ORCID Profile
0000-0002-1216-477X
Current Organisation
University of North Carolina at Chapel Hill
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Publisher: American Association for Cancer Research (AACR)
Date: 15-09-2023
Publisher: American Association for Cancer Research (AACR)
Date: 14-08-2023
DOI: 10.1158/1078-0432.23938319.V1
Abstract: Heatmap showing clustering of all module scores filtered for a significant interaction with treatment. Our original clusters are shown against the new clusters at the top of the heatmap.
Publisher: American Association for Cancer Research (AACR)
Date: 14-08-2023
DOI: 10.1158/1078-0432.23938319
Abstract: Heatmap showing clustering of all module scores filtered for a significant interaction with treatment. Our original clusters are shown against the new clusters at the top of the heatmap.
Publisher: American Association for Cancer Research (AACR)
Date: 15-09-2023
Publisher: American Association for Cancer Research (AACR)
Date: 14-08-2023
DOI: 10.1158/1078-0432.23938310
Abstract: Supplemetary table 3 - Change in signature scores from primary to recurrence
Publisher: American Association for Cancer Research (AACR)
Date: 14-08-2023
DOI: 10.1158/1078-0432.23938325.V1
Abstract: Heatmap of signatures used for clustering by the resulting novel clusters.
Publisher: Frontiers Media SA
Date: 04-01-2019
Publisher: American Association for Cancer Research (AACR)
Date: 14-08-2023
DOI: 10.1158/1078-0432.23938313
Abstract: Supplementary table 2 - Model estimates for logistic regression models of objective response rate and linear regression models of restricted PFS by treatment group
Publisher: American Association for Cancer Research (AACR)
Date: 15-09-2023
Publisher: American Association for Cancer Research (AACR)
Date: 14-08-2023
DOI: 10.1158/1078-0432.23938316
Abstract: Supplementary table 1 - Biomarkers of interest
Publisher: American Association for Cancer Research (AACR)
Date: 15-09-2023
Publisher: Elsevier BV
Date: 04-2018
Publisher: Elsevier BV
Date: 04-2018
Publisher: Elsevier BV
Date: 04-2018
Publisher: American Association for Cancer Research (AACR)
Date: 15-09-2023
Publisher: American Association for Cancer Research (AACR)
Date: 15-09-2023
Publisher: American Association for Cancer Research (AACR)
Date: 15-09-2023
Publisher: American Association for Cancer Research (AACR)
Date: 15-09-2023
Publisher: American Association for Cancer Research (AACR)
Date: 15-09-2023
Publisher: American Association for Cancer Research (AACR)
Date: 15-09-2023
Publisher: American Association for Cancer Research (AACR)
Date: 14-08-2023
DOI: 10.1158/1078-0432.23938322
Abstract: This is an ex le of DDR-deficient case with high TILs and low gene-expression measurements. These cases were confirmed to have high TIL content (black delineation) and are characterized by both high tumour area- stromal area ratio as well as a high tumour cell- stromal cell ratio. Moreover, all these cases were characterized by high grade features, such as necrosis (blue delineation), high mitotic activity (green arrow), and high levels of atypia (blue arrow), and all had a solid growth pattern, with no formation of glands.
Publisher: American Association for Cancer Research (AACR)
Date: 15-09-2023
Publisher: American Association for Cancer Research (AACR)
Date: 14-08-2023
DOI: 10.1158/1078-0432.23938325
Abstract: Heatmap of signatures used for clustering by the resulting novel clusters.
Publisher: American Association for Cancer Research (AACR)
Date: 14-08-2023
DOI: 10.1158/1078-0432.23938328.V1
Abstract: Changes in A. CIN70, B. RPS and C. PARPi7 from treatment naïve primary tumours to post-treatment metastatic s les in an independent dataset. Multiple metastatic s les are included for some patients. 𝛃 coefficients and p-values presented for timepoint term from linear regression models with a random effect for patient to account for multiple s les from patients.
Publisher: American Association for Cancer Research (AACR)
Date: 14-08-2023
DOI: 10.1158/1078-0432.23938328
Abstract: Changes in A. CIN70, B. RPS and C. PARPi7 from treatment naïve primary tumours to post-treatment metastatic s les in an independent dataset. Multiple metastatic s les are included for some patients. 𝛃 coefficients and p-values presented for timepoint term from linear regression models with a random effect for patient to account for multiple s les from patients.
