Rainer Will
YOU?
Author Swipe
View article: High 4E-BP1 expression associates with chromosome 8 gain and CDK4/6 sensitivity in Ewing sarcoma
High 4E-BP1 expression associates with chromosome 8 gain and CDK4/6 sensitivity in Ewing sarcoma Open
Chromosome 8 (chr8) gains are common in cancer, but their contribution to tumor heterogeneity is largely unexplored. Ewing sarcoma (EwS) is defined by FET::ETS fusions with few other recurrent mutations to explain clinical diversity. In Ew…
View article: P08.16.B UTILIZATION OF UNIVERSAL-TARGETING MSA2 CAR-T CELLS FOR THE TREATMENT OF GLIOBLASTOMA
P08.16.B UTILIZATION OF UNIVERSAL-TARGETING MSA2 CAR-T CELLS FOR THE TREATMENT OF GLIOBLASTOMA Open
BACKGROUND Glioblastoma (GB) remains refractory to chimeric antigen receptor (CAR)-T cell therapy, mainly attributed to tumor heterogeneity and antigen escape. CAR-T cells utilizing monomeric streptavidin-2 (mSA2) instead of a traditional …
View article: Exploration of oncogenic cooperation between germline variation and somatic mutation in prostate cancer progression
Exploration of oncogenic cooperation between germline variation and somatic mutation in prostate cancer progression Open
Prostate carcinoma (PCa) is the most common cancer of men, associated with a still unresolved issue of accurate risk-stratification. While recent advances in omics technologies have provided clues as to how molecular changes shape the onse…
View article: Autophagy suppression via SRC induction represents a therapeutic vulnerability for <i>BAP1</i> -mutant cancers
Autophagy suppression via SRC induction represents a therapeutic vulnerability for <i>BAP1</i> -mutant cancers Open
BAP1 is a tumor suppressor and epigenetic modifier that is frequently mutated in cancer, leading to increased aggressiveness and metastasis, as well as poor patient survival. Unfortunately, there are currently no specific therapies for met…
View article: Utilization of universal-targeting mSA2 CAR-T cells for the treatment of glioblastoma
Utilization of universal-targeting mSA2 CAR-T cells for the treatment of glioblastoma Open
Glioblastoma (GB) remains refractory to chimeric antigen receptor (CAR)-T cell therapy, mainly attributed to tumor heterogeneity and antigen escape. CAR-T cells utilizing monomeric streptavidin-2 (mSA2) instead of a traditional target bind…
View article: Loss of<i>SMARCB1</i>evokes targetable epigenetic vulnerabilities in Epithelioid Sarcoma
Loss of<i>SMARCB1</i>evokes targetable epigenetic vulnerabilities in Epithelioid Sarcoma Open
Dysfunction of epigenetic modulators, such as the SWI/SNF complex, is a wide-spread but relatively ill-defined feature of a broad spectrum of cancer entities. Among SWI/SNF-mutant entities, SMARCB1 -deficient cancers, such as the highly ag…
View article: PDCD10 Is a Key Player in TMZ-Resistance and Tumor Cell Regrowth: Insights into Its Underlying Mechanism in Glioblastoma Cells
PDCD10 Is a Key Player in TMZ-Resistance and Tumor Cell Regrowth: Insights into Its Underlying Mechanism in Glioblastoma Cells Open
Overcoming temozolomide (TMZ)-resistance is a major challenge in glioblastoma therapy. Therefore, identifying the key molecular player in chemo-resistance becomes urgent. We previously reported the downregulation of PDCD10 in primary gliob…
View article: Clonal heterogeneity in ER+ breast cancer reveals the proteasome and PKC as potential therapeutic targets
Clonal heterogeneity in ER+ breast cancer reveals the proteasome and PKC as potential therapeutic targets Open
Intratumoral heterogeneity impacts the success or failure of anti-cancer therapies. Here, we investigated the evolution and mechanistic heterogeneity in clonal populations of cell models for estrogen receptor positive breast cancer. To thi…
View article: EMP3 sustains oncogenic EGFR/CDK2 signaling by restricting receptor degradation in glioblastoma
EMP3 sustains oncogenic EGFR/CDK2 signaling by restricting receptor degradation in glioblastoma Open
