Michael Linnebacher
YOU?
Author Swipe
View article: Targeting the Met-RIPK1 signaling axis to enforce apoptosis and necroptosis in colorectal cancer
Targeting the Met-RIPK1 signaling axis to enforce apoptosis and necroptosis in colorectal cancer Open
Resistance to cell death remains a critical challenge in the therapy of colorectal cancer (CRC). Smac mimetics (SM) are cytotoxic agents specifically designed to maximize tumor cell killing mediated via endogenous tumor necrosis factor (TN…
View article: Pan‐ERBB Inhibitors Synergize With KRAS Inhibitors in Rectal Cancer
Pan‐ERBB Inhibitors Synergize With KRAS Inhibitors in Rectal Cancer Open
Background Emerging RAS inhibitors show promise in treating KRAS‐mutated malignancies, but resistance mechanisms limit their clinical efficacy. Given recent clinical findings associating KRAS mutations with reduced response to neoadjuvant …
View article: Author Correction: Sequential orthogonal assays for longitudinal and endpoint characterization of three-dimensional spheroids
Author Correction: Sequential orthogonal assays for longitudinal and endpoint characterization of three-dimensional spheroids Open
View article: Mutational Patterns in Colorectal Cancer: Do PDX Models Retain the Heterogeneity of the Original Tumor?
Mutational Patterns in Colorectal Cancer: Do PDX Models Retain the Heterogeneity of the Original Tumor? Open
Colorectal cancer (CRC) remains a leading cause of cancer-related mortality worldwide, highlighting the need for a deeper understanding of the genetic mechanisms driving its development and progression. Identifying genetic mutations that a…
View article: Coupling Immunoprecipitation with Multiplexed Digital PCR for Cell-Free DNA Methylation Detection in Small Plasma Volumes of Early-Onset Colorectal Cancer
Coupling Immunoprecipitation with Multiplexed Digital PCR for Cell-Free DNA Methylation Detection in Small Plasma Volumes of Early-Onset Colorectal Cancer Open
Colorectal cancer (CRC) remains a major global health challenge, with an increasing incidence of early-onset cases among young adults. Targeted analysis of cell-free DNA (cfDNA) methylation in blood has emerged as a promising minimally inv…
View article: Optimization of Tumor Treating Fields (<scp>TTF</scp>ields) Frequency and Treatment Duration in Colorectal Cancer Cells
Optimization of Tumor Treating Fields (<span>TTF</span>ields) Frequency and Treatment Duration in Colorectal Cancer Cells Open
Introduction Colorectal cancer (CRC) is one of the most prevalent malignancies worldwide. Tumor Treating Fields (TTFields), a novel anticancer therapy using intermediate frequency and low‐intensity alternating electric fields, has demonstr…
View article: Supplementary Fig. 4 from Tumor Vessel Normalization via PFKFB3 Inhibition Alleviates Hypoxia and Increases Tumor Necrosis in Rectal Cancer upon Radiotherapy
Supplementary Fig. 4 from Tumor Vessel Normalization via PFKFB3 Inhibition Alleviates Hypoxia and Increases Tumor Necrosis in Rectal Cancer upon Radiotherapy Open
Supplementary Fig. 4
View article: Supplementary Fig. 6 from Tumor Vessel Normalization via PFKFB3 Inhibition Alleviates Hypoxia and Increases Tumor Necrosis in Rectal Cancer upon Radiotherapy
Supplementary Fig. 6 from Tumor Vessel Normalization via PFKFB3 Inhibition Alleviates Hypoxia and Increases Tumor Necrosis in Rectal Cancer upon Radiotherapy Open
Supplementary Fig. 6
View article: Supplementary Fig. 3 from Tumor Vessel Normalization via PFKFB3 Inhibition Alleviates Hypoxia and Increases Tumor Necrosis in Rectal Cancer upon Radiotherapy
Supplementary Fig. 3 from Tumor Vessel Normalization via PFKFB3 Inhibition Alleviates Hypoxia and Increases Tumor Necrosis in Rectal Cancer upon Radiotherapy Open
Supplementary Fig. 3
View article: Supplementary Fig. 5 from Tumor Vessel Normalization via PFKFB3 Inhibition Alleviates Hypoxia and Increases Tumor Necrosis in Rectal Cancer upon Radiotherapy