Publisher: American Association for Cancer Research (AACR)
Date: 15-09-2023
Publisher: Elsevier BV
Date: 04-2018
Publisher: American Association for Cancer Research (AACR)
Date: 14-08-2023
DOI: 10.1158/1078-0432.23938331.V1
Abstract: Additional associations between signatures. A. Distribution of CIN70 by HRD score and genomic scars (NtAI tertiles, AiCna tertiles and HLAMP). B Distribution of RPS by HRD score and genomic scars (NtAI tertiles, AiCna tertiles and HLAMP). C. Distribution of PARPi7 by HRD score and genomic scars (NtAI tertiles, AiCna tertiles and HLAMP). D. Distribution of TILs by HRD score, E. Distribution of ConcensusTME average score by HRD score F. ConsensusTME cell type estimates are highly correlated excluding fibroblasts.Correlation assessed using Spearman correlation. HRD = HRD low HRD≥42 = HRD high.
Publisher: Elsevier BV
Date: 04-2018
Publisher: Elsevier BV
Date: 04-2018
Publisher: Elsevier BV
Date: 04-2018
Publisher: American Association for Cancer Research (AACR)
Date: 14-08-2023
DOI: 10.1158/1078-0432.23938310.V1
Abstract: Supplemetary table 3 - Change in signature scores from primary to recurrence
Publisher: Elsevier BV
Date: 04-2018
Publisher: American Association for Cancer Research (AACR)
Date: 17-09-2023
Publisher: American Association for Cancer Research (AACR)
Date: 15-09-2023
Publisher: Springer Science and Business Media LLC
Date: 09-07-0077
DOI: 10.1038/NATURE13385
Publisher: Elsevier BV
Date: 08-2017
Publisher: American Association for Cancer Research (AACR)
Date: 15-09-2023
Publisher: American Association for Cancer Research (AACR)
Date: 15-09-2023
Publisher: Elsevier BV
Date: 03-2018
Publisher: American Association for Cancer Research (AACR)
Date: 15-09-2023
DOI: 10.1158/1078-0432.C.6787739
Abstract: AbstractPurpose: The TNT trial (NCT00532727) showed no evidence of carboplatin superiority over docetaxel in metastatic triple-negative breast cancer (mTNBC), but carboplatin benefit was observed in the germline i BRCA1/2 /i mutation subgroup. Broader response-predictive biomarkers are needed. We explored the predictive ability of DNA damage response (DDR) and immune markers. Patients and Methods: Tumor-infiltrating lymphocytes were evaluated for 222 of 376 patients. Primary tumors (PT) from 186 TNT participants (13 matched recurrences) were profiled using total RNA sequencing. Four transcriptional DDR-related and 25 immune-related signatures were evaluated. We assessed their association with objective response rate (ORR) and progression-free survival (PFS). Conditional inference forest clustering was applied to integrate multimodal data. The biology of subgroups was characterized by 693 gene expression modules and other markers. Results: Transcriptional DDR-related biomarkers were not predictive of ORR to either treatment overall. Changes from PT to recurrence were demonstrated in chemotherapy-naïve patients, transcriptional DDR markers separated carboplatin responders from nonresponders ( i P /i values = 0.017 0.046). High immune infiltration was associated with docetaxel ORR (interaction i P /i values 0.05). Six subgroups were identified the immune-enriched cluster had preferential docetaxel response [62.5% (D) vs. 29.4% (C) i P /i = 0.016]. The immune-depleted cluster had preferential carboplatin response [8.0% (D) vs. 40.0% (C) i P /i = 0.011]. DDR-related subgroups were too small to assess ORR. Conclusions: High immune features predict docetaxel response, and high DDR signature scores predict carboplatin response in treatment-naïve mTNBC. Integrating multimodal DDR and immune-related markers identifies subgroups with differential treatment sensitivity. Treatment options for patients with immune-low and DDR-proficient tumors remains an outstanding need. Caution is needed using PT-derived transcriptional signatures to direct treatment in mTNBC, particularly DDR-related markers following prior chemotherapy. /
Publisher: American Association for Cancer Research (AACR)
Date: 15-09-2023
Publisher: Elsevier BV
Date: 03-2018
Publisher: American Association for Cancer Research (AACR)
Date: 15-09-2023
Publisher: Elsevier BV
Date: 06-2015
Publisher: American Association for Cancer Research (AACR)
Date: 14-08-2023
DOI: 10.1158/1078-0432.CCR-23-0370
Abstract: The TNT trial (NCT00532727) showed no evidence of carboplatin superiority over docetaxel in metastatic triple-negative breast cancer (mTNBC), but carboplatin benefit was observed in the germline BRCA1/2 mutation subgroup. Broader response-predictive biomarkers are needed. We explored the predictive ability of DNA damage response (DDR) and immune markers. Tumor-infiltrating lymphocytes were evaluated for 222 of 376 patients. Primary tumors (PT) from 186 TNT participants (13 matched recurrences) were profiled using total RNA sequencing. Four transcriptional DDR-related and 25 immune-related signatures were evaluated. We assessed their association with objective response rate (ORR) and progression-free survival (PFS). Conditional inference forest clustering was applied to integrate multimodal data. The biology of subgroups was characterized by 693 gene expression modules and other markers. Transcriptional DDR-related biomarkers were not predictive of ORR to either treatment overall. Changes from PT to recurrence were demonstrated in chemotherapy-naïve patients, transcriptional DDR markers separated carboplatin responders from nonresponders (P values = 0.017 0.046). High immune infiltration was associated with docetaxel ORR (interaction P values & 0.05). Six subgroups were identified the immune-enriched cluster had preferential docetaxel response [62.5% (D) vs. 29.4% (C) P = 0.016]. The immune-depleted cluster had preferential carboplatin response [8.0% (D) vs. 40.0% (C) P = 0.011]. DDR-related subgroups were too small to assess ORR. High immune features predict docetaxel response, and high DDR signature scores predict carboplatin response in treatment-naïve mTNBC. Integrating multimodal DDR and immune-related markers identifies subgroups with differential treatment sensitivity. Treatment options for patients with immune-low and DDR-proficient tumors remains an outstanding need. Caution is needed using PT-derived transcriptional signatures to direct treatment in mTNBC, particularly DDR-related markers following prior chemotherapy.
