Benjamin J. Drapkin
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View article: Marked under-diagnosis of Lambert-Eaton myasthenic syndrome in small cell lung cancer: an analysis of real-world claims data
Marked under-diagnosis of Lambert-Eaton myasthenic syndrome in small cell lung cancer: an analysis of real-world claims data Open
Background Lambert-Eaton myasthenic syndrome (LEMS) is an autoimmune neurologic condition causing progressive muscle weakness that can occur as a paraneoplastic disorder, most commonly in patients with small cell lung cancer (SCLC). In lim…
View article: Peak Mitotic Cyclin Permits Mitotic Exit
Peak Mitotic Cyclin Permits Mitotic Exit Open
In eukaryotes, DNA replication, mitosis, and cytokinesis are all regulated by Cyclin-dependent kinase (Cdk). Cyclin/Cdk complexes promote replication origin firing and mitotic entry, and conversely, inhibit pre-replication origin loading a…
View article: Supplementary Table 1 from KSR1 Mediates Small Cell Lung Carcinoma Tumor Initiation and Cisplatin Resistance
Supplementary Table 1 from KSR1 Mediates Small Cell Lung Carcinoma Tumor Initiation and Cisplatin Resistance Open
The table contains the statistical tests conducted for all the ELDAs in the study
View article: Supplementary Fig. S5 from KSR1 Mediates Small Cell Lung Carcinoma Tumor Initiation and Cisplatin Resistance
Supplementary Fig. S5 from KSR1 Mediates Small Cell Lung Carcinoma Tumor Initiation and Cisplatin Resistance Open
The figure contains Multi well resistance assays with control and KSR1 KO cells at different cisplatin doses
View article: Supplementary Fig. S2 from KSR1 Mediates Small Cell Lung Carcinoma Tumor Initiation and Cisplatin Resistance
Supplementary Fig. S2 from KSR1 Mediates Small Cell Lung Carcinoma Tumor Initiation and Cisplatin Resistance Open
Cisplatin and Trametinib dose response curves for SCLC cell lines
View article: Supplementary Fig. S4 from KSR1 Mediates Small Cell Lung Carcinoma Tumor Initiation and Cisplatin Resistance
Supplementary Fig. S4 from KSR1 Mediates Small Cell Lung Carcinoma Tumor Initiation and Cisplatin Resistance Open
The figure contains SCLC PDX data.
View article: Data from KSR1 Mediates Small Cell Lung Carcinoma Tumor Initiation and Cisplatin Resistance
Data from KSR1 Mediates Small Cell Lung Carcinoma Tumor Initiation and Cisplatin Resistance Open
Small cell lung cancer (SCLC) has a dismal 5-year survival rate of less than 7%, with limited advances in first-line treatment over the past four decades. Tumor-initiating cells (TIC) contribute to resistance and relapse, a major impedimen…
View article: Supplementary Fig. S3 from KSR1 Mediates Small Cell Lung Carcinoma Tumor Initiation and Cisplatin Resistance
Supplementary Fig. S3 from KSR1 Mediates Small Cell Lung Carcinoma Tumor Initiation and Cisplatin Resistance Open
Cisplatin dose response curves for SCLC cell lines with and without KSR1
View article: Supplementary Fig. S1 from KSR1 Mediates Small Cell Lung Carcinoma Tumor Initiation and Cisplatin Resistance
Supplementary Fig. S1 from KSR1 Mediates Small Cell Lung Carcinoma Tumor Initiation and Cisplatin Resistance Open
The figure contains images of western blots of SCLC Cell lines used in the study
View article: Jumonji histone demethylases are therapeutic targets in small cell lung cancer
Jumonji histone demethylases are therapeutic targets in small cell lung cancer Open
Small cell lung cancer (SCLC) is a recalcitrant cancer of neuroendocrine (NE) origin. Changes in therapeutic approaches against SCLC have been lacking over the decades. Here, we use preclinical models to identify a new therapeutic vulnerab…
View article: Mammalian SWI/SNF complex activity regulates POU2F3 and constitutes a targetable dependency in small cell lung cancer