Supplementary Fig. 5 from Tumor Vessel Normalization via PFKFB3 Inhibition Alleviates Hypoxia and Increases Tumor Necrosis in Rectal Cancer upon Radiotherapy Open
Supplementary Fig. 5
View article: Supplementary Fig. 2 from Tumor Vessel Normalization via PFKFB3 Inhibition Alleviates Hypoxia and Increases Tumor Necrosis in Rectal Cancer upon Radiotherapy
Supplementary Fig. 2 from Tumor Vessel Normalization via PFKFB3 Inhibition Alleviates Hypoxia and Increases Tumor Necrosis in Rectal Cancer upon Radiotherapy Open
Supplementary Fig. 2
View article: Supplementary Fig.1 from Tumor Vessel Normalization via PFKFB3 Inhibition Alleviates Hypoxia and Increases Tumor Necrosis in Rectal Cancer upon Radiotherapy
Supplementary Fig.1 from Tumor Vessel Normalization via PFKFB3 Inhibition Alleviates Hypoxia and Increases Tumor Necrosis in Rectal Cancer upon Radiotherapy Open
Supplementary Fig.1
View article: Supplementary Fig. 7 from Tumor Vessel Normalization via PFKFB3 Inhibition Alleviates Hypoxia and Increases Tumor Necrosis in Rectal Cancer upon Radiotherapy
Supplementary Fig. 7 from Tumor Vessel Normalization via PFKFB3 Inhibition Alleviates Hypoxia and Increases Tumor Necrosis in Rectal Cancer upon Radiotherapy Open
Supplementary Fig. 7
View article: Addressing Challenges in Targeted Therapy for Metastatic Colorectal Cancer
Addressing Challenges in Targeted Therapy for Metastatic Colorectal Cancer Open
This review article aims to address the challenges associated with targeted therapy for the treatment of metastatic colorectal cancer (mCRC). We will first provide an overview of approved targeted therapies for treating mCRC, which include…
View article: The impact of SEC23A on 5-FU chemotherapy sensitivity and its involvement in endoplasmic reticulum stress-induced apoptosis in colorectal cancer
The impact of SEC23A on 5-FU chemotherapy sensitivity and its involvement in endoplasmic reticulum stress-induced apoptosis in colorectal cancer Open
Background: Colorectal cancer (CRC) represents a significant global health burden, with chemotherapy resistance representing a significant challenge to effective treatment. SEC23A, a core component of the COPII vesicle trafficking system, …
View article: A Dot-Blot Screening for Identifying the Temozolomide-Regulated Proteins as Potential Targets for Glioma Multi-OMICS Studies
A Dot-Blot Screening for Identifying the Temozolomide-Regulated Proteins as Potential Targets for Glioma Multi-OMICS Studies Open
Background: Malignant gliomas represent a heterogenous group of brain cancers that are characterized by infiltrative growth that lacks a clearly identifiable tumor border. The lack of the possibility of radical surgical resection and targe…
View article: DNA demethylation triggers cell free DNA release in colorectal cancer cells
DNA demethylation triggers cell free DNA release in colorectal cancer cells Open
Background Liquid biopsy based on cell-free DNA (cfDNA) analysis holds significant promise as a minimally invasive approach for the diagnosis, genotyping, and monitoring of solid malignancies. Human tumors release cfDNA in the bloodstream …
View article: Supplementary Fig. 7 from Tumor Vessel Normalization via PFKFB3 Inhibition Alleviates Hypoxia and Increases Tumor Necrosis in Rectal Cancer upon Radiotherapy
Supplementary Fig. 7 from Tumor Vessel Normalization via PFKFB3 Inhibition Alleviates Hypoxia and Increases Tumor Necrosis in Rectal Cancer upon Radiotherapy Open
Supplementary Fig. 7
View article: Supplementary Fig.1 from Tumor Vessel Normalization via PFKFB3 Inhibition Alleviates Hypoxia and Increases Tumor Necrosis in Rectal Cancer upon Radiotherapy
Supplementary Fig.1 from Tumor Vessel Normalization via PFKFB3 Inhibition Alleviates Hypoxia and Increases Tumor Necrosis in Rectal Cancer upon Radiotherapy Open
Supplementary Fig.1
View article: Supplementary Fig. 5 from Tumor Vessel Normalization via PFKFB3 Inhibition Alleviates Hypoxia and Increases Tumor Necrosis in Rectal Cancer upon Radiotherapy
Supplementary Fig. 5 from Tumor Vessel Normalization via PFKFB3 Inhibition Alleviates Hypoxia and Increases Tumor Necrosis in Rectal Cancer upon Radiotherapy Open
