scholarly journals Severe EGFR inhibitor-induced acneiform eruption responding to dapsone

2021 ◽  
Vol 27 (7) ◽  
Author(s):  
Abram Beshay ◽  
Marta Petersen ◽  
Jamie L W Rhoads
Keyword(s):  
Egfr Inhibitor ◽  
Acneiform Eruption

scholarly journals Cetuximab Induced Hidrocystomas: A Case Report

2020 ◽  
Vol 4 (5) ◽  
pp. 443-445
Author(s):  
Nicole Nagrani ◽  
David E Castillo ◽  
Mariya Miteva ◽  
Anna Nichols
Keyword(s):  
Hair Follicle ◽  
Growth Factor Receptor ◽  
Sweat Glands ◽  
Egfr Inhibitor ◽  
Sweat Duct ◽  
Metastatic Colorectal Carcinoma ◽  
Eccrine Gland ◽  
First Case ◽  
Acneiform Eruption ◽  
Epidermal Growth

Cetuximab is an epidermal growth factor receptor (EGFR) inhibitor that commonly results in follicular-based acneiform eruptions. EGFR is expressed in the epidermis, hair follicle epithelium, sweat gland apparatus, and plays an important role in the differentiation and development of the hair follicle. In this report we describe a 70-year-old man who developed an acneiform eruption on his nose, cheeks, neck, and back when cetuximab was started for metastatic colorectal carcinoma.  This initial eruption improved with cessation of cetuximab but left residual cystic papules on his nose and multiple superficial white cysts on his bilateral cheeks, neck and back. Skin biopsy of a representative lesion on the nose revealed a cyst-like cavity lined with epithelium similar to sweat glands within the dermis consistent with a hidrocystoma. In this case, it is plausible that the use of an EGFR inhibitor resulted in a cutaneous inflammatory reaction, that subsequently healed with blockage of the sweat duct apparatus causing the formation of cutaneous cysts, including both hidrocystomas and milia. Alternatively, the blockage of the duct may have resulted from inhibition of basal cell migration and increased cell adhesion within the eccrine gland causing accumulation of eccrine gland secretion, and eventually hidrocystomas. To our knowledge, this is the first case describing the resolution of a typical cetuximab-induced acneiform eruption with residual hidrocystomas and milia.

A case of successfully treated recalcitrant EGFR inhibitor-induced acneiform eruption following non-ablative fractional laser

2016 ◽  
Vol 29 (4) ◽  
pp. 252-254 ◽  
Author(s):  
Joong Woon Choi ◽  
Tae In Kim ◽  
Ki-Heon Jeong ◽  
Min Kyung Shin
Keyword(s):  
Egfr Inhibitor ◽  
Fractional Laser ◽  
Acneiform Eruption ◽  
Ablative Fractional Laser

scholarly journals DRES-13. DUAL KINASE INHIBITION TO COMBAT EGFR-INHIBITOR RESISTANCE IN GLIOBLASTOMA

2019 ◽  
Vol 21 (Supplement_6) ◽  
pp. vi74-vi74
Author(s):  
Erin Smithberger ◽  
Abigail Shelton ◽  
Madison Butler ◽  
Alex Flores ◽  
Ryan Bash ◽  
...  
Keyword(s):  
Kinase Inhibitors ◽  
Alternative Pathway ◽  
Growth Factor Receptor ◽  
Cell Types ◽  
Genetically Engineered ◽  
Differentially Expressed ◽  
Egfr Inhibitor ◽  
Tumor Resistance ◽  
Pten Deletion ◽  
In Cells

