Publications by authors named "Erin Schenk"

Article Synopsis
  • This study investigates the effects of continuing osimertinib alongside platinum-pemetrexed chemotherapy for patients with EGFR mutant non-small cell lung cancer (NSCLC) who have had disease progression on osimertinib.
  • It analyzed data from 159 eligible patients out of 421 identified, comparing outcomes between two groups: one continuing osimertinib with chemotherapy and the other receiving chemotherapy alone.
  • Results showed that the group continuing osimertinib experienced a significant improvement in progression-free survival (9.0 months vs. 4.5 months), indicating a potential clinical benefit in this treatment strategy.
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Background: Gene copy number gain (CNG) is a continuous variable. The relevant cutpoint for HER2, KRAS and MET CNG in non-mall cell lung cancer remains uncertain. As de novo driver oncogenes are largely mutually exclusive, oncogene overlap analysis can be used to explore CNG thresholds.

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Purpose: To assess the safety and efficacy of the third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor osimertinib as neoadjuvant therapy in patients with surgically resectable stage I-IIIA -mutated non-small cell lung cancer (NSCLC).

Patients And Methods: This was a multi-institutional phase II trial of neoadjuvant osimertinib for patients with surgically resectable stage I-IIIA (American Joint Committee on Cancer [AJCC] V7) -mutated (L858R or exon 19 deletion) NSCLC (ClinicalTrials.gov identifier: NCT03433469).

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Aberrant activation of GLI transcription factors has been implicated in the pathogenesis of different tumor types including pancreatic ductal adenocarcinoma. However, the mechanistic link with established drivers of this disease remains in part elusive. In this study, using a new genetically engineered mouse model overexpressing constitutively active mouse form of GLI2 and a combination of genome-wide assays, we provide evidence of a novel mechanism underlying the interplay between KRAS, a major driver of pancreatic ductal adenocarcinoma development, and GLI2 to control oncogenic gene expression.

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Purpose: We first described the role of local radiation therapy (LT) for oligoprogressive disease (OPD) on targeted therapy in 2012. Here, we present an updated and larger data set and extend the analysis beyond EGFR and ALK.

Methods: A retrospective review of patients with metastatic NSCLC harboring V600E mutations, or rearrangements, who had OPD on respective tyrosine-kinase inhibitor (TKI) and treated with LT was performed.

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Article Synopsis
  • The purpose of this guideline is to provide updated, evidence-based treatment recommendations for patients with stage IV non-small cell lung cancer (NSCLC) who do not have specific genetic driver alterations.
  • The recommendations are based on recent systematic reviews and randomized clinical trials, focusing on both efficacy and safety, and were developed by an Expert Panel with diverse expertise.
  • The latest update identified ten new randomized clinical trials and consolidates previous recommendations, covering treatment options for first, second, and subsequent lines of therapy.
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Article Synopsis
  • The guideline aims to provide evidence-based recommendations for treating stage IV non-small cell lung cancer patients with specific driver alterations.
  • It is regularly updated based on systematic reviews of clinical trials, with the latest review covering studies from February to October 2023.
  • The latest update identified eight new randomized controlled trials and refined treatment recommendations for different stages of therapy based on targetable driver alterations.
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Introduction: Acquired gene amplification, exon 14 skip mutations, or fusions can emerge as resistance mechanisms to tyrosine kinase inhibitors (TKIs) in patients with lung cancer. The efficacy and safety of combining MET TKIs (such as crizotinib, capmatinib, or tepotinib) with parent TKIs to target acquired MET resistance are not well characterized.

Methods: Multi-institutional retrospective chart review identified 83 patients with metastatic oncogene-driven NSCLC that were separated into the following two pairwise matched cohorts: (1) MET cohort (n = 41)-patients with acquired MET resistance continuing their parent TKI with a MET TKI added or (2) Chemotherapy cohort (n = 42)-patients without any actionable resistance continuing their parent TKI with a platinum-pemetrexed added.

