Walter J. Curran
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View article: Omitting Regional Nodal Irradiation after Response to Neoadjuvant Chemotherapy
Omitting Regional Nodal Irradiation after Response to Neoadjuvant Chemotherapy Open
The addition of adjuvant regional nodal irradiation did not decrease the risk of invasive breast cancer recurrence or death from breast cancer in patients who had negative axillary nodes after neoadjuvant chemotherapy. (Funded by the Natio…
View article: Primary Results of NRG-RTOG1106/ECOG-ACRIN 6697: A Randomized Phase II Trial of Individualized Adaptive (chemo)Radiotherapy Using Midtreatment <sup>18</sup> F-Fluorodeoxyglucose Positron Emission Tomography/Computed Tomography in Stage III Non–Small Cell Lung Cancer
Primary Results of NRG-RTOG1106/ECOG-ACRIN 6697: A Randomized Phase II Trial of Individualized Adaptive (chemo)Radiotherapy Using Midtreatment <sup>18</sup> F-Fluorodeoxyglucose Positron Emission Tomography/Computed Tomography in Stage III Non–Small Cell Lung Cancer Open
PURPOSE NRG-RTOG0617 demonstrated a detrimental effect of uniform high-dose radiation in stage III non–small cell lung cancer. NRG-RTOG1106/ECOG-ACRIN6697 (ClinicalTrials.gov identifier: NCT01507428 ), a randomized phase II trial, studied …
View article: Quality-of-life outcomes from NRG Oncology NSABP B-39/RTOG 0413: whole-breast irradiation vs accelerated partial-breast irradiation after breast-conserving surgery
Quality-of-life outcomes from NRG Oncology NSABP B-39/RTOG 0413: whole-breast irradiation vs accelerated partial-breast irradiation after breast-conserving surgery Open
Background NRG Oncology NSABP B-39/RTOG 0413 compared whole-breast irradiation (WBI) to accelerated partial-breast irradiation (APBI). APBI was not equivalent to WBI in local tumor control. Secondary outcome was quality of life (QOL). Meth…
View article: Radiotherapy Plus Cisplatin With or Without Lapatinib for Non–Human Papillomavirus Head and Neck Carcinoma
Radiotherapy Plus Cisplatin With or Without Lapatinib for Non–Human Papillomavirus Head and Neck Carcinoma Open
Importance Patients with locally advanced non–human papillomavirus (HPV) head and neck cancer (HNC) carry an unfavorable prognosis. Chemoradiotherapy (CRT) with cisplatin or anti–epidermal growth factor receptor (EGFR) antibody improves ov…
View article: Cancer Informatics for Cancer Centers: Sharing Ideas on How to Build an Artificial Intelligence–Ready Informatics Ecosystem for Radiation Oncology
Cancer Informatics for Cancer Centers: Sharing Ideas on How to Build an Artificial Intelligence–Ready Informatics Ecosystem for Radiation Oncology Open
In August 2022, the Cancer Informatics for Cancer Centers brought together cancer informatics leaders for its biannual symposium, Precision Medicine Applications in Radiation Oncology, co-chaired by Quynh-Thu Le, MD (Stanford University), …
View article: Data from Rapamycin Induces Bad Phosphorylation in Association with Its Resistance to Human Lung Cancer Cells
Data from Rapamycin Induces Bad Phosphorylation in Association with Its Resistance to Human Lung Cancer Cells Open
Inhibition of mTOR signaling by rapamycin has been shown to activate extracellular signal-regulated kinase 1 or 2 (ERK1/2) and Akt in various types of cancer cells, which contributes to rapamycin resistance. However, the downstream effect …
View article: Supplementary Methods, Figures 1-4 from Rapamycin Induces Bad Phosphorylation in Association with Its Resistance to Human Lung Cancer Cells
Supplementary Methods, Figures 1-4 from Rapamycin Induces Bad Phosphorylation in Association with Its Resistance to Human Lung Cancer Cells Open
PDF file - 476K
View article: Supplementary Figure 1 from Niclosamide Overcomes Acquired Resistance to Erlotinib through Suppression of STAT3 in Non–Small Cell Lung Cancer
Supplementary Figure 1 from Niclosamide Overcomes Acquired Resistance to Erlotinib through Suppression of STAT3 in Non–Small Cell Lung Cancer Open
PDF file, 171K, Inhibition of EGFR by erlotinib (Erlo) results in STAT3 phosphorylation at Tyr 705 and increased Bcl2/Bcl-XL in human lung cancer H1650 and H1975 cells.
