Immunohistochemical analysis of lichenoid reactions in patients treated with anti‐PD‐L1 and anti‐PD‐1 therapy

Schaberg, Kurt B.; Novoa, Roberto A.; Wakelee, Heather A.; Kim, Jinah; Cheung, Christine; Srinivas, Sandhya; Kwong, Bernice Y.

doi:10.1111/cup.12666

Cited by 115 publications

(140 citation statements)

References 13 publications

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“…In line with our report, Lindner et al [13], in 2009, reported the case of a metastatic renal cell carcinoma patient who developed an “immune-mediated” lichen ruber 6 months after starting nivolumab therapy. Later, various groups reported the occurrence of lichenoid lesion during anti-PD-1/anti-PD-L1 therapy [14, 15]. Additionally, in our patient the development of lichen ruber might be related to the infection with HCV, representing an important risk factor for this disease [16].…”

Section: Discussion/conclusionmentioning

confidence: 60%

Excellent Response to Anti-PD-1 Therapy in a Patient with Hepatocellular Carcinoma Intolerant to Sorafenib

et al. 2019

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Background: Hepatocellular carcinoma (HCC) represents the most common primary carcinoma of the liver. Most patients present with advanced or metastatic HCC at diagnosis and face a very limited prognosis. Systemic treatment with the tyrosine-kinase inhibitors sorafenib or lenvatinib is considered as the treatment of choice in these patients. In patients intolerant to tyrosine-kinase inhibitors, no standard therapy is approved so far, but several agents have demonstrated efficacy in clinical trials. As such, the checkpoint inhibitors nivolumab and pembrolizumab have been shown to induce tumor response and to prolong survival in patients with advanced HCC, both when intolerant to sorafenib or after failure of a first-line therapy with sorafenib. Case Report: We here report the case of a patient with advanced HCC that demonstrated severe toxicity upon first-line treatment with sorafenib. Administration of sorafenib was discontinued and after careful consideration the patient started a second-line treatment with the PD-1 antibody nivolumab. Strikingly, this treatment led to a significant regression of tumor size and a drastic reduction of alpha-fetoprotein serum concentrations. At 17 months after initiation of treatment, the patient is still alive in excellent condition with sustained tumor response. Conclusion: In summary, we report on a very rare case of a patient with HCC demonstrating an almost complete response to checkpoint inhibitor treatment.

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Section: Discussion/conclusionmentioning

confidence: 60%

Excellent Response to Anti-PD-1 Therapy in a Patient with Hepatocellular Carcinoma Intolerant to Sorafenib

et al. 2019

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“…These lesions generally occurred several months after treatment induction. Histopathology and immunophenotypic analysis of the lichenoid lesions associated with anti-PD1 and anti-PDL-1 therapy seem to reveal greater histiocytic infiltrate than that observed in similar nondrug-related lichenoid reactions (i.e., lichen planus, lichen planus-like keratoses) [172].…”

Section: Lichenoid Reactionsmentioning

confidence: 74%

“…Recently, more characteristic oral lesions with PD-1 or PD-L1 inhibitors have been described [20,38,171,172].…”

Section: Pigmentary Changesmentioning

confidence: 99%

“…Schaberg et al [172] reported one case of lichenoid lesion with PDL-1 inhibitor therapy and Hofmann et al [171] reported one case of oral lichen planus with pembrolizumab. We have also observed several cases of mucosal lesions, which were clinically and histologically consistent with oral lichenoid lesions, developing as a result of treatment with PD-1 and PD-L-1 [20].…”

Section: Lichenoid Reactionsmentioning

confidence: 99%

“…Patients may report pain or soreness but the lesions can also be asymptomatic. The perianal area or vulva can also be affected [172]. Topical corticosteroids should be considered if lesions are painful (Table 5).…”

Section: Lichenoid Reactionsmentioning

confidence: 99%

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Oral mucosal changes induced by anticancer targeted therapies and immune checkpoint inhibitors

Vigarios

Epstein

Sibaud

2017

Support Care Cancer

148

136

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Development of biological targeted therapies and immune checkpoint inhibitors has redefined the treatment for many cancers; however, the increasing use of new protocols has led to physicians observing a new spectrum of toxicities. To date, oral adverse events induced by these new anticancer therapies have been mainly reported using nonspecific terminology (Bstomatitis,^Bmucosal inflammation,^Bmucositis^) and remain poorly characterized, with the exception of mammalian target of rapamycin (mTOR) inhibitor-associated stomatitis. Oral toxicities of targeted therapies often display very characteristic features which clearly differ from classic oral injuries observed with cytotoxic chemotherapy and/or radiotherapy. In addition, they frequently affect more than 20% of treated patients and can lead to a significant morbidity or permanent treatment discontinuation. Oral mucosal toxicities described in this review include mTOR inhibitor-associated stomatitis (mIAS); stomatitis, benign migratory glossitis, and osteonecrosis of the jaw associated with multi-targeted kinase inhibitors of the VEGF and PDGF receptors; mucositis induced by EGFR inhibitors (in monotherapy or in combination with head and neck radiotherapy and/or chemotherapy); hyperkeratotic lesions with BRAF inhibitors; pigmentary changes and lichenoid reactions secondary to imatinib; and more recent data on the BOsler-Weber-Rendu-like syndrome^described with the antibody-drug conjugate, TDM-1. Finally, we provide, to our knowledge, the first available structured data on oral toxicities induced by the new recently FDA-and EMA-approved monoclonal antibodies targeting PD-1. Clinical management of these targeted therapy-related oral changes is also discussed.

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Clinical and Histologic Features of Lichenoid Mucocutaneous Eruptions Due to Anti–Programmed Cell Death 1 and Anti–Programmed Cell Death Ligand 1 Immunotherapy

et al. 2016

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Importance: Antagonist antibodies to programmed cell death 1 (PD-1) and programmed cell death ligand 1 (PD-L1) have shown remarkable activity in multiple tumor types. Recent US Food and Drug Administration approval of such agents for advanced melanoma, non-small cell lung cancer, and renal cell carcinoma has hastened the need to better characterize their unique toxicity profiles.Objective: To provide a clinical and pathologic description of the lichenoid mucocutaneous adverse effects seen in patients receiving anti-PD-1/PD-L1 treatment.Design, Setting, and Participants: Patients with advanced cancer who were referred to dermatology at Yale-New Haven Hospital, a tertiary care hospital, after developing cutaneous adverse effects while receiving an anti-PD-1 or PD-L1 antibody therapy either as monotherapy or in combination with another agent were identified. Medical records from 2010 to 2015 and available skin biopsy specimens were retrospectively reviewed.

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Immunohistochemical analysis of lichenoid reactions in patients treated with anti‐PD‐L1 and anti‐PD‐1 therapy

Abstract: These findings expand the literature of immune-related toxicities of PD-L1 and PD-1 blockade to include lichenoid dermatitis and lichenoid mucositis. Of note, these cutaneous side effects were amenable to topical treatment, without the need for medication dose reduction or discontinuation.

Cited by 115 publications

References 13 publications

Excellent Response to Anti-PD-1 Therapy in a Patient with Hepatocellular Carcinoma Intolerant to Sorafenib

Excellent Response to Anti-PD-1 Therapy in a Patient with Hepatocellular Carcinoma Intolerant to Sorafenib

Oral mucosal changes induced by anticancer targeted therapies and immune checkpoint inhibitors

Clinical and Histologic Features of Lichenoid Mucocutaneous Eruptions Due to Anti–Programmed Cell Death 1 and Anti–Programmed Cell Death Ligand 1 Immunotherapy

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