Kristopher Attwood
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Kristopher Attwood has a total of 378 co-authors. Here are the top co-authors by number of shared publications:
- Grace K. Dy
Department of Medicine, Roswell Park Comprehensive Cancer Center, Buffalo, New York
76 shared publications - Chang-Chieh Hsu
University at Buffalo 1 Department of Biomedical Engineering The State University of New York, Buffalo, New York
57 shared publications - Kate Rittenhouse-Olson
Department of Biotechnical and Clinical Laboratory Sciences, State University of New York at Buffalo, Buffalo, NY, USA
57 shared publications - Mary E. Reid
Roswell Park Comprehensive Cancer Center 3 Department of Medicine Buffalo, New York
57 shared publications - Wilfrido Mojica
Department of Pathology and Anatomical Sciences, University at Buffalo, The State University of New York, Buffalo, New York. 4
57 shared publications - Yafei Su
Department of Biomedical Engineering, University at Buffalo, The State University of New York, Buffalo, NY 14260, USA
57 shared publications
Latest Publications
- Open Access
- 2 July 2026
- Published by American Association for Cancer Research (AACR)
Table S2 from Tumor-Derived Complement C3 Overexpression in STK11-Mutant Lung Adenocarcinoma Drives Tumor Growth and Immune Checkpoint Inhibitor Resistance
Antibodies used in Flow Cytometry, Multi-spectral Flow Cytometry, and PhenoCycler Immunofluorescence.
- 2 July 2026
- Published by American Association for Cancer Research (AACR)
Open AccessTable S2 from Tumor-Derived Complement C3 Overexpression in STK11-Mutant Lung Adenocarcinoma Drives Tumor Growth and Immune Checkpoint Inhibitor Resistance
Antibodies used in Flow Cytometry, Multi-spectral Flow Cytometry, and PhenoCycler Immunofluorescence.
- Open Access
- 2 July 2026
- Published by American Association for Cancer Research (AACR)
Figure S5 from Tumor-Derived Complement C3 Overexpression in STK11-Mutant Lung Adenocarcinoma Drives Tumor Growth and Immune Checkpoint Inhibitor Resistance
STK11 deletion results in increased neutrophilic and decreased T cell inflammation in the TME.
- 2 July 2026
- Published by American Association for Cancer Research (AACR)
Open AccessFigure S5 from Tumor-Derived Complement C3 Overexpression in STK11-Mutant Lung Adenocarcinoma Drives Tumor Growth and Immune Checkpoint Inhibitor Resistance
STK11 deletion results in increased neutrophilic and decreased T cell inflammation in the TME.
- Open Access
- 2 July 2026
- Published by American Association for Cancer Research (AACR)
Figure S4 from Tumor-Derived Complement C3 Overexpression in STK11-Mutant Lung Adenocarcinoma Drives Tumor Growth and Immune Checkpoint Inhibitor Resistance
ScRNA-seq of CMT167-STK11KO versus CMT167-STK11WT tumor subsets and orthotopic implantation.
- 2 July 2026
- Published by American Association for Cancer Research (AACR)
Open AccessFigure S4 from Tumor-Derived Complement C3 Overexpression in STK11-Mutant Lung Adenocarcinoma Drives Tumor Growth and Immune Checkpoint Inhibitor Resistance
ScRNA-seq of CMT167-STK11KO versus CMT167-STK11WT tumor subsets and orthotopic implantation.
- Open Access
- 2 July 2026
- Published by American Association for Cancer Research (AACR)
Figure S1 from Tumor-Derived Complement C3 Overexpression in STK11-Mutant Lung Adenocarcinoma Drives Tumor Growth and Immune Checkpoint Inhibitor Resistance
Gene Expression Analysis of TCGA KRAS/STK11 mutant NSCLC RNAseq.
- 2 July 2026
- Published by American Association for Cancer Research (AACR)
Open AccessFigure S1 from Tumor-Derived Complement C3 Overexpression in STK11-Mutant Lung Adenocarcinoma Drives Tumor Growth and Immune Checkpoint Inhibitor Resistance
Gene Expression Analysis of TCGA KRAS/STK11 mutant NSCLC RNAseq.