View article: Data from Niclosamide Overcomes Acquired Resistance to Erlotinib through Suppression of STAT3 in Non–Small Cell Lung Cancer
Data from Niclosamide Overcomes Acquired Resistance to Erlotinib through Suppression of STAT3 in Non–Small Cell Lung Cancer Open
The emergence of resistance to EGF receptor (EGFR) inhibitor therapy is a major clinical problem for patients with non–small cell lung cancer (NSCLC). The mechanisms underlying tumor resistance to inhibitors of the kinase activity of EGFR …
View article: Supplementary Methods, Figures 1-4 from Rapamycin Induces Bad Phosphorylation in Association with Its Resistance to Human Lung Cancer Cells
Supplementary Methods, Figures 1-4 from Rapamycin Induces Bad Phosphorylation in Association with Its Resistance to Human Lung Cancer Cells Open
PDF file - 476K
View article: Supplementary Figure 4 from Niclosamide Overcomes Acquired Resistance to Erlotinib through Suppression of STAT3 in Non–Small Cell Lung Cancer
Supplementary Figure 4 from Niclosamide Overcomes Acquired Resistance to Erlotinib through Suppression of STAT3 in Non–Small Cell Lung Cancer Open
PDF file, 161K, Toxicity analysis for treatments with erlotinib and niclosamide in mice bearing HCC827 xenografts.
View article: Data from Rapamycin Induces Bad Phosphorylation in Association with Its Resistance to Human Lung Cancer Cells
Data from Rapamycin Induces Bad Phosphorylation in Association with Its Resistance to Human Lung Cancer Cells Open
Inhibition of mTOR signaling by rapamycin has been shown to activate extracellular signal-regulated kinase 1 or 2 (ERK1/2) and Akt in various types of cancer cells, which contributes to rapamycin resistance. However, the downstream effect …
View article: Supplementary Figure 5 from Niclosamide Overcomes Acquired Resistance to Erlotinib through Suppression of STAT3 in Non–Small Cell Lung Cancer
Supplementary Figure 5 from Niclosamide Overcomes Acquired Resistance to Erlotinib through Suppression of STAT3 in Non–Small Cell Lung Cancer Open
PDF file, 152K, Toxicity analysis for treatments with erlotinib and niclosamide in mice bearing HCC827/ER xenografts.
View article: Supplementary Figure 3 from Niclosamide Overcomes Acquired Resistance to Erlotinib through Suppression of STAT3 in Non–Small Cell Lung Cancer
Supplementary Figure 3 from Niclosamide Overcomes Acquired Resistance to Erlotinib through Suppression of STAT3 in Non–Small Cell Lung Cancer Open
PDF file, 78K, Treatment of mice with human lung cancer HCC827/ER xenografts using a combination of erlotinib and niclosamide results in a long term tumor-free survival.
View article: Supplementary Figure 2 from Niclosamide Overcomes Acquired Resistance to Erlotinib through Suppression of STAT3 in Non–Small Cell Lung Cancer
Supplementary Figure 2 from Niclosamide Overcomes Acquired Resistance to Erlotinib through Suppression of STAT3 in Non–Small Cell Lung Cancer Open
PDF file, 46K, Structures of erlotinib and niclosamide.
View article: Supplementary Figure 2 from Niclosamide Overcomes Acquired Resistance to Erlotinib through Suppression of STAT3 in Non–Small Cell Lung Cancer
Supplementary Figure 2 from Niclosamide Overcomes Acquired Resistance to Erlotinib through Suppression of STAT3 in Non–Small Cell Lung Cancer Open
PDF file, 46K, Structures of erlotinib and niclosamide.
View article: Supplementary Figure 1 from Niclosamide Overcomes Acquired Resistance to Erlotinib through Suppression of STAT3 in Non–Small Cell Lung Cancer
Supplementary Figure 1 from Niclosamide Overcomes Acquired Resistance to Erlotinib through Suppression of STAT3 in Non–Small Cell Lung Cancer Open
PDF file, 171K, Inhibition of EGFR by erlotinib (Erlo) results in STAT3 phosphorylation at Tyr 705 and increased Bcl2/Bcl-XL in human lung cancer H1650 and H1975 cells.
View article: Supplementary Figure 5 from Niclosamide Overcomes Acquired Resistance to Erlotinib through Suppression of STAT3 in Non–Small Cell Lung Cancer
Supplementary Figure 5 from Niclosamide Overcomes Acquired Resistance to Erlotinib through Suppression of STAT3 in Non–Small Cell Lung Cancer Open
PDF file, 152K, Toxicity analysis for treatments with erlotinib and niclosamide in mice bearing HCC827/ER xenografts.
