Saadia A. Karim
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View article: Activation of PP2A-B56α leads to aberrant EGFR signaling and proliferative phenotypes in PDAC
Activation of PP2A-B56α leads to aberrant EGFR signaling and proliferative phenotypes in PDAC Open
Pancreatic ductal adenocarcinoma (PDAC) stands to become the second most deadly cancer by 2030. The small GTPase, KRAS, is mutated in over 90% of PDAC patients and considered the primary driver mutation. Despite being an almost ubiquitous …
View article: Targeting PIKfyve-driven lipid metabolism in pancreatic cancer
Targeting PIKfyve-driven lipid metabolism in pancreatic cancer Open
Pancreatic ductal adenocarcinoma (PDAC) subsists in a nutrient-deregulated microenvironment, making it particularly susceptible to treatments that interfere with cancer metabolism 1,2 . For example, PDAC uses, and is dependent on, high lev…
View article: A precision image-guided model of stereotactic ablative radiotherapy for hepatocellular carcinoma
A precision image-guided model of stereotactic ablative radiotherapy for hepatocellular carcinoma Open
Liver tumours, both primary and metastatic, are diseases of unmet clinical need. Hepatocellular carcinoma (HCC), the most common primary liver tumour, like many other cancers, can be treated by stereotactic ablative radiotherapy (SABR), re…
View article: Targeted irradiation in an autochthonous mouse model of pancreatic cancer
Targeted irradiation in an autochthonous mouse model of pancreatic cancer Open
The value of radiotherapy in the treatment of pancreatic cancer has been the subject of much debate but limited preclinical research. We hypothesise that the poor translation of radiation research into clinical trials of radiotherapy in pa…
View article: Optimisation of Sample Preparation from Primary Mouse Tissue to Maintain RNA Integrity for Methods Examining Translational Control
Optimisation of Sample Preparation from Primary Mouse Tissue to Maintain RNA Integrity for Methods Examining Translational Control Open
The protein output of different mRNAs can vary by two orders of magnitude; therefore, it is critical to understand the processes that control gene expression operating at the level of translation. Translatome-wide techniques, such as polys…
View article: Defining the spatial distribution of extracellular adenosine revealed a myeloid-dependent immunosuppressive microenvironment in pancreatic ductal adenocarcinoma
Defining the spatial distribution of extracellular adenosine revealed a myeloid-dependent immunosuppressive microenvironment in pancreatic ductal adenocarcinoma Open
Background The prognosis for patients with pancreatic ductal adenocarcinoma (PDAC) remains extremely poor. It has been suggested that the adenosine pathway contributes to the ability of PDAC to evade the immune system and hence, its resist…
View article: Optimisation of sample preparation from primary mouse tissue to maintain RNA integrity for methods examining translational control
Optimisation of sample preparation from primary mouse tissue to maintain RNA integrity for methods examining translational control Open
Protein output of different mRNAs can vary by two orders of magnitude therefore it is critical to understand the processes that control gene expression that operate at the level of translation. Translatome-wide techniques such as polysome …
View article: Table S4 from Repression of the Type I Interferon Pathway Underlies MYC- and KRAS-Dependent Evasion of NK and B Cells in Pancreatic Ductal Adenocarcinoma
Table S4 from Repression of the Type I Interferon Pathway Underlies MYC- and KRAS-Dependent Evasion of NK and B Cells in Pancreatic Ductal Adenocarcinoma Open
Spreadsheet of genes co-regulated by MYC & Miz1 in KMC PDAC cells
View article: Data from Repression of the Type I Interferon Pathway Underlies MYC- and KRAS-Dependent Evasion of NK and B Cells in Pancreatic Ductal Adenocarcinoma