Publisher: American Association for Cancer Research (AACR)
Date: 15-09-2023
Publisher: American Association for Cancer Research (AACR)
Date: 15-09-2023
Publisher: Elsevier BV
Date: 04-2018
Publisher: Elsevier BV
Date: 04-2018
Publisher: American Association for Cancer Research (AACR)
Date: 14-08-2023
DOI: 10.1158/1078-0432.23938307.V1
Abstract: Supplementary Table 4 - Representativeness of Study Participants
Publisher: Elsevier BV
Date: 04-2018
Publisher: Elsevier BV
Date: 04-2018
Publisher: Elsevier BV
Date: 04-2018
Publisher: American Association for Cancer Research (AACR)
Date: 14-08-2023
DOI: 10.1158/1078-0432.23938331
Abstract: Additional associations between signatures. A. Distribution of CIN70 by HRD score and genomic scars (NtAI tertiles, AiCna tertiles and HLAMP). B Distribution of RPS by HRD score and genomic scars (NtAI tertiles, AiCna tertiles and HLAMP). C. Distribution of PARPi7 by HRD score and genomic scars (NtAI tertiles, AiCna tertiles and HLAMP). D. Distribution of TILs by HRD score, E. Distribution of ConcensusTME average score by HRD score F. ConsensusTME cell type estimates are highly correlated excluding fibroblasts.Correlation assessed using Spearman correlation. HRD = HRD low HRD≥42 = HRD high.
Publisher: American Association for Cancer Research (AACR)
Date: 09-05-2012
DOI: 10.1158/1078-0432.23938313.V1
Abstract: Supplementary table 2 - Model estimates for logistic regression models of objective response rate and linear regression models of restricted PFS by treatment group
Publisher: Springer Science and Business Media LLC
Date: 18-07-2012
DOI: 10.1038/NATURE11252
Publisher: American Association for Cancer Research (AACR)
Date: 15-09-2023
Publisher: Elsevier BV
Date: 04-2018
Publisher: American Association for Cancer Research (AACR)
Date: 14-08-2023
DOI: 10.1158/1078-0432.C.6787739.V1
Abstract: AbstractPurpose: The TNT trial (NCT00532727) showed no evidence of carboplatin superiority over docetaxel in metastatic triple-negative breast cancer (mTNBC), but carboplatin benefit was observed in the germline i BRCA1/2 /i mutation subgroup. Broader response-predictive biomarkers are needed. We explored the predictive ability of DNA damage response (DDR) and immune markers. Patients and Methods: Tumor-infiltrating lymphocytes were evaluated for 222 of 376 patients. Primary tumors (PT) from 186 TNT participants (13 matched recurrences) were profiled using total RNA sequencing. Four transcriptional DDR-related and 25 immune-related signatures were evaluated. We assessed their association with objective response rate (ORR) and progression-free survival (PFS). Conditional inference forest clustering was applied to integrate multimodal data. The biology of subgroups was characterized by 693 gene expression modules and other markers. Results: Transcriptional DDR-related biomarkers were not predictive of ORR to either treatment overall. Changes from PT to recurrence were demonstrated in chemotherapy-naïve patients, transcriptional DDR markers separated carboplatin responders from nonresponders ( i P /i values = 0.017 0.046). High immune infiltration was associated with docetaxel ORR (interaction i P /i values 0.05). Six subgroups were identified the immune-enriched cluster had preferential docetaxel response [62.5% (D) vs. 29.4% (C) i P /i = 0.016]. The immune-depleted cluster had preferential carboplatin response [8.0% (D) vs. 40.0% (C) i P /i = 0.011]. DDR-related subgroups were too small to assess ORR. Conclusions: High immune features predict docetaxel response, and high DDR signature scores predict carboplatin response in treatment-naïve mTNBC. Integrating multimodal DDR and immune-related markers identifies subgroups with differential treatment sensitivity. Treatment options for patients with immune-low and DDR-proficient tumors remains an outstanding need. Caution is needed using PT-derived transcriptional signatures to direct treatment in mTNBC, particularly DDR-related markers following prior chemotherapy. /
Publisher: American Association for Cancer Research (AACR)
Date: 15-09-2023
Publisher: American Association for Cancer Research (AACR)
