phase Ib/II Study of Copanlisib in Combination with Rucaparib in Patients with Metastatic Castration-Resistant Prostate Cancer (mCRPC)
Figure 1 from BrUOG360: A Phase Ib/II Study of Copanlisib in Combination with Rucaparib in Patients with Metastatic Castration-Resistant Prostate Cancer (mCRPC) Open
Plasma concentration for copanlisib (BAY 80-6946). Plasma concentration of copanlisib (BAY 80-6946) was measured in samples from nine patients collected on cycle 1 day 15 before infusion (pre-dose) and at 0.5, 1, 2, 4, 6, 8, and 24 hours a…
View article: Table 1 from BrUOG360: A Phase Ib/II Study of Copanlisib in Combination with Rucaparib in Patients with Metastatic Castration-Resistant Prostate Cancer (mCRPC)
Table 1 from BrUOG360: A Phase Ib/II Study of Copanlisib in Combination with Rucaparib in Patients with Metastatic Castration-Resistant Prostate Cancer (mCRPC) Open
Baseline patient characteristics.
View article: Data from BrUOG360: A Phase Ib/II Study of Copanlisib in Combination with Rucaparib in Patients with Metastatic Castration-Resistant Prostate Cancer (mCRPC)
Data from BrUOG360: A Phase Ib/II Study of Copanlisib in Combination with Rucaparib in Patients with Metastatic Castration-Resistant Prostate Cancer (mCRPC) Open
Purpose:Metastatic castration-resistant prostate cancer with homologous recombination (HR) deficiency (HRD) is sensitive to PARP inhibitors (PARPi). PI3K inhibitors (PI3Ki) sensitize to PARPi by disrupting HR in preclinical models. This ph…
View article: Table 2 from BrUOG360: A Phase Ib/II Study of Copanlisib in Combination with Rucaparib in Patients with Metastatic Castration-Resistant Prostate Cancer (mCRPC)
Table 2 from BrUOG360: A Phase Ib/II Study of Copanlisib in Combination with Rucaparib in Patients with Metastatic Castration-Resistant Prostate Cancer (mCRPC) Open
HRD pathogenic genomic alterations.
View article: Supplementary Figure 1 from Metastatic Prostate Cancers with <i>BRCA2</i> versus <i>ATM</i> Mutations Exhibit Divergent Molecular Features and Clinical Outcomes
Supplementary Figure 1 from Metastatic Prostate Cancers with <i>BRCA2</i> versus <i>ATM</i> Mutations Exhibit Divergent Molecular Features and Clinical Outcomes Open
Overall survival of ATM, BRCA2 mutant, and HRDother mPCs.
View article: Supplementary Table 2 from Metastatic Prostate Cancers with <i>BRCA2</i> versus <i>ATM</i> Mutations Exhibit Divergent Molecular Features and Clinical Outcomes
Supplementary Table 2 from Metastatic Prostate Cancers with <i>BRCA2</i> versus <i>ATM</i> Mutations Exhibit Divergent Molecular Features and Clinical Outcomes Open
Comparison of the frequencies of additional molecular features between non-castrate (NC) and castrate (C) samples in ATMm, BRCA2m, HRDother, and HRP groups. The significant differences between the two groups are highlighted (red box).
View article: Supplementary Table 1 from Metastatic Prostate Cancers with <i>BRCA2</i> versus <i>ATM</i> Mutations Exhibit Divergent Molecular Features and Clinical Outcomes
Supplementary Table 1 from Metastatic Prostate Cancers with <i>BRCA2</i> versus <i>ATM</i> Mutations Exhibit Divergent Molecular Features and Clinical Outcomes Open
Composition and rates of all detectable genomic features detectable through the Caris diagnostic platform.
View article: Supplementary Figure 3 from Metastatic Prostate Cancers with <i>BRCA2</i> versus <i>ATM</i> Mutations Exhibit Divergent Molecular Features and Clinical Outcomes
Supplementary Figure 3 from Metastatic Prostate Cancers with <i>BRCA2</i> versus <i>ATM</i> Mutations Exhibit Divergent Molecular Features and Clinical Outcomes Open
AR activities and NEPC signatures in ATM- and BRCA2- mutated tumors.