Data from Repression of the Type I Interferon Pathway Underlies MYC- and KRAS-Dependent Evasion of NK and B Cells in Pancreatic Ductal Adenocarcinoma Open
MYC is implicated in the development and progression of pancreatic cancer, yet the precise level of MYC deregulation required to contribute to tumor development has been difficult to define. We used modestly elevated expression of human MY…
View article: Supplementary Material from Repression of the Type I Interferon Pathway Underlies MYC- and KRAS-Dependent Evasion of NK and B Cells in Pancreatic Ductal Adenocarcinoma
Supplementary Material from Repression of the Type I Interferon Pathway Underlies MYC- and KRAS-Dependent Evasion of NK and B Cells in Pancreatic Ductal Adenocarcinoma Open
6 supplementary Figures with legends under each; 3 Supplementary Tables; Supplementary Methods and References
View article: Supplementary Material from Repression of the Type I Interferon Pathway Underlies MYC- and KRAS-Dependent Evasion of NK and B Cells in Pancreatic Ductal Adenocarcinoma
Supplementary Material from Repression of the Type I Interferon Pathway Underlies MYC- and KRAS-Dependent Evasion of NK and B Cells in Pancreatic Ductal Adenocarcinoma Open
6 supplementary Figures with legends under each; 3 Supplementary Tables; Supplementary Methods and References
View article: Data from Repression of the Type I Interferon Pathway Underlies MYC- and KRAS-Dependent Evasion of NK and B Cells in Pancreatic Ductal Adenocarcinoma
Data from Repression of the Type I Interferon Pathway Underlies MYC- and KRAS-Dependent Evasion of NK and B Cells in Pancreatic Ductal Adenocarcinoma Open
MYC is implicated in the development and progression of pancreatic cancer, yet the precise level of MYC deregulation required to contribute to tumor development has been difficult to define. We used modestly elevated expression of human MY…
View article: Table S4 from Repression of the Type I Interferon Pathway Underlies MYC- and KRAS-Dependent Evasion of NK and B Cells in Pancreatic Ductal Adenocarcinoma
Table S4 from Repression of the Type I Interferon Pathway Underlies MYC- and KRAS-Dependent Evasion of NK and B Cells in Pancreatic Ductal Adenocarcinoma Open
Spreadsheet of genes co-regulated by MYC & Miz1 in KMC PDAC cells
View article: Supplemental Tables 1 through 3 from mTORC2 Signaling Drives the Development and Progression of Pancreatic Cancer
Supplemental Tables 1 through 3 from mTORC2 Signaling Drives the Development and Progression of Pancreatic Cancer Open
Table S1: Antibodies for immunohistochemistry. Table S2: shRNA sequences. Table S3: Antibodies for western blotting.
View article: Data from mTORC2 Signaling Drives the Development and Progression of Pancreatic Cancer
Data from mTORC2 Signaling Drives the Development and Progression of Pancreatic Cancer Open
mTOR signaling controls several critical cellular functions and is deregulated in many cancers, including pancreatic cancer. To date, most efforts have focused on inhibiting the mTORC1 complex. However, clinical trials of mTORC1 inhibitors…
View article: Data from mTORC2 Signaling Drives the Development and Progression of Pancreatic Cancer
Data from mTORC2 Signaling Drives the Development and Progression of Pancreatic Cancer Open
mTOR signaling controls several critical cellular functions and is deregulated in many cancers, including pancreatic cancer. To date, most efforts have focused on inhibiting the mTORC1 complex. However, clinical trials of mTORC1 inhibitors…
View article: Supplemental Tables 1 through 3 from mTORC2 Signaling Drives the Development and Progression of Pancreatic Cancer
Supplemental Tables 1 through 3 from mTORC2 Signaling Drives the Development and Progression of Pancreatic Cancer Open
Table S1: Antibodies for immunohistochemistry. Table S2: shRNA sequences. Table S3: Antibodies for western blotting.
