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This article discusses a case of a 64-year-old man who presented with back pain and cough. Imaging revealed masses in the chest and abdomen, as well as pleural effusions. Pathological examination of the tissue revealed a poorly differentiated malignant neoplasm that initially appeared to be anaplastic large-cell lymphoma (ALCL) based on immunohistochemical staining. However, further molecular testing confirmed a diagnosis of ALK-rearranged lung adenocarcinoma. The patient has responded to ALK-inhibitor therapy. The article emphasizes the importance of careful interpretation of immunohistochemical stains in cases of poorly differentiated ALK+/CD30+ neoplasms. [Extracted from the article]

The programmed death‐1 (PD‐1) receptor checkpoint inhibitors nivolumab and pembrolizumab represent an important therapeutic advance in the treatment of relapsed or refractory classical Hodgkin lymphoma (cHL). Clinical trials have shown substantial therapeutic activity and an acceptable safety profile in heavily pretreated patients, resulting in U.S. Food and Drug Administration approval of nivolumab for the treatment of cHL that has relapsed or progressed after either autologous hematopoietic cell transplantation (auto‐HCT) and brentuximab vedotin treatment or three or more lines of systemic therapy (including auto‐HCT), and of pembrolizumab for adult or pediatric patients with refractory cHL or cHL that has relapsed after three or more prior therapies. Mechanistically, anti‐PD‐1 therapy prevents inhibitory signaling through PD‐1 receptors on T cells, thereby releasing a 'block' to antitumor T‐cell responses. However, this disinhibition can also lead to inappropriate T‐cell activation and responses against healthy tissues, resulting in immune‐mediated adverse events (IMAEs) that affect a number of organ systems. The skin, gastrointestinal, hepatic, and endocrine systems are most commonly involved, typically resulting in rash, colitis, abnormal liver enzyme levels, and thyroiditis, respectively. Notably, pneumonitis is a potentially fatal complication of checkpoint inhibitor immunotherapy. Hematologic oncologists who treat cHL with PD‐1 immune checkpoint inhibitors should monitor patients for IMAEs, as early recognition and treatment can rapidly reduce morbidity and mortality. This review focuses on IMAEs during the treatment of relapsed or refractory cHL with nivolumab and pembrolizumab. Implications for Practice: This article highlights the importance of monitoring for immune‐mediated adverse events (IMAEs) in patients with Hodgkin lymphoma (HL) who receive anti‐programmed death‐1 (anti‐PD‐1) therapy, with particular attention given to the recognition and management of such events. The risk of individual IMAEs differs between patients with HL and those with solid tumors, as prior treatments may predispose certain organ systems to specific IMAEs. Accurate and prompt diagnosis of IMAEs is essential for optimal management, allowing PD‐1 inhibitor therapy to be restarted in order to maintain disease control. Potential difficulties, such as distinguishing disease progression from pneumonitis, or colitis from diarrhea, are highlighted to raise clinical awareness. This review focuses on immune‐mediated adverse events (IMAEs) reported during the treatment of relapsed or refractory classical Hodgkin lymphoma with the programmed death‐1 (PD‐1) immune checkpoint inhibitors nivolumab and pembrolizumab, describing strategies for promptly recognizing and managing IMAEs in these patients, with the aim of ensuring timely recovery and minimizing discontinuation of anti‐PD‐1 therapy to improve overall disease control. [ABSTRACT FROM AUTHOR]

The authors are grateful to the Editor of I Molecular and Clinical Oncology i for allowing them the opportunity to publish this corrigendum, and regret any confusion that the wording of this sentence may have caused for readers. Mol Clin Oncol 14:Article no. 34, 2021; DOI: 10.3892/mco.2020.2196 Following the publication of this article, the authors have realized that a sentence in the Introduction was written incorrectly from the perspective of its comprehension. The sentence on the first page, right-hand column, lines 5-7, written as "When a diagnosis of LCNEC cannot be made..." should have been written as follows (changes highlighted in bold): "When a diagnosis of LCNEC cannot be made on a morphological basis, immunohistochemical markers exist that B may aid in the differentiation of b the disease from SCLC". [Extracted from the article]