Mammalian SWI/SNF complex activity regulates POU2F3 and constitutes a targetable dependency in small cell lung cancer Open
Small cell lung cancers (SCLCs) are composed of heterogeneous subtypes marked by lineage-specific transcription factors, including ASCL1, NEUROD1, and POU2F3. POU2F3-positive SCLCs, ∼12% of all cases, are uniquely dependent on POU2F3 itsel…
View article: Data from Acquired Cross-Resistance in Small Cell Lung Cancer due to Extrachromosomal DNA Amplification of <i>MYC</i> Paralogs
Data from Acquired Cross-Resistance in Small Cell Lung Cancer due to Extrachromosomal DNA Amplification of <i>MYC</i> Paralogs Open
Small cell lung cancer (SCLC) presents as a highly chemosensitive malignancy but acquires cross-resistance after relapse. This transformation is nearly inevitable in patients but has been difficult to capture in laboratory models. Here, we…
View article: Supplementary Tables from Acquired Cross-Resistance in Small Cell Lung Cancer due to Extrachromosomal DNA Amplification of <i>MYC</i> Paralogs
Supplementary Tables from Acquired Cross-Resistance in Small Cell Lung Cancer due to Extrachromosomal DNA Amplification of <i>MYC</i> Paralogs Open
Supplementary Table S1. Clinical Histories of PDX Models.Supplementary Table S2. Differential Gene Expression for MGH1518 Serial Models.Supplementary Table S3. Mutations in the ecMYC region in MGH1518-3A.Supplementary Table S4. Mutations i…
View article: Supplementary Figure S4 from Acquired Cross-Resistance in Small Cell Lung Cancer due to Extrachromosomal DNA Amplification of <i>MYC</i> Paralogs
Supplementary Figure S4 from Acquired Cross-Resistance in Small Cell Lung Cancer due to Extrachromosomal DNA Amplification of <i>MYC</i> Paralogs Open
Genomic analysis of chromosome 17 focal amplification in MGH1531-5BX and analysis of ecDNA junction mutations in MGH1518-3A.
View article: Supplementary Figure S3 from Acquired Cross-Resistance in Small Cell Lung Cancer due to Extrachromosomal DNA Amplification of <i>MYC</i> Paralogs
Supplementary Figure S3 from Acquired Cross-Resistance in Small Cell Lung Cancer due to Extrachromosomal DNA Amplification of <i>MYC</i> Paralogs Open
Genomic analysis of chromosome 8 focal amplification in MGH1518-3A
View article: Supplementary Figure S2 from Acquired Cross-Resistance in Small Cell Lung Cancer due to Extrachromosomal DNA Amplification of <i>MYC</i> Paralogs
Supplementary Figure S2 from Acquired Cross-Resistance in Small Cell Lung Cancer due to Extrachromosomal DNA Amplification of <i>MYC</i> Paralogs Open
Comparison gene expression and H3K27ac between MGH1518 serial models
View article: Supplementary Figure S9 from Acquired Cross-Resistance in Small Cell Lung Cancer due to Extrachromosomal DNA Amplification of <i>MYC</i> Paralogs
Supplementary Figure S9 from Acquired Cross-Resistance in Small Cell Lung Cancer due to Extrachromosomal DNA Amplification of <i>MYC</i> Paralogs Open
Reconstruction of ecDNAs containing MYC paralogs and MYCL FISH in MGH1501-1A metaphase chromosomes.
View article: Supplementary Figure S6 from Acquired Cross-Resistance in Small Cell Lung Cancer due to Extrachromosomal DNA Amplification of <i>MYC</i> Paralogs
Supplementary Figure S6 from Acquired Cross-Resistance in Small Cell Lung Cancer due to Extrachromosomal DNA Amplification of <i>MYC</i> Paralogs Open
Levels of ecMYC in untreated and treated MGH1518-3A xenografts
View article: Supplementary Figure S14 from Acquired Cross-Resistance in Small Cell Lung Cancer due to Extrachromosomal DNA Amplification of <i>MYC</i> Paralogs
Supplementary Figure S14 from Acquired Cross-Resistance in Small Cell Lung Cancer due to Extrachromosomal DNA Amplification of <i>MYC</i> Paralogs Open
MYC paralog amplifications that were detected or omitted by segmented copy number analysis, and patient survival compared with ecDNA status of PDX models.