Date: 15-09-2023
Publisher: American Association for Cancer Research (AACR)
Date: 15-09-2023
Publisher: American Association for Cancer Research (AACR)
Date: 14-08-2023
DOI: 10.1158/1078-0432.23938307
Abstract: Supplementary Table 4 - Representativeness of Study Participants
Publisher: American Association for Cancer Research (AACR)
Date: 15-09-2023
Publisher: American Association for Cancer Research (AACR)
Date: 15-09-2023
Publisher: American Association for Cancer Research (AACR)
Date: 14-08-2023
DOI: 10.1158/1078-0432.23938316.V1
Abstract: Supplementary table 1 - Biomarkers of interest
Publisher: American Association for Cancer Research (AACR)
Date: 15-09-2023
Publisher: American Association for Cancer Research (AACR)
Date: 14-08-2023
DOI: 10.1158/1078-0432.23938322.V1
Abstract: This is an ex le of DDR-deficient case with high TILs and low gene-expression measurements. These cases were confirmed to have high TIL content (black delineation) and are characterized by both high tumour area- stromal area ratio as well as a high tumour cell- stromal cell ratio. Moreover, all these cases were characterized by high grade features, such as necrosis (blue delineation), high mitotic activity (green arrow), and high levels of atypia (blue arrow), and all had a solid growth pattern, with no formation of glands.
Publisher: American Association for Cancer Research (AACR)
Date: 16-05-0015
Publisher: American Association for Cancer Research (AACR)
Date: 15-09-2023
Publisher: Elsevier BV
Date: 04-2018
Publisher: Elsevier BV
Date: 04-2018
Publisher: American Association for Cancer Research (AACR)
Date: 15-09-2023
Publisher: Elsevier BV
Date: 04-2018
Publisher: Elsevier BV
Date: 04-2018
Publisher: American Association for the Advancement of Science (AAAS)
Date: 26-10-2018
Abstract: The Cancer Genome Atlas (TCGA) provides a high-quality resource of molecular data on a large variety of human cancers. Corces et al. used a recently modified assay to profile chromatin accessibility to determine the accessible chromatin landscape in 410 TCGA s les from 23 cancer types (see the Perspective by Taipale). When the data were integrated with other omics data available for the same tumor s les, inherited risk loci for cancer predisposition were revealed, transcription factors and enhancers driving molecular subtypes of cancer with patient survival differences were identified, and noncoding mutations associated with clinical prognosis were discovered. Science , this issue p. eaav1898 see also p. 401
Publisher: American Association for Cancer Research (AACR)
Date: 15-09-2023
Publisher: Elsevier BV
Date: 04-2018
Publisher: Springer Science and Business Media LLC
Date: 05-2013
DOI: 10.1038/NATURE12113
Publisher: Elsevier BV
Date: 10-2018
Publisher: Elsevier BV
Date: 04-2018
Publisher: Springer Science and Business Media LLC
Date: 04-11-2022
DOI: 10.1038/S41467-022-33980-9
Abstract: Urothelial Cancer - Genomic Analysis to Improve Patient Outcomes and Research (NCT02643043), UC-GENOME, is a genomic analysis and biospecimen repository study in 218 patients with metastatic urothelial carcinoma. Here we report on the primary outcome of the UC-GENOME—the proportion of subjects who received next generation sequencing (NGS) with treatment options—and present the initial genomic analyses and clinical correlates. 69.3% of subjects had potential treatment options, however only 5.0% received therapy based on NGS. We found an increased frequency of TP53 E285K mutations as compared to non-metastatic cohorts and identified features associated with benefit to chemotherapy and immune checkpoint inhibition, including: Ba/Sq and Stroma-rich subtypes, APOBEC mutational signature (SBS13), and inflamed tumor immune phenotype. Finally, we derive a computational model incorporating both genomic and clinical features predictive of immune checkpoint inhibitor response. Future work will utilize the biospecimens alongside these foundational analyses toward a better understanding of urothelial carcinoma biology.
Location: United States of America
No related grants have been discovered for Katherine Hoadley.