View article: Data from Niclosamide Overcomes Acquired Resistance to Erlotinib through Suppression of STAT3 in Non–Small Cell Lung Cancer
Data from Niclosamide Overcomes Acquired Resistance to Erlotinib through Suppression of STAT3 in Non–Small Cell Lung Cancer Open
The emergence of resistance to EGF receptor (EGFR) inhibitor therapy is a major clinical problem for patients with non–small cell lung cancer (NSCLC). The mechanisms underlying tumor resistance to inhibitors of the kinase activity of EGFR …
View article: Supplementary Figure 3 from Niclosamide Overcomes Acquired Resistance to Erlotinib through Suppression of STAT3 in Non–Small Cell Lung Cancer
Supplementary Figure 3 from Niclosamide Overcomes Acquired Resistance to Erlotinib through Suppression of STAT3 in Non–Small Cell Lung Cancer Open
PDF file, 78K, Treatment of mice with human lung cancer HCC827/ER xenografts using a combination of erlotinib and niclosamide results in a long term tumor-free survival.
View article: Supplementary Figure 4 from Niclosamide Overcomes Acquired Resistance to Erlotinib through Suppression of STAT3 in Non–Small Cell Lung Cancer
Supplementary Figure 4 from Niclosamide Overcomes Acquired Resistance to Erlotinib through Suppression of STAT3 in Non–Small Cell Lung Cancer Open
PDF file, 161K, Toxicity analysis for treatments with erlotinib and niclosamide in mice bearing HCC827 xenografts.
View article: Supplementary Data from Mcl-1 Interacts with Akt to Promote Lung Cancer Progression
Supplementary Data from Mcl-1 Interacts with Akt to Promote Lung Cancer Progression Open
Supplementary Figure 1. Knockout of Mcl-1 from H1299 by CRISPR/Cas9 system results in decreased cell proliferation and increased caspase 3/7 activity. Supplementary Figure 2. Expression of constitutive active form of Akt in H1299 Mcl-1 kno…
View article: Data from Mcl-1 Interacts with Akt to Promote Lung Cancer Progression
Data from Mcl-1 Interacts with Akt to Promote Lung Cancer Progression Open
Mcl-1 is a unique antiapoptotic Bcl2 family protein that functions as a gatekeeper in manipulating apoptosis and survival in cancer cells. Akt is an oncogenic kinase that regulates multiple cellular functions and its activity is significan…
View article: Supplementary Data from Mcl-1 Interacts with Akt to Promote Lung Cancer Progression
Supplementary Data from Mcl-1 Interacts with Akt to Promote Lung Cancer Progression Open
Supplementary Figure 1. Knockout of Mcl-1 from H1299 by CRISPR/Cas9 system results in decreased cell proliferation and increased caspase 3/7 activity. Supplementary Figure 2. Expression of constitutive active form of Akt in H1299 Mcl-1 kno…
View article: Data from Mcl-1 Interacts with Akt to Promote Lung Cancer Progression
Data from Mcl-1 Interacts with Akt to Promote Lung Cancer Progression Open
Mcl-1 is a unique antiapoptotic Bcl2 family protein that functions as a gatekeeper in manipulating apoptosis and survival in cancer cells. Akt is an oncogenic kinase that regulates multiple cellular functions and its activity is significan…
View article: Supplementary Data and Methods from Modulation of Bax and mTOR for Cancer Therapeutics
Supplementary Data and Methods from Modulation of Bax and mTOR for Cancer Therapeutics Open
Figure S1. Bak BH3 peptide position in Bak protein. Figure S2. Dephosphorylation of Bax by lambdaPPase in vitro. Figure S3. Bax activators CYD-2-11 and SMBA1 failed to induce Bak oligomerization. Figure S4. Analysis of CYD-2-11 toxicity in…
View article: Data from Modulation of Bax and mTOR for Cancer Therapeutics
Data from Modulation of Bax and mTOR for Cancer Therapeutics Open
A rationale exists for pharmacologic manipulation of the serine (S)184 phosphorylation site of the proapoptotic Bcl2 family member Bax as an anticancer strategy. Here, we report the refinement of the Bax agonist SMBA1 to generate CYD-2-11,…
View article: Supplementary Data and Methods from Modulation of Bax and mTOR for Cancer Therapeutics
Supplementary Data and Methods from Modulation of Bax and mTOR for Cancer Therapeutics Open
Figure S1. Bak BH3 peptide position in Bak protein. Figure S2. Dephosphorylation of Bax by lambdaPPase in vitro. Figure S3. Bax activators CYD-2-11 and SMBA1 failed to induce Bak oligomerization. Figure S4. Analysis of CYD-2-11 toxicity in…
View article: Data from Modulation of Bax and mTOR for Cancer Therapeutics
Data from Modulation of Bax and mTOR for Cancer Therapeutics Open
A rationale exists for pharmacologic manipulation of the serine (S)184 phosphorylation site of the proapoptotic Bcl2 family member Bax as an anticancer strategy. Here, we report the refinement of the Bax agonist SMBA1 to generate CYD-2-11,…
View article: Supplementary Methods from Novel Small-Molecule Inhibitors of Bcl-XL to Treat Lung Cancer
Supplementary Methods from Novel Small-Molecule Inhibitors of Bcl-XL to Treat Lung Cancer Open
PDF file, 31K.