Publications by authors named "Julian Marin-Acevedo"

A major paradigm shift in the diagnosis, management, and survival outcomes of early and advanced non-small cell lung cancer has transpired over the past few decades in thoracic oncology with the incorporation of molecular testing, targeted therapy, immunotherapy, neoadjuvant, and adjuvant approaches. However, transformation in the management and survival outcomes of rare lung tumors is lacking. Given the scarcity of these tumor types, randomized trials are rarely performed, and treatment is extrapolated from case series, tumor-agnostic trials, or cancers with similar histology.

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Genomic mutations impact non-small cell lung cancer (NSCLC) biology. The influence of sex and age on the distribution of these alterations is unclear. We analyzed circulating-tumor DNA from individuals with advanced NSCLC from March 2018 to October 2020.

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Anti-PD1 therapy demonstrated impressive, prolonged responses in advanced cutaneous squamous cell carcinoma (CSCC). Therapy for ICI-refractory/ineligible disease remains unclear. We performed a retrospective analysis in locally-advanced/metastatic CSCC using cetuximab across three cohorts: immediately after ICI failure (A), not immediately following ICI failure (B), or without prior ICI (C).

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The development of targeted therapies over the past two decades has led to a dramatic change in the management of -mutant non-small cell lung cancer (NSCLC). While there are currently five approved EGFR tyrosine kinase inhibitors (TKIs) for treating -mutant NSCLC in the first-line setting, therapy selection after progression on EGFR TKIs remains complex. Multiple groups are investigating novel therapies and drug combinations to determine the optimal therapy and treatment sequence for these patients.

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Limited-stage small cell lung cancer (LS-SCLC) is a potentially curable disease. However, most patients develop disease relapse shortly after definitive treatment. The landmark trials IMpower133 and CASPIAN demonstrated a survival benefit with the addition of immunotherapy to first-line platinum/etoposide for extensive-stage small cell lung cancer.

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Co-stimulatory and co-inhibitory molecules play a critical role in T cell function. Tumor cells escape immune surveillance by promoting immunosuppression. Immunotherapy targeting inhibitory molecules like anti-CTLA-4 and anti-PD-1/PD-L1 were developed to overcome these immunosuppressive effects.

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The treatment paradigm for patients with advanced non-small cell lung cancer has substantially changed with the discovery of immunotherapy. The incorporation of immunotherapy into treatment algorithms has resulted in better outcomes for patients, with fewer side effects compared with classic chemotherapeutic agents. Multiple treatment options are now available for patients with advanced non-small cell lung cancer, ranging from single-agent immunotherapy to quadruple therapy, which involves dual immune checkpoint inhibitor plus chemotherapy or immune checkpoint inhibitor plus chemotherapy plus anti-vascular endothelial growth factor drugs.

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The immune system is the core defense against cancer development and progression. Failure of the immune system to recognize and eliminate malignant cells plays an important role in the pathogenesis of cancer. Tumor cells evade immune recognition, in part, due to the immunosuppressive features of the tumor microenvironment.

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With improving survivorship in chronic lymphocytic leukemia (CLL), the risk of second primary malignancies (SPMs) has not been systematically addressed. Differences in risk for SPMs among CLL survivors from the Surveillance, Epidemiology, and End Results (SEER) database (1973-2015) were compared to risk of individual malignancies expected in the general population. In ~270,000 person-year follow-up, 6487 new SPMs were diagnosed with a standardized incidence ratio (SIR) of 1.

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Hyperprogression and pseudoprogression are two atypical responses to immune checkpoint inhibitor therapy that affect therapeutic decisions and prognosis. Identification of predictive biomarkers for atypical responses either before or during treatment remains a huge unmet need in cancer immunotherapy. Many studies have looked at potential biomarkers, including clinical factors and laboratory findings (e.

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Article Synopsis
  • - Immune checkpoint inhibitors boost the body's immune response to fight tumors, transforming cancer treatment since their success in advanced melanoma and now being used for other cancers.
  • - These therapies can lead to immune-related adverse events, which manifest as autoimmune-like toxicities affecting various organs, with skin and colon being the most common sites.
  • - Management of these adverse effects often involves corticosteroids or other immunosuppressive treatments, and may necessitate stopping immunotherapy based on the toxicity severity.
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Immune checkpoint inhibitors have changed the treatment paradigm for patients with cancer. Though a majority of patients tolerate treatment, some develop hematologic toxicities, including eosinophilia. Eosinophilia has been associated with better responses in some patients with melanoma, but this has not been investigated in non-small-cell lung cancer.

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Background: Anti-programmed cell death 1 (PD-1) antibodies have demonstrated improved overall survival (OS) and progression-free survival (PFS) in a subset of patients with metastatic or locally advanced non-small cell lung cancer (NSCLC). To date, no blood biomarkers have been identified in NSCLC to predict clinical outcomes of treatment with anti-PD-1 antibodies.

Patient And Methods: We performed an analysis of retrospectively registered data of 157 patients with advanced NSCLC treated with anti-PD-1 antibodies at Mayo Clinic in Florida and Rochester.

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Article Synopsis
  • * When symptoms do appear, they tend to be vague and can sometimes lead to severe outcomes, making diagnosis difficult.
  • * Effective treatment focuses on managing inflammation and preventing heart damage, but the overall outlook for patients remains concerning, as shown in a case where initial symptoms did not lead to immediate diagnosis.
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Infiltrative cardiomyopathies include a variety of disorders that lead to myocardial thickening resulting in a constellation of clinical manifestations and eventually heart failure that could be the first clue to reach the diagnosis. Among the more described infiltrative diseases of the heart is amyloid cardiomyopathy. The disease usually presents with subtle, nonspecific symptoms.

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Immune checkpoints consist of inhibitory and stimulatory pathways that maintain self-tolerance and assist with immune response. In cancer, immune checkpoint pathways are often activated to inhibit the nascent anti-tumor immune response. Immune checkpoint therapies act by blocking or stimulating these pathways and enhance the body's immunological activity against tumors.

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Since their introduction for melanoma treatment, the use of immune checkpoint inhibitors (ICIs) has rapidly expanded. Though their impact on survival is irrefutable, these medications have been associated with autoimmune-like adverse events related to their ability to induce the immune system. One of the most commonly affected organ systems is the gastrointestinal (GI) tract, in which manifestations range from mild diarrhea to severe colitis with intestinal perforation.

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Malignant cells have the capacity to rapidly grow exponentially and spread in part by suppressing, evading, and exploiting the host immune system. Immunotherapy is a form of oncologic treatment directed towards enhancing the host immune system against cancer. In recent years, manipulation of immune checkpoints or pathways has emerged as an important and effective form of immunotherapy.

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A 54-year-old man presented to the emergency department with acute left-sided chest pain and left upper quadrant abdominal pain. He had a significant history of squamous cell carcinoma of the lung previously treated with right pneumonectomy who ; is currently receiving adjuvant chemotherapy with cisplatin. Physical examination was remarkable for tachycardia, hypertension and mild abdominal tenderness.

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