Publications by authors named "Brett H Herzog"

Non-small cell lung cancer (NSCLC) is a leading cause of cancer-related deaths. Immune checkpoint blockade has improved survival for many patients with NSCLC, but most fail to obtain long-term benefit. Understanding the factors leading to reduced immune surveillance in NSCLC is critical in improving patient outcomes.

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Introduction: The American Cancer Society has recently reported an increase in the percentage of patients with localized lung cancer from 2004 to 2018, coinciding with the initial lung cancer screening guidelines issued in 2013. We conducted a National Cancer Database (NCDB) study to further evaluate the trends in stage I according to patient and tumor characteristics.

Methods: We selected patients with lung cancer from the NCDB Public Benchmark Report diagnosed between 2010 and 2017.

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Article Synopsis
  • Targeting focal adhesion kinase (FAK) with the drug defactinib, combined with gemcitabine and pembrolizumab, shows promise in treating pancreatic ductal adenocarcinoma (PDAC) in a multi-center phase I study.* -
  • The study involved two phases: one to determine the optimal dosage and another to treat patients with either refractory or stable PDAC, where an 80% disease control rate was observed among those with refractory disease.* -
  • Preliminary results indicate the treatment combination is well-tolerated and shows potential efficacy, suggesting future studies may benefit from using stronger chemotherapy agents alongside it.*
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Objectives: The treatment options for patients with stage IV non-small cell lung cancer (NSCLC) who develop tumor progression after platinum-based chemotherapy and immune checkpoint inhibitors (ICIs) are limited. The combination of ICI with inhibitors of vascular endothelial growth receptor (VEGFR) signaling has shown promising results in previously untreated patients.

Materials And Methods: In this single institution phase II study, patients with advanced stage NSCLC previously treated with at least one line including ICI received ramucirumab 10 mg/kg and atezolizumab 1,200 mg intravenously every 21 days until tumor progression or intolerable toxicity.

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SCLC is an aggressive form of lung cancer with a very poor prognosis. Although SCLC initially responds very well to platinum-based chemotherapy, it eventually recurs and at recurrence is nearly universally resistant to therapy. In light of the recent advances in understanding regarding the biology of SCLC, we review findings related to SCLC chemotherapy resistance.

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Here, we utilized spontaneous models of pancreatic and lung cancer to examine how neoantigenicity shapes tumor immunity and progression. As expected, neoantigen expression during lung adenocarcinoma development leads to T cell-mediated immunity and disease restraint. By contrast, neoantigen expression in pancreatic ductal adenocarcinoma (PDAC) results in exacerbation of a fibro-inflammatory microenvironment that drives disease progression and metastasis.

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Purpose: Patients with SCLC rarely undergo biopsies at relapse. When pursued, tissue obtained can be inadequate for molecular testing, posing a challenge in identifying potentially targetable alterations in a clinically meaningful time frame. We examined the feasibility of circulating tumor DNA (ctDNA) testing in identifying potentially targetable alterations in SCLC.

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The kidney's filtration activity is essential for removing toxins and waste products from the body. The vascular endothelial cells of the glomerulus are fenestrated, flattened, and surrounded by podocytes, specialized cells that support glomerular endothelial cells. Mucin-type core 1-derived glycans (-glycans) are highly expressed on both glomerular capillary endothelial cells and their supporting podocytes, but their biological role is unclear.

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Mucin-type core 1-derived O-glycans, one of the major types of O-glycans, are highly expressed in mammary gland epithelium. Abnormal O-glycans such as Tn antigen are found in over 90% of breast cancers; however, the in vivo role of these aberrant O-glycans in the etiology of breast cancer is unclear. We generated mice with mammary epithelial specific deletion of core 1-derived O-glycans.

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Vascular endothelial cells, in addition to many other mammalian cell types, express proteins that are highly modified with mucin-type O-glycosylation, a specific type of glycosylation that begins with the addition of an N-acetylgalactosamine moiety to serine or threonine residues within the peptide backbone. Recently, it has become evident that O-glycosylation governs the separation of blood and lymphatic vessels throughout life and plays a critical role in maintaining vascular integrity in specific tissues such as the brain and lymph node. This mini-review seeks to highlight some of these recent advances regarding in vivo functions of mucin-type O-glycans.

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Lymphomas originate in and spread primarily along the lymphatic system. However, whether lymphatic vessels contribute to the growth and spreading of lymphomas is largely unclear. Mantle cell lymphoma (MCL) represents an aggressive non-Hodgkin's lymphoma.

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Circulating lymphocytes continuously enter lymph nodes for immune surveillance through specialized blood vessels named high endothelial venules, a process that increases markedly during immune responses. How high endothelial venules (HEVs) permit lymphocyte transmigration while maintaining vascular integrity is unknown. Here we report a role for the transmembrane O-glycoprotein podoplanin (PDPN, also known as gp38 and T1α) in maintaining HEV barrier function.

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