View article: The evolving landscape of antibody-drug conjugates (ADCs) for treatment of prostate cancer
The evolving landscape of antibody-drug conjugates (ADCs) for treatment of prostate cancer Open
View article: BrUOG360: A Phase Ib/II Study of Copanlisib in Combination with Rucaparib in Patients with Metastatic Castration-Resistant Prostate Cancer (mCRPC)
BrUOG360: A Phase Ib/II Study of Copanlisib in Combination with Rucaparib in Patients with Metastatic Castration-Resistant Prostate Cancer (mCRPC) Open
Purpose: Metastatic castration-resistant prostate cancer with homologous recombination (HR) deficiency (HRD) is sensitive to PARP inhibitors (PARPi). PI3K inhibitors (PI3Ki) sensitize to PARPi by disrupting HR in preclinical models. This p…
View article: 1344 AgenT-797, an allogeneic iNKT cell therapy, demonstrates durable clinical activity in solid tumors: updated phase 1 findings
1344 AgenT-797, an allogeneic iNKT cell therapy, demonstrates durable clinical activity in solid tumors: updated phase 1 findings Open
View article: 517 A phase 1 trial of NM32–2668, a ROR1-CD3-HSA trispecific T-cell engager in patients with ROR1-expressing solid tumors
517 A phase 1 trial of NM32–2668, a ROR1-CD3-HSA trispecific T-cell engager in patients with ROR1-expressing solid tumors Open
View article: Supplementary Figure S2 from Genomic and Epigenomic ctDNA Profiling in Liquid Biopsies from Heavily Pretreated Patients with DNA Damage Response–Deficient Tumors
Supplementary Figure S2 from Genomic and Epigenomic ctDNA Profiling in Liquid Biopsies from Heavily Pretreated Patients with DNA Damage Response–Deficient Tumors Open
Relationship between TF measures and clinical disease burden.
View article: Supplementary Figure S3 from Genomic and Epigenomic ctDNA Profiling in Liquid Biopsies from Heavily Pretreated Patients with DNA Damage Response–Deficient Tumors
Supplementary Figure S3 from Genomic and Epigenomic ctDNA Profiling in Liquid Biopsies from Heavily Pretreated Patients with DNA Damage Response–Deficient Tumors Open
ctDNA-based enrollment PV detection and allelic status calls.
View article: Supplementary Figure S4 from Genomic and Epigenomic ctDNA Profiling in Liquid Biopsies from Heavily Pretreated Patients with DNA Damage Response–Deficient Tumors
Supplementary Figure S4 from Genomic and Epigenomic ctDNA Profiling in Liquid Biopsies from Heavily Pretreated Patients with DNA Damage Response–Deficient Tumors Open
cHRD scores based on tumor type, genotype and tumor or ctDNA-derived allelic status.
View article: Supplementary Figure S6 from Genomic and Epigenomic ctDNA Profiling in Liquid Biopsies from Heavily Pretreated Patients with DNA Damage Response–Deficient Tumors
Supplementary Figure S6 from Genomic and Epigenomic ctDNA Profiling in Liquid Biopsies from Heavily Pretreated Patients with DNA Damage Response–Deficient Tumors Open
a, b) Lollipop plot of the a) TP53BP1 and b) RIF1 mutations identified in a patient with BRCA1-altered pancreatic cancer.
View article: Supplementary Figure S1 from Genomic and Epigenomic ctDNA Profiling in Liquid Biopsies from Heavily Pretreated Patients with DNA Damage Response–Deficient Tumors
Supplementary Figure S1 from Genomic and Epigenomic ctDNA Profiling in Liquid Biopsies from Heavily Pretreated Patients with DNA Damage Response–Deficient Tumors Open
Relationship between genomic and epigenomic measures of tumor fraction.
View article: Supplementary Figure S7 from Genomic and Epigenomic ctDNA Profiling in Liquid Biopsies from Heavily Pretreated Patients with DNA Damage Response–Deficient Tumors
Supplementary Figure S7 from Genomic and Epigenomic ctDNA Profiling in Liquid Biopsies from Heavily Pretreated Patients with DNA Damage Response–Deficient Tumors Open
IGV screenshots for two patients with ATM reversions.
