Imaging features of toxicities associated with immune checkpoint inhibitors
Name:
Publisher version
View Source
Access full-text PDFOpen Access
View Source
Check access options
Check access options
Authors
Gosangi, BabinaMcIntosh, Lacey
Keraliya, Abhishek
Irugu, David Victor Kumar
Baheti, Akshay
Khandelwal, Ashish
Thomas, Richard
Braschi-Amirfarzan, Marta
UMass Chan Affiliations
RadiologyDocument Type
Journal ArticlePublication Date
2022-08-08Keywords
AIP, acute interstitial pneumonitisARDS, acute respiratory distress syndrome
CTCAE, Common Terminology Criteria for Adverse Events
CTLA-4 inhibitor, Cytotoxic T-lymphocyte antigen- 4 inhibitor
Colitis
FDA, Food and Drug Administration
Hepatitis
ICI, Immune check point inhibitor
Immune check point inhibitors toxicity
LGE, late Gadolinium enhancement
NSCLC, non-small cell lung cancer
NSIP, non-specific interstitial pneumonia
OP, organizing pneumonia
PD-1 inhibitor, programmed cell death-1 inhibitor
PD-L1 inhibitor, programmed cell death ligand-1 inhibitor
PFS, progression free survival
Pancreatitis
Pneumonitis
RRP, radiation recall pneumonitis
irAE, immune-related adverse event
Metadata
Show full item recordAbstract
The past decade has witnessed a change in landscape of cancer management with the advent of precision oncology. Immune checkpoint inhibitors (ICIs) have revolutionized cancer treatment and have played an important role in improving patient survival. While the patients are living longer, treatment with ICIs are sometimes associated with adverse effects, some of which could be fatal. Radiologists can play a crucial role by early identification of some of these adverse effects during restaging scans. Our paper focuses on the imaging features of commonly occurring ICI toxicities based on organ system.Source
Gosangi B, McIntosh L, Keraliya A, Irugu DVK, Baheti A, Khandelwal A, Thomas R, Braschi-Amirfarzan M. Imaging features of toxicities associated with immune checkpoint inhibitors. Eur J Radiol Open. 2022 Aug 8;9:100434. doi: 10.1016/j.ejro.2022.100434. PMID: 35967881; PMCID: PMC9372737.DOI
10.1016/j.ejro.2022.100434Permanent Link to this Item
http://hdl.handle.net/20.500.14038/51263PubMed ID
35967881Rights
© 2022 The Authors. Published by Elsevier Ltd. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).; Attribution 4.0 InternationalDistribution License
http://creativecommons.org/licenses/by/4.0/ae974a485f413a2113503eed53cd6c53
10.1016/j.ejro.2022.100434
Scopus Count
Collections
The following license files are associated with this item:
- Creative Commons
Except where otherwise noted, this item's license is described as © 2022 The Authors. Published by Elsevier Ltd. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).
Related items
Showing items related by title, author, creator and subject.
-
Risk of COVID-19 in Dermatologic Patients on Long-term Immunomodulatory TherapyHolcomb, Zachary E.; Santillan, Monica Rosales; Morss-Walton, Peyton C; Salian, Prerna; Her, Min Ji; Giannotti, Nicole M.; Kimball, Alexa B.; Porter, Martina L. (2020-07-01)As the COVID-19 pandemic has rapidly spread around the globe, concern has been raised regarding susceptibility of patients on immunomodulatory therapies to severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection. While general guidance has been put forth, data regarding infection rate and outcomes in immunosuppressed patients is still rare.1 Recent articles, including the work by Gisondi, et al, suggest that outcomes of patients on systemic immunomodulatory therapies infected with SARS-CoV-2 are similar to the general population.2 These findings may relate to the aberrant cytokine and inflammatory responses in severe COVID-19, which may be treated or partially blunted by cytokine-targeted therapy.3 Given the substantial outbreak of COVID-19 in our community, we tested whether, in addition to similar outcomes, patients on systemic immunomodulatory therapy had similar infection rates compared to the general population.
-
Hippocampal c-Jun-N-terminal kinases serve as negative regulators of associative learningSherrin, Tessi; Blank, Thomas; Hippel, Cathrin; Rayner, Martin; Davis, Roger J.; Todorovic, Cedomir (2010-10-06)In the adult mouse, signaling through c-Jun N-terminal kinases (JNKs) links exposure to acute stress to various physiological responses. Inflammatory cytokines, brain injury and ischemic insult, or exposure to psychological acute stressors induce activation of hippocampal JNKs. Here we report that exposure to acute stress caused activation of JNKs in the hippocampal CA1 and CA3 subfields, and impaired contextual fear conditioning. Conversely, intrahippocampal injection of JNKs inhibitors sp600125 (30 mum) or D-JNKI1 (8 mum) reduced activity of hippocampal JNKs and rescued stress-induced deficits in contextual fear. In addition, intrahippocampal administration of anisomycin (100 mug/mul), a potent JNKs activator, mimicked memory-impairing effects of stress on contextual fear. This anisomycin-induced amnesia was abolished after cotreatment with JNKs selective inhibitor sp600125 without affecting anisomycin's ability to effectively inhibit protein synthesis as measured by c-Fos immunoreactivity. We also demonstrated milder and transient activation of the JNKs pathway in the CA1 subfield of the hippocampus during contextual fear conditioning and an enhancement of contextual fear after pharmacological inhibition of JNKs under baseline conditions. Finally, using combined biochemical and transgenic approaches with mutant mice lacking different members of the JNK family (Jnk1, Jnk2, and Jnk3), we provided evidence that JNK2 and JNK3 are critically involved in stress-induced deficit of contextual fear, while JNK1 mainly regulates baseline learning in this behavioral task. Together, these results support the possibility that hippocampal JNKs serve as a critical molecular regulator in the formation of contextual fear.
-
Immortalization of human mammary epithelial cells is associated with inactivation of the p14ARF-p53 pathwayShamanin, Vladimir A.; Androphy, Elliot J. (2004-02-18)Inactivation of the ARF-p53 tumor suppressor pathway leads to immortalization of murine fibroblasts. The role of this pathway in immortalization of human epithelial cells is not clear. We analyzed the functionality of the p14(ARF)-p53 pathway in human mammary epithelial cells (MEC) immortalized by human papillomavirus 16 (HPV16) E6, the p53 degradation-defective E6 mutant Y54D, or hTERT. E6-MEC or E6Y54D-MEC maintains high-level expression of p14(ARF). Late-passage hTERT-immortalized MEC express p53 but down-regulate p14(ARF). Enforced expression of p14(ARF) induces p53-dependent senescence in hTERT-MEC, while both E6-MEC and E6Y54D-MEC are resistant. We show that E6Y54D inhibits p14(ARF)-induced activation of p53 without inactivation of the p53-dependent DNA damage response. Hence, p53 degradation and inhibition of p14(ARF) signaling to p53 are independent functions of HPV16 E6. Our observations imply that long-term proliferation of MEC requires inactivation of the p14(ARF)-p53 pathway.