Epithelial membrane protein 3 (EMP3) is an N -glycosylated tetraspanin with a putative trafficking function. It is highly expressed in isocitrate dehydrogenase-wild-type glioblastoma (IDH-wt GBM), and its high expression correlates with po…
View article: CNSC-09. CHI3L1 IS A MOLECULAR MARKER FOR GLIOBLASTOMA NETWORK CONNECTIVITY AND FUNCTIONALLY ORCHESTRATES TUMOR MICROTUBE FORMATION
CNSC-09. CHI3L1 IS A MOLECULAR MARKER FOR GLIOBLASTOMA NETWORK CONNECTIVITY AND FUNCTIONALLY ORCHESTRATES TUMOR MICROTUBE FORMATION Open
Chitinase 3-like 1 (CHI3L1) is a secreted glycoprotein and its RNA expression elevated in glioblastoma (GB) compared to other tumor types and related normal tissues. Furthermore, transcript levels in GB dictate aggressiveness through modul…
View article: NLGN4X TCR transgenic T cells to treat gliomas
NLGN4X TCR transgenic T cells to treat gliomas Open
Background Neuroligin 4 X-linked (NLGN4X) harbors a human leukocyte antigen (HLA)-A*02-restricted tumor-associated antigen, overexpressed in human gliomas, that was found to induce specific cytotoxic T cell responses following multi-peptid…
View article: Novel Function of Cancer Stem Cell Marker ALDH1A3 in Glioblastoma: Pro-Angiogenesis through Paracrine PAI-1 and IL-8
Novel Function of Cancer Stem Cell Marker ALDH1A3 in Glioblastoma: Pro-Angiogenesis through Paracrine PAI-1 and IL-8 Open
Hyper-angiogenesis is a typical feature of glioblastoma (GBM), the most aggressive brain tumor. We have reported the expression of aldehyde dehydrogenase 1A3 (ALDH1A3) in proliferating vasculature in GBM patients. We hypothesized that ALDH…
View article: P06.12.A NLGN4X-SPECIFIC TCR T CELLS TARGETING EXPERIMENTAL GLIOMAS
P06.12.A NLGN4X-SPECIFIC TCR T CELLS TARGETING EXPERIMENTAL GLIOMAS Open
BACKGROUND A human leukocyte antigen (HLA)-A*02-restricted tumor associated antigen in the neuroligin 4 X-linked (NLGN4X) protein was found to be specifically overexpressed in human gliomas. Individualized multipeptide vaccination targeted…
View article: P858: FUNCTIONAL STUDIES IN MULTIPLE MYELOMA CELL LINESWITH OVEREXPRESSION OF NRAS Q61R MUTATION
P858: FUNCTIONAL STUDIES IN MULTIPLE MYELOMA CELL LINESWITH OVEREXPRESSION OF NRAS Q61R MUTATION Open
Topic: 13. Myeloma and other monoclonal gammopathies - Biology & Translational Research Background: Multiple myeloma (MM) is one of the most common hematological malignancies, accounting for 20% of all newly diagnosed hematological cancers…
View article: Clonal heterogeneity in ER+ breast cancer reveals the proteasome and PKC as potential therapeutic targets
Clonal heterogeneity in ER+ breast cancer reveals the proteasome and PKC as potential therapeutic targets Open
Intratumoral heterogeneity drastically impacts the success or failure of anti-cancer therapies. Here, we investigated the evolution and mechanistic heterogeneity in clonal populations of cell models for estrogen receptor positive breast ca…
View article: EMP3 sustains oncogenic EGFR/CDK2 signaling by restricting receptor degradation in glioblastoma
EMP3 sustains oncogenic EGFR/CDK2 signaling by restricting receptor degradation in glioblastoma Open
Epithelial membrane protein 3 (EMP3) is an N-glycosylated tetraspanin with a putative trafficking function. It is highly expressed in isocitrate dehydrogenase-wild-type glioblastoma (IDH-wt GBM), and its high expression correlates with poo…
View article: Supplementary Figure from AXL and Error-Prone DNA Replication Confer Drug Resistance and Offer Strategies to Treat EGFR-Mutant Lung Cancer
Supplementary Figure from AXL and Error-Prone DNA Replication Confer Drug Resistance and Offer Strategies to Treat EGFR-Mutant Lung Cancer Open
Supplementary Figure from AXL and Error-Prone DNA Replication Confer Drug Resistance and Offer Strategies to Treat EGFR-Mutant Lung Cancer
View article: Supplementary Data from AXL and Error-Prone DNA Replication Confer Drug Resistance and Offer Strategies to Treat EGFR-Mutant Lung Cancer
Supplementary Data from AXL and Error-Prone DNA Replication Confer Drug Resistance and Offer Strategies to Treat EGFR-Mutant Lung Cancer Open