View article: Supplemental Figures 1 through 8 from mTORC2 Signaling Drives the Development and Progression of Pancreatic Cancer
Supplemental Figures 1 through 8 from mTORC2 Signaling Drives the Development and Progression of Pancreatic Cancer Open
Figure S1: Loss of Rictor does not prevent pancreatic formation or function. Figure S2: Rictor deletion decreases proliferation in PanIN1 lesions. Figure S3: Rictor deletion alters CDKI and BMI1 expression and localization. Figure S4: Rict…
View article: Supplemental Figure Legends from mTORC2 Signaling Drives the Development and Progression of Pancreatic Cancer
Supplemental Figure Legends from mTORC2 Signaling Drives the Development and Progression of Pancreatic Cancer Open
Supplementary figure legends for Figures S1-S8
View article: Supplemental Figure Legends from mTORC2 Signaling Drives the Development and Progression of Pancreatic Cancer
Supplemental Figure Legends from mTORC2 Signaling Drives the Development and Progression of Pancreatic Cancer Open
Supplementary figure legends for Figures S1-S8
View article: Supplemental Methods from mTORC2 Signaling Drives the Development and Progression of Pancreatic Cancer
Supplemental Methods from mTORC2 Signaling Drives the Development and Progression of Pancreatic Cancer Open
Supplementary materials and methods
View article: Supplemental Figures 1 through 8 from mTORC2 Signaling Drives the Development and Progression of Pancreatic Cancer
Supplemental Figures 1 through 8 from mTORC2 Signaling Drives the Development and Progression of Pancreatic Cancer Open
Figure S1: Loss of Rictor does not prevent pancreatic formation or function. Figure S2: Rictor deletion decreases proliferation in PanIN1 lesions. Figure S3: Rictor deletion alters CDKI and BMI1 expression and localization. Figure S4: Rict…
View article: Supplemental Methods from mTORC2 Signaling Drives the Development and Progression of Pancreatic Cancer
Supplemental Methods from mTORC2 Signaling Drives the Development and Progression of Pancreatic Cancer Open
Supplementary materials and methods
View article: Supplementary Methods from Intravital FLIM-FRET Imaging Reveals Dasatinib-Induced Spatial Control of Src in Pancreatic Cancer
Supplementary Methods from Intravital FLIM-FRET Imaging Reveals Dasatinib-Induced Spatial Control of Src in Pancreatic Cancer Open
Supplementary Methods - PDF file 83K, Additional experimental procedures including Multiphoton TCSPC FLIM, Frequency domain FLIM, Data Analysis, and Western Blotting
View article: Supplementary Figure 10 from Spatial Regulation of RhoA Activity during Pancreatic Cancer Cell Invasion Driven by Mutant p53
Supplementary Figure 10 from Spatial Regulation of RhoA Activity during Pancreatic Cancer Cell Invasion Driven by Mutant p53 Open
Supplementary Figure 10 from Spatial Regulation of RhoA Activity during Pancreatic Cancer Cell Invasion Driven by Mutant p53
View article: Supplementary Movie 1 from Intravital FLIM-FRET Imaging Reveals Dasatinib-Induced Spatial Control of Src in Pancreatic Cancer
Supplementary Movie 1 from Intravital FLIM-FRET Imaging Reveals Dasatinib-Induced Spatial Control of Src in Pancreatic Cancer Open
Supplementary Movie 1 - WMV file 4865K, Mutant p53R172H PDACs expressing Src biosensor (green) on organotypic assay with SHG signal from ECM components (purple), interacting with fibroblasts (red) during invasion
View article: Supplementary Figure S1 from Intravital FLIM-FRET Imaging Reveals Dasatinib-Induced Spatial Control of Src in Pancreatic Cancer
Supplementary Figure S1 from Intravital FLIM-FRET Imaging Reveals Dasatinib-Induced Spatial Control of Src in Pancreatic Cancer Open
Supplementary Figure S1 - PDF file 273K, Characterization of the Src-biosensor in vitro
View article: Supplementary Figure S3 from Intravital FLIM-FRET Imaging Reveals Dasatinib-Induced Spatial Control of Src in Pancreatic Cancer
Supplementary Figure S3 from Intravital FLIM-FRET Imaging Reveals Dasatinib-Induced Spatial Control of Src in Pancreatic Cancer Open
Supplementary Figure S3 - PDF file 150K, SHG identification of invasive border versus tumour centre
View article: Supplementary Methods, Figure and Movie Legends from Spatial Regulation of RhoA Activity during Pancreatic Cancer Cell Invasion Driven by Mutant p53
Supplementary Methods, Figure and Movie Legends from Spatial Regulation of RhoA Activity during Pancreatic Cancer Cell Invasion Driven by Mutant p53 Open
Supplementary Methods, Figure and Movie Legends from Spatial Regulation of RhoA Activity during Pancreatic Cancer Cell Invasion Driven by Mutant p53