View article: Supplementary Figure S6 from Acquired Cross-Resistance in Small Cell Lung Cancer due to Extrachromosomal DNA Amplification of <i>MYC</i> Paralogs
Supplementary Figure S6 from Acquired Cross-Resistance in Small Cell Lung Cancer due to Extrachromosomal DNA Amplification of <i>MYC</i> Paralogs Open
Levels of ecMYC in untreated and treated MGH1518-3A xenografts
View article: Supplementary Figure S4 from Acquired Cross-Resistance in Small Cell Lung Cancer due to Extrachromosomal DNA Amplification of <i>MYC</i> Paralogs
Supplementary Figure S4 from Acquired Cross-Resistance in Small Cell Lung Cancer due to Extrachromosomal DNA Amplification of <i>MYC</i> Paralogs Open
Genomic analysis of chromosome 17 focal amplification in MGH1531-5BX and analysis of ecDNA junction mutations in MGH1518-3A.
View article: Supplementary Figure S13 from Acquired Cross-Resistance in Small Cell Lung Cancer due to Extrachromosomal DNA Amplification of <i>MYC</i> Paralogs
Supplementary Figure S13 from Acquired Cross-Resistance in Small Cell Lung Cancer due to Extrachromosomal DNA Amplification of <i>MYC</i> Paralogs Open
MYC paralog copy number and ecDNA status in SCLC cell lines, PDX models and biopsy samples derived before treatment or after relapse.
View article: Supplementary Figure S8 from Acquired Cross-Resistance in Small Cell Lung Cancer due to Extrachromosomal DNA Amplification of <i>MYC</i> Paralogs
Supplementary Figure S8 from Acquired Cross-Resistance in Small Cell Lung Cancer due to Extrachromosomal DNA Amplification of <i>MYC</i> Paralogs Open
Comparison of chemotherapy regimen delta-AUC and comparison of average delta-AUC by PDX source.
View article: Supplementary Figure S13 from Acquired Cross-Resistance in Small Cell Lung Cancer due to Extrachromosomal DNA Amplification of <i>MYC</i> Paralogs
Supplementary Figure S13 from Acquired Cross-Resistance in Small Cell Lung Cancer due to Extrachromosomal DNA Amplification of <i>MYC</i> Paralogs Open
MYC paralog copy number and ecDNA status in SCLC cell lines, PDX models and biopsy samples derived before treatment or after relapse.
View article: Supplementary Figure S8 from Acquired Cross-Resistance in Small Cell Lung Cancer due to Extrachromosomal DNA Amplification of <i>MYC</i> Paralogs
Supplementary Figure S8 from Acquired Cross-Resistance in Small Cell Lung Cancer due to Extrachromosomal DNA Amplification of <i>MYC</i> Paralogs Open
Comparison of chemotherapy regimen delta-AUC and comparison of average delta-AUC by PDX source.
View article: Supplementary Tables from Acquired Cross-Resistance in Small Cell Lung Cancer due to Extrachromosomal DNA Amplification of <i>MYC</i> Paralogs
Supplementary Tables from Acquired Cross-Resistance in Small Cell Lung Cancer due to Extrachromosomal DNA Amplification of <i>MYC</i> Paralogs Open
Supplementary Table S1. Clinical Histories of PDX Models.Supplementary Table S2. Differential Gene Expression for MGH1518 Serial Models.Supplementary Table S3. Mutations in the ecMYC region in MGH1518-3A.Supplementary Table S4. Mutations i…
View article: Supplementary Figure S14 from Acquired Cross-Resistance in Small Cell Lung Cancer due to Extrachromosomal DNA Amplification of <i>MYC</i> Paralogs
Supplementary Figure S14 from Acquired Cross-Resistance in Small Cell Lung Cancer due to Extrachromosomal DNA Amplification of <i>MYC</i> Paralogs Open
MYC paralog amplifications that were detected or omitted by segmented copy number analysis, and patient survival compared with ecDNA status of PDX models.
View article: Supplementary Figure S7 from Acquired Cross-Resistance in Small Cell Lung Cancer due to Extrachromosomal DNA Amplification of <i>MYC</i> Paralogs
Supplementary Figure S7 from Acquired Cross-Resistance in Small Cell Lung Cancer due to Extrachromosomal DNA Amplification of <i>MYC</i> Paralogs Open
Untreated PDX growth curves.