Supplementary Data from AXL and Error-Prone DNA Replication Confer Drug Resistance and Offer Strategies to Treat EGFR-Mutant Lung Cancer
View article: Supplementary Data from AXL and Error-Prone DNA Replication Confer Drug Resistance and Offer Strategies to Treat EGFR-Mutant Lung Cancer
Supplementary Data from AXL and Error-Prone DNA Replication Confer Drug Resistance and Offer Strategies to Treat EGFR-Mutant Lung Cancer Open
Supplementary Data from AXL and Error-Prone DNA Replication Confer Drug Resistance and Offer Strategies to Treat EGFR-Mutant Lung Cancer
View article: Supplementary Data from AXL and Error-Prone DNA Replication Confer Drug Resistance and Offer Strategies to Treat EGFR-Mutant Lung Cancer
Supplementary Data from AXL and Error-Prone DNA Replication Confer Drug Resistance and Offer Strategies to Treat EGFR-Mutant Lung Cancer Open
Supplementary Data from AXL and Error-Prone DNA Replication Confer Drug Resistance and Offer Strategies to Treat EGFR-Mutant Lung Cancer
View article: Supplementary Data from AXL and Error-Prone DNA Replication Confer Drug Resistance and Offer Strategies to Treat EGFR-Mutant Lung Cancer
Supplementary Data from AXL and Error-Prone DNA Replication Confer Drug Resistance and Offer Strategies to Treat EGFR-Mutant Lung Cancer Open
Supplementary Data from AXL and Error-Prone DNA Replication Confer Drug Resistance and Offer Strategies to Treat EGFR-Mutant Lung Cancer
View article: Data from AXL and Error-Prone DNA Replication Confer Drug Resistance and Offer Strategies to Treat EGFR-Mutant Lung Cancer
Data from AXL and Error-Prone DNA Replication Confer Drug Resistance and Offer Strategies to Treat EGFR-Mutant Lung Cancer Open
Anticancer therapies have been limited by the emergence of mutations and other adaptations. In bacteria, antibiotics activate the SOS response, which mobilizes error-prone factors that allow for continuous replication at the cost of mutage…
View article: Supplementary Figure from AXL and Error-Prone DNA Replication Confer Drug Resistance and Offer Strategies to Treat EGFR-Mutant Lung Cancer
Supplementary Figure from AXL and Error-Prone DNA Replication Confer Drug Resistance and Offer Strategies to Treat EGFR-Mutant Lung Cancer Open
Supplementary Figure from AXL and Error-Prone DNA Replication Confer Drug Resistance and Offer Strategies to Treat EGFR-Mutant Lung Cancer
View article: Supplementary Data from AXL and Error-Prone DNA Replication Confer Drug Resistance and Offer Strategies to Treat EGFR-Mutant Lung Cancer
Supplementary Data from AXL and Error-Prone DNA Replication Confer Drug Resistance and Offer Strategies to Treat EGFR-Mutant Lung Cancer Open
Supplementary Data from AXL and Error-Prone DNA Replication Confer Drug Resistance and Offer Strategies to Treat EGFR-Mutant Lung Cancer
View article: Supplementary Data from AXL and Error-Prone DNA Replication Confer Drug Resistance and Offer Strategies to Treat EGFR-Mutant Lung Cancer
Supplementary Data from AXL and Error-Prone DNA Replication Confer Drug Resistance and Offer Strategies to Treat EGFR-Mutant Lung Cancer Open
Supplementary Data from AXL and Error-Prone DNA Replication Confer Drug Resistance and Offer Strategies to Treat EGFR-Mutant Lung Cancer
View article: Data from AXL and Error-Prone DNA Replication Confer Drug Resistance and Offer Strategies to Treat EGFR-Mutant Lung Cancer
Data from AXL and Error-Prone DNA Replication Confer Drug Resistance and Offer Strategies to Treat EGFR-Mutant Lung Cancer Open
Anticancer therapies have been limited by the emergence of mutations and other adaptations. In bacteria, antibiotics activate the SOS response, which mobilizes error-prone factors that allow for continuous replication at the cost of mutage…
View article: Clonal heterogeneity of endocrine therapy resistance in breast cancer
Clonal heterogeneity of endocrine therapy resistance in breast cancer Open
We barcoded endocrine therapy sensitive cell lines (MCF7 and T47D) and rendered them resistant to commonly applied first line endocrine therapeutics (Tamoxifen and estrogen deprivation). Next, we isolated single cell clones of endocrine th…