Abstract Glioblastoma (GBM) is an aggressive primary brain tumor with a poor survival rate. One of the most common molecular alterations seen in GBM is amplification and/or mutation of the Epidermal Growth Factor Receptor (EGFR), which has made it an attractive therapeutic target. However, several EGFR tyrosine kinase inhibitors have been tested clinically in GBM with minimal success. One reason for this lack of efficacy could be due to acute, adaptive resistance via alternative pathway activation. To investigate this mechanism of tumor resistance, we used RNA-seq and multiplex inhibitor bead/mass spectrometry (MIB-MS) to analyze the transcriptomes and kinomes of genetically engineered murine astrocytes with common GBM genotypes. We have previously shown that 38% of the expressed kinome varied among a panel of diverse nGEM astrocytes harboring Cdkn2a deletion (C) plus Pten deletion (CP), wild-type human EGFR (CE) or EGFRvIII (CEv3) overexpression or both EGFRvIII overexpression and Pten deletion (CEv3P). Although CE have a similar transcriptional profile to C cells at baseline, when treated with the EGFR inhibitor afatinib, CE respond more similarly to CEv3 cells. When cells containing endogenous murine EGFR (C and CP) are treated with afatinib, fewer than 0.5% of kinases showed differential expression. In cells with EGFR overexpression alone, more than 6% of kinases were differentially expressed upon afatinib treatment, including Ntrk3, Fgfr2 and 3, Lyn, Bmx, Epha2 and 5, Fn3k, a kinase involved in fructosamine processing, and Nrbp2, a kinase involved in regulation of apoptosis. This effect was blunted in cells lacking Pten in addition to having EGFRvIII (CEv3P), resulting in less than 2% of kinases being differentially expressed. The only kinase upregulated in all three EGFR-overexpressing cell types was Coq8a, which is involved in electron transport and response to DNA damage. Given this overlap in response, Coq8a could be a potential dual treatment target for GBM.

scholarly journals BEBT-109, a pan-mutant-selective EGFR inhibitor with potent antitumor activity in EGFR-mutant non-small cell lung cancer

2021 ◽  
Vol 14 (2) ◽  
pp. 100961
Author(s):  
Fushun Fan ◽  
Minhua Zhou ◽  
Xiaolan Ye ◽  
Zhenxian Mo ◽  
Yaru Ma ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Antitumor Activity ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Egfr Inhibitor ◽  
Small Cell Lung ◽  
Egfr Mutant

scholarly journals CALM1 promotes progression and dampens chemosensitivity to EGFR inhibitor in esophageal squamous cell carcinoma

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Tao Liu ◽  
Xiujuan Han ◽  
Shutao Zheng ◽  
Qing Liu ◽  
Aerziguli Tuerxun ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Prognostic Significance ◽  
Xenograft Model ◽  
Combined Effect ◽  
Egfr Inhibitor ◽  
Knock Out ◽  
And Migration

Abstract Background Calmodulin1 (CALM1) has been identified as one of the overexpression genes in a variety of cancers and EGFR inhibitor have been widely used in clinical treatment but it is unknown whether CALM1 and epidermal growth factor receptor (EGFR) have a synergistic effect in esophageal squamous cell carcinoma (ESCC). The aim of the present study was to explore the synergistic effects of knock-out CALM1 combined with EGFR inhibitor (Afatinib) and to elucidate the role of CALM1 in sensitizing the resistance to Afatinib in ESCC. Method Immunohistochemistry (IHC) and qRT-PCR were used to examine the expression of CALM1 and EGFR in ESCC tissues. Kaplan–Meier survival analysis was used to analyze the clinical and prognostic significance of CALM1 and EGFR expression in ESCC. Furthermore, to evaluate the biological function of CALM1 in ESCC, the latest gene editing technique CRISPR/Cas9(Clustered regularly interspaced short palindromic repeats)was applied to knockout CALM1 in ESCC cell lines KYSE150, Eca109 and TE-1. MTT, flow cytometry, Transwell migration, scratch wound-healing and colony formation assays were performed to assay the combined effect of knock-out CALM1 and EGFR inhibitor on ESCC cell proliferation and migration. In addition, nude mice xenograft model was used to observe the synergistic inhibition of knock-out CALM1 and Afatinib. Results Both CALM1 and EGFR were found to be significantly over-expressed in ESCC compared with paired normal control. Over-expressed CALM1 and EGFR were significantly associated with clinical stage, T classification and poor overall prognosis, respectively. In vitro, the combined effect of knock-out CALM1 mediated by the lentivirus and EGFR inhibitor was shown to be capable of inhibiting the proliferation, inducing cell cycle arrest at G1/S stage and increasing apoptosis of KYSE-150 and Eca109 cells; invasion and migration were also suppressed. In vivo, the results of tumor weight and total fluorescence were markedly reduced compared with the sgCtrl-infected group and sgCAML1 group. Conclusion Our data demonstrated that knock-out of CALM1 could sensitize ESCC cells to EGFR inhibitor, and it may exert oncogenic role via promotion of EMT. Taken together, CALM1 may be a tempting target to overcome Afatinib resistance.

cSCC: EGFR-Inhibitor bei immunkompromittierten Patienten

2020 ◽  
Vol 23 (4) ◽  
pp. 59-59
Author(s):  
Friederike Klein
Keyword(s):  
Egfr Inhibitor
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