Erupsi Akneiformis Pada AML Dengan Regimen Kemoterapi “3 + 7”

Bayu Prio Septiantoro; Indra Pradipta

doi:10.36408/mhjcm.v8i2.609

Erupsi Akneiformis Pada AML Dengan Regimen Kemoterapi “3 + 7”

Medica Hospitalia : Journal of Clinical Medicine ◽

10.36408/mhjcm.v8i2.609 ◽

2021 ◽

Vol 8 (2) ◽

pp. 248-251

Author(s):

Bayu Prio Septiantoro ◽

Indra Pradipta

Keyword(s):

Egfr Inhibitor ◽

Akne Vulgaris

Latar belakang: Kemoterapi bertanggung jawab terhadap sebagian besar manifestasi kulit dalam perawatan pasien kanker. Daunorubicin selama 3 hari ditambah sitarabin selama 7 hari untuk kemoterapi induksi pada pasien dengan AML dikenal sebagai regimen “3 + 7.” Walaupun erupsi akneiformis biasanya muncul pada pasien yang mendapatkan agen penghambat EGFR dan antibodi monoclonal, reaksi kulit ini juga dapat dialami pasien yang mendapatkan regime daunorubicin atau sitarabin. Laporan kasus: Seorang wanita berusia 19 tahun dengan diagnosa AML masuk rumah sakit untuk menjalani kemoterapi dengan regimen 3+7 (daunorubicin 45mg/m2 selama 3 hari dan sitarabin 100mg/m2 selama 7 hari). Setelah hari pertama kemoterapi diberikan, muncul akne berupa bintik merah di wajah dan bertambah berat setelah sesi kemoterapi selesai dimana meluas hingga ke leher, dada dan punggung bahkan ke daerah kulit kepala, dengan adanya rasa gatal, papul dan eritema. Ia terdiagnosa erupsi akneiformis. Tujuan: Untuk melaporkan kasus reaksi kulit berupa erupsi aneiformis pada pasien dengan diagnose AML yang menjalani kemoterapi dengan regime 3+7. Pembahasan: Lesi erupsi akneiformis biasanya muncul sebagai papula dan pustula inflamasi monomorfik yang biasanya melibatkan wajah, leher, dada, punggung atas dan dapat diperluas hingga selain daerah seboroik. Beberapa karakteristik dapat membantu untuk mendukung hubungan potensial antara obat dengan munculnya akne. Diantaranya yang teridentifikasi pada pasien ini yaitu timbulnya akne secara tiba-tiba tanpa adanya riwayat akne vulgaris sebelumnya, lesi monomorfik dengan inflamasi, serta sedikit komedo dan kista. Terdapat empat tingkatan yang dapat digunakan dