title: Spared pre-irradiated area in pustular lesions induced by icotinib showing decreased expressions of CD1a+ langerhans cells and FGFR2.
abstract: Icotinib hydrochloride, a novel inhibitor of epidermal growth factor receptor tyrosine kinase, has been approved by the State Food and Drug Administration for the treatment of advanced non-small-cell lung cancer. Up to date, cutaneous response to icotinib is largely unknown. Here we report an uncommon lesional phenomenon in a 56-year-old Chinese male with non-small-cell lung cancer, who received icotinib as a second-line treatment. Characteristic papulopustular rash on the chest and back was observed 4 days later. Interestingly, the rash completely spares a pre-irradiated area. The immunohistochemical study in the lesional skin area and spared skin area revealed a significant decrease in CD1a(+) Langerhans cells, Ki-67 as well as FGFR2 in the spared area than in the lesional area. Thus, the present case indicated that loss of the basal layer of proliferative cells and antigen-presenting cells (Langerhans cell), as well as the down-regulation of FGFR2 signaling in the pre-irradiated skin area, may join forces in inhibiting icotinib-associated cutaneous reactions. To our knowledge, this is the first report of both lesional area and lesion-spared area in a Chinese male receiving treatment with a new epidermal growth factor receptor-tyrosine kinase inhibitor (icotinib). The immunohistochemical reactions described here also provide new insight into the pathogenesis of epidermal growth factor receptor-tyrosine kinase inhibitor-related skin toxicities, and the role that other tyrosine kinase receptors (including FGFR) played in non-small-cell lung cancer.
authors.affiliation: Department of Thoracic Oncology, 1st Affiliated Hospital, Zhejiang University School of Medicine, 79 Qing Chun Road, Hangzhou 310003, China.
authors.forename: Qiong
authors.initials: Q
authors.lastname: Zhao
authors.forename: Yi Na
authors.initials: YN
authors.lastname: Wang
authors.forename: Bo
authors.initials: B
authors.lastname: Wang
mesh_terms: D017486:Acneiform Eruptions / Q000139:chemically induced* / Q000378:metabolism; D000230:Adenocarcinoma / Q000188:drug therapy / Q000378:metabolism / Q000532:radiotherapy; D000077192:Adenocarcinoma of Lung; D018949:Antigens, CD1 / Q000378:metabolism*; D000970:Antineoplastic Agents / Q000008:administration & dosage / Q000009:adverse effects*; D001706:Biopsy; D001768:Blister / Q000139:chemically induced; D017024:Chemotherapy, Adjuvant; D043844:Crown Ethers / Q000008:administration & dosage / Q000009:adverse effects*; D019583:Dose Fractionation, Radiation; D015536:Down-Regulation / Q000187:drug effects; D003875:Drug Eruptions / Q000209:etiology* / Q000378:metabolism; D004791:Enzyme Inhibitors / Q000009:adverse effects; D066246:ErbB Receptors / Q000378:metabolism*; D005145:Face; D005499:Folliculitis / Q000139:chemically induced; D006801:Humans; D007150:Immunohistochemistry; D019394:Ki-67 Antigen / Q000378:metabolism; D007801:Langerhans Cells / Q000378:metabolism*; D008175:Lung Neoplasms / Q000188:drug therapy / Q000378:metabolism / Q000532:radiotherapy; D008297:Male; D008875:Middle Aged; D011505:Protein-Tyrosine Kinases / Q000037:antagonists & inhibitors; D011799:Quinazolines / Q000008:administration & dosage / Q000009:adverse effects*; D051497:Receptor, Fibroblast Growth Factor, Type 2 / Q000378:metabolism*; D012867:Skin / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D035441:Thoracic Wall
chemical_list: D018949:Antigens, CD1; D000970:Antineoplastic Agents; C419393:CD1a antigen; D043844:Crown Ethers; D004791:Enzyme Inhibitors; D019394:Ki-67 Antigen; D011799:Quinazolines; C531470:icotinib; D066246:ErbB Receptors; C496353:FGFR2 protein, human; D011505:Protein-Tyrosine Kinases; D051497:Receptor, Fibroblast Growth Factor, Type 2