View article: Supplementary Methods S1 from Genomic and Epigenomic ctDNA Profiling in Liquid Biopsies from Heavily Pretreated Patients with DNA Damage Response–Deficient Tumors
Supplementary Methods S1 from Genomic and Epigenomic ctDNA Profiling in Liquid Biopsies from Heavily Pretreated Patients with DNA Damage Response–Deficient Tumors Open
Supplemental methods
View article: Supplementary Table S2 from Genomic and Epigenomic ctDNA Profiling in Liquid Biopsies from Heavily Pretreated Patients with DNA Damage Response–Deficient Tumors
Supplementary Table S2 from Genomic and Epigenomic ctDNA Profiling in Liquid Biopsies from Heavily Pretreated Patients with DNA Damage Response–Deficient Tumors Open
Details of reversion alterations in reversion evaluable patients
View article: Supplementary Figure S5 from Genomic and Epigenomic ctDNA Profiling in Liquid Biopsies from Heavily Pretreated Patients with DNA Damage Response–Deficient Tumors
Supplementary Figure S5 from Genomic and Epigenomic ctDNA Profiling in Liquid Biopsies from Heavily Pretreated Patients with DNA Damage Response–Deficient Tumors Open
Reversion detection by clinical and genomic characteristics.
View article: Supplementary Table S1 from Genomic and Epigenomic ctDNA Profiling in Liquid Biopsies from Heavily Pretreated Patients with DNA Damage Response–Deficient Tumors
Supplementary Table S1 from Genomic and Epigenomic ctDNA Profiling in Liquid Biopsies from Heavily Pretreated Patients with DNA Damage Response–Deficient Tumors Open
Study representation
View article: Data from Genomic and Epigenomic ctDNA Profiling in Liquid Biopsies from Heavily Pretreated Patients with DNA Damage Response–Deficient Tumors
Data from Genomic and Epigenomic ctDNA Profiling in Liquid Biopsies from Heavily Pretreated Patients with DNA Damage Response–Deficient Tumors Open
Purpose:The development of DNA damage response (DDR)-directed therapies is a major area of clinical investigation; however, to date, PARP inhibitors (PARPi) remain the only approved therapy in this space. Major challenges to DDR-targeted t…
View article: Figure 3 from IPH5201, an Anti-CD39 mAb, as Monotherapy or in Combination with Durvalumab in Advanced Solid Tumors
Figure 3 from IPH5201, an Anti-CD39 mAb, as Monotherapy or in Combination with Durvalumab in Advanced Solid Tumors Open
IPH5201 treatment decreases tumoral CD39 enzymatic activity. The Wachstein–Meisel assay detects the presence of phosphates hydrolyzed from ATP due to enzymatic activity of CD39. A, Representative histology images of tumor tissues wi…
View article: Table 2 from IPH5201, an Anti-CD39 mAb, as Monotherapy or in Combination with Durvalumab in Advanced Solid Tumors
Table 2 from IPH5201, an Anti-CD39 mAb, as Monotherapy or in Combination with Durvalumab in Advanced Solid Tumors Open
Safety summarya.
View article: Data from IPH5201, an Anti-CD39 mAb, as Monotherapy or in Combination with Durvalumab in Advanced Solid Tumors
Data from IPH5201, an Anti-CD39 mAb, as Monotherapy or in Combination with Durvalumab in Advanced Solid Tumors Open
Purpose:Blocking enzymatic activity of cluster of differentiation 39 (CD39) with IPH5201 may promote antitumor immunity by increasing immunostimulatory ATP and reducing immunosuppressive adenosine levels in the tumor microenvironment. This…
View article: Table S1 from IPH5201, an Anti-CD39 mAb, as Monotherapy or in Combination with Durvalumab in Advanced Solid Tumors
Table S1 from IPH5201, an Anti-CD39 mAb, as Monotherapy or in Combination with Durvalumab in Advanced Solid Tumors Open
TEAEs of any grade occurring in >10% of all patients.