- Open Access
- 2 July 2026
- Published by American Association for Cancer Research (AACR)
Figure S7 from Tumor-Derived Complement C3 Overexpression in STK11-Mutant Lung Adenocarcinoma Drives Tumor Growth and Immune Checkpoint Inhibitor Resistance
CMT167-STK11KO tumor growth in wildtype versus immunodeficient nude mice.
- 2 July 2026
- Published by American Association for Cancer Research (AACR)
Open AccessFigure S7 from Tumor-Derived Complement C3 Overexpression in STK11-Mutant Lung Adenocarcinoma Drives Tumor Growth and Immune Checkpoint Inhibitor Resistance
CMT167-STK11KO tumor growth in wildtype versus immunodeficient nude mice.
- Open Access
- 2 July 2026
- Published by American Association for Cancer Research (AACR)
Figure S3 from Tumor-Derived Complement C3 Overexpression in STK11-Mutant Lung Adenocarcinoma Drives Tumor Growth and Immune Checkpoint Inhibitor Resistance
STK11 deletion in syngeneic Lacun3 LUAD mouse model results in increased C3 expression and resistance to anti–PD-1 therapy.
- 2 July 2026
- Published by American Association for Cancer Research (AACR)
Open AccessFigure S3 from Tumor-Derived Complement C3 Overexpression in STK11-Mutant Lung Adenocarcinoma Drives Tumor Growth and Immune Checkpoint Inhibitor Resistance
STK11 deletion in syngeneic Lacun3 LUAD mouse model results in increased C3 expression and resistance to anti–PD-1 therapy.
- Open Access
- 2 July 2026
- Published by American Association for Cancer Research (AACR)
Figure S8 from Tumor-Derived Complement C3 Overexpression in STK11-Mutant Lung Adenocarcinoma Drives Tumor Growth and Immune Checkpoint Inhibitor Resistance
Cytokine evaluation of CMT167-STK11KO and STK11WT tumors.
- 2 July 2026
- Published by American Association for Cancer Research (AACR)
Open AccessFigure S8 from Tumor-Derived Complement C3 Overexpression in STK11-Mutant Lung Adenocarcinoma Drives Tumor Growth and Immune Checkpoint Inhibitor Resistance
Cytokine evaluation of CMT167-STK11KO and STK11WT tumors.
- Open Access
- 2 July 2026
- Published by American Association for Cancer Research (AACR)
Figure S10 from Tumor-Derived Complement C3 Overexpression in STK11-Mutant Lung Adenocarcinoma Drives Tumor Growth and Immune Checkpoint Inhibitor Resistance
Neutrophil depletion with anti-Ly6G treatment in mice enhanced the effect of anti–PD-1 therapy in CMT167-STK11KO tumors.
- 2 July 2026
- Published by American Association for Cancer Research (AACR)
Open AccessFigure S10 from Tumor-Derived Complement C3 Overexpression in STK11-Mutant Lung Adenocarcinoma Drives Tumor Growth and Immune Checkpoint Inhibitor Resistance
Neutrophil depletion with anti-Ly6G treatment in mice enhanced the effect of anti–PD-1 therapy in CMT167-STK11KO tumors.
- Open Access
- 2 July 2026
- Published by American Association for Cancer Research (AACR)
Figure S9 from Tumor-Derived Complement C3 Overexpression in STK11-Mutant Lung Adenocarcinoma Drives Tumor Growth and Immune Checkpoint Inhibitor Resistance
CXCL2KO alters the phenotype of neutrophils in STK11KO TME.
- 2 July 2026
- Published by American Association for Cancer Research (AACR)
Open AccessFigure S9 from Tumor-Derived Complement C3 Overexpression in STK11-Mutant Lung Adenocarcinoma Drives Tumor Growth and Immune Checkpoint Inhibitor Resistance
CXCL2KO alters the phenotype of neutrophils in STK11KO TME.