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Background: Anaplastic lymphoma kinase () rearrangement is one of the most important drivers in non-small cell lung cancer (NSCLC). Despite the effectiveness to canonical 3'- fusions, the clinical efficacy of ALK inhibitors in patients with complex fusions, such as nonreciprocal/reciprocal translocation remains uncertain. Exploring the optimal therapeutic regimens for this subset of patients is of crucial clinical significance.

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Background And Objective: Patients with metastatic anaplastic lymphoma kinase (ALK)+ non-small cell lung cancer (NSCLC) often experience years of disease control on targeted therapies but the disease eventually develops resistance and progresses. Multiple clinical trial efforts to incorporate PD-1/PD-L1 immunotherapy into the treatment paradigm for ALK+ NSCLC have resulted in significant toxicities without clear improvement in patient outcomes. Observations from clinical trials, translational studies, and preclinical models suggest the immune system interacts with ALK+ NSCLC and this interaction is heightened with the initiation of targeted therapy.

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Article Synopsis
  • The study explores using tyrosine kinase inhibitors (TKIs) to treat patients with extensive brain metastases (BrM) from lung cancer, aiming to downstage their condition and avoid whole-brain radiotherapy.
  • Twelve patients with ALK, EGFR, and ROS1-driven non-small cell lung cancer (NSCLC) were treated with CNS-active TKIs, showing significant reductions in both the number and volume of BrMs.
  • Most patients experienced CNS progression after initial treatment, yet the overall survival rate from starting TKIs was promising, averaging 43.2 months.
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Lung cancers bearing oncogenic EML4-ALK fusions respond to targeted tyrosine kinase inhibitors (TKIs; e.g., alectinib), with variation in the degree of shrinkage and duration of treatment (DOT).

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Patients with metastatic NSCLC bearing a ROS1 gene fusion usually experience prolonged disease control with ROS1-targeting tyrosine kinase inhibitors (TKI), but significant clinical heterogeneity exists in part due to the presence of co-occurring genomic alterations. Here, we report on a patient with metastatic NSCLC with a concurrent ROS1 fusion and KRAS p.G12C mutation at diagnosis who experienced a short duration of disease control on entrectinib, a ROS1 TKI.

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Patients with early-stage lung adenocarcinoma have a high risk of recurrent or metastatic disease despite undergoing curative intent therapy. We hypothesized that increased CD14+ cells within the tumor microenvironment (TME) could stratify patient outcomes. Immunohistochemistry for CD14 was performed on 189 specimens from patients with lung adenocarcinoma who underwent curative intent surgery.

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Objective: Multiplex immunohistochemistry (mIHC) and multiplexed ion beam imaging (MIBI) images are usually phenotyped using a manual thresholding process. The thresholding is prone to biases, especially when examining multiple images with high cellularity.

Results: Unsupervised cell-phenotyping methods including PhenoGraph, flowMeans, and SamSPECTRAL, primarily used in flow cytometry data, often perform poorly or need elaborate tuning to perform well in the context of mIHC and MIBI data.

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The tumor microenvironment (TME), which characterizes the tumor and its surroundings, plays a critical role in understanding cancer development and progression. Recent advances in imaging techniques enable researchers to study spatial structure of the TME at a single-cell level. Investigating spatial patterns and interactions of cell subtypes within the TME provides useful insights into how cells with different biological purposes behave, which may consequentially impact a subject's clinical outcomes.

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Purpose: Targeting the vascular endothelial growth factor (VEGF) pathway improves progression free survival in multiple advanced malignancies but durable responses are uncommon. Inhibition of the VEGF pathway at multiple levels of signal transduction may improve clinical outcomes. Preclinical data with cediranib, an inhibitor of all 3 VEGF receptors, in combination with selumetinib, an inhibitor of MEK 1/2, demonstrated improved tumor control experimentally.

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Introduction: In patients with NSCLC, the prognostic significance of the tumor microenvironment (TME) immune composition has been revealed using single- or dual-marker staining on sequential tissue sections. Although these studies reveal that relative abundance and localization of immune cells are important parameters, deeper analyses of the NSCLC TME are necessary to refine the potential application of these findings to clinical care. Currently, the complex spatial relationships between cells of the NSCLC TME and potential drivers contributing to its immunologic composition remain unknown.

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