Interstitial lung disease (ILD) is a well-known extra-articular manifestation of rheumatoid arthritis (RA). RA-associated ILD (RA-ILD) exists on a wide spectrum, with variable levels of inflammatory and fibrotic activity, although all subtypes are regarded as irreversible pathologic conditions. In both articular and pulmonary manifestations, TNF is a significant pathogenic factor. Whereas anti-TNF therapy alleviates joint pathologic conditions, it exacerbates fibrotic RA-ILD. The TNF-transgenic (TNF-Tg) murine model of RA develops both inflammatory arthritis and an ILD that mimics a cellular nonspecific interstitial pneumonia pattern dominated by an interstitial accumulation of inflammatory cells with minimal-to-absent fibrosis. Given the model's potential to elucidate the genesis of inflammatory RA-ILD, we aim to achieve the following: 1) characterize the cellular accumulations in TNF-Tg lungs, and 2) assess the reversibility of inflammatory ILD following anti-TNF therapy known to resolve TNF-Tg inflammatory arthritis. TNF-Tg mice with established disease were randomized to anti-TNF or placebo therapy and evaluated with imaging, histology, and flow cytometric analyses, together with wild-type controls. Flow cytometry of TNF-Tg versus wildtype lungs revealed significant increases in activated monocytes, conventional dendritic cells, and CD21+/CD23- B cells that are phenotypically distinct from the B cells in inflamed nodes, which are known to accumulate in joint-draining lymph nodes. In contrast to human RA-ILD, anti-TNF treatment significantly alleviated both joint and lung inflammation. These results identify a potential role for activated monocytes, conventional dendritic cells, and CD21+/CD23- B cells in the genesis of RA-ILD, which exist in a previously unknown, reversible, prefibrotic stage of the disease. [ABSTRACT FROM AUTHOR]

Interstitial lung disease (ILD) is a well-known extra-articular manifestation of rheumatoid arthritis (RA). RA-associated ILD (RA-ILD) exists on a wide spectrum, with variable levels of inflammatory and fibrotic activity, although all subtypes are regarded as irreversible pathologic conditions. In both articular and pulmonary manifestations, TNF is a significant pathogenic factor. Whereas anti-TNF therapy alleviates joint pathologic conditions, it exacerbates fibrotic RA-ILD. The TNF-transgenic (TNF-Tg) murine model of RA develops both inflammatory arthritis and an ILD that mimics a cellular nonspecific interstitial pneumonia pattern dominated by an interstitial accumulation of inflammatory cells with minimal-to-absent fibrosis. Given the model's potential to elucidate the genesis of inflammatory RA-ILD, we aim to achieve the following: 1) characterize the cellular accumulations in TNF-Tg lungs, and 2) assess the reversibility of inflammatory ILD following anti-TNF therapy known to resolve TNF-Tg inflammatory arthritis. TNF-Tg mice with established disease were randomized to anti-TNF or placebo therapy and evaluated with imaging, histology, and flow cytometric analyses, together with wild-type controls. Flow cytometry of TNF-Tg versus wild-type lungs revealed significant increases in activated monocytes, conventional dendritic cells, and CD21 + /CD23 - B cells that are phenotypically distinct from the B cells in inflamed nodes, which are known to accumulate in joint-draining lymph nodes. In contrast to human RA-ILD, anti-TNF treatment significantly alleviated both joint and lung inflammation. These results identify a potential role for activated monocytes, conventional dendritic cells, and CD21 + /CD23 - B cells in the genesis of RA-ILD, which exist in a previously unknown, reversible, prefibrotic stage of the disease., (Copyright © 2019 by The American Association of Immunologists, Inc.)