Supplementary Fig. 5
View article: Supplementary Fig. 4 from Tumor Vessel Normalization via PFKFB3 Inhibition Alleviates Hypoxia and Increases Tumor Necrosis in Rectal Cancer upon Radiotherapy
Supplementary Fig. 4 from Tumor Vessel Normalization via PFKFB3 Inhibition Alleviates Hypoxia and Increases Tumor Necrosis in Rectal Cancer upon Radiotherapy Open
Supplementary Fig. 4
View article: Supplementary Fig. 6 from Tumor Vessel Normalization via PFKFB3 Inhibition Alleviates Hypoxia and Increases Tumor Necrosis in Rectal Cancer upon Radiotherapy
Supplementary Fig. 6 from Tumor Vessel Normalization via PFKFB3 Inhibition Alleviates Hypoxia and Increases Tumor Necrosis in Rectal Cancer upon Radiotherapy Open
Supplementary Fig. 6
View article: Supplementary Fig. 2 from Tumor Vessel Normalization via PFKFB3 Inhibition Alleviates Hypoxia and Increases Tumor Necrosis in Rectal Cancer upon Radiotherapy
Supplementary Fig. 2 from Tumor Vessel Normalization via PFKFB3 Inhibition Alleviates Hypoxia and Increases Tumor Necrosis in Rectal Cancer upon Radiotherapy Open
Supplementary Fig. 2
View article: Supplementary Fig. 3 from Tumor Vessel Normalization via PFKFB3 Inhibition Alleviates Hypoxia and Increases Tumor Necrosis in Rectal Cancer upon Radiotherapy
Supplementary Fig. 3 from Tumor Vessel Normalization via PFKFB3 Inhibition Alleviates Hypoxia and Increases Tumor Necrosis in Rectal Cancer upon Radiotherapy Open
Supplementary Fig. 3
View article: Mutation patterns in colorectal cancer and their relationship with prognosis
Mutation patterns in colorectal cancer and their relationship with prognosis Open
View article: Figure 2 from Tumor Vessel Normalization via PFKFB3 Inhibition Alleviates Hypoxia and Increases Tumor Necrosis in Rectal Cancer upon Radiotherapy
Figure 2 from Tumor Vessel Normalization via PFKFB3 Inhibition Alleviates Hypoxia and Increases Tumor Necrosis in Rectal Cancer upon Radiotherapy Open
3PO reduces colorectal cancer cell invasion and endothelial cell sprouting capabilities. A, Invasion assay performed with HCT-116, HT-29, SW-1463, and SW-837 cancer cells. Cells were plated in a Boyden multi-well chamber and treated…
View article: Figure 1 from Tumor Vessel Normalization via PFKFB3 Inhibition Alleviates Hypoxia and Increases Tumor Necrosis in Rectal Cancer upon Radiotherapy
Figure 1 from Tumor Vessel Normalization via PFKFB3 Inhibition Alleviates Hypoxia and Increases Tumor Necrosis in Rectal Cancer upon Radiotherapy Open
3PO affects normal epithelial and colorectal cancer cell proliferation and viability in a concentration-dependent manner. A, xCELLigence assay performed with HCT-116, HT-29, SW-1463, SW-837, HUVECs, and RPE-1 cells. Real-time cell a…
View article: Supplementary Fig. 4 from Tumor Vessel Normalization via PFKFB3 Inhibition Alleviates Hypoxia and Increases Tumor Necrosis in Rectal Cancer upon Radiotherapy
Supplementary Fig. 4 from Tumor Vessel Normalization via PFKFB3 Inhibition Alleviates Hypoxia and Increases Tumor Necrosis in Rectal Cancer upon Radiotherapy Open
Supplementary Fig. 4
View article: Supplementary Fig. 6 from Tumor Vessel Normalization via PFKFB3 Inhibition Alleviates Hypoxia and Increases Tumor Necrosis in Rectal Cancer upon Radiotherapy
Supplementary Fig. 6 from Tumor Vessel Normalization via PFKFB3 Inhibition Alleviates Hypoxia and Increases Tumor Necrosis in Rectal Cancer upon Radiotherapy Open
Supplementary Fig. 6
View article: Figure 6 from Tumor Vessel Normalization via PFKFB3 Inhibition Alleviates Hypoxia and Increases Tumor Necrosis in Rectal Cancer upon Radiotherapy
Figure 6 from Tumor Vessel Normalization via PFKFB3 Inhibition Alleviates Hypoxia and Increases Tumor Necrosis in Rectal Cancer upon Radiotherapy Open
In vivo 3PO administration in combination with radiotherapy induces TVN and alleviates hypoxia in RC. A, Representative images of CD31+αSMA+ co-stained sections of PDX tumors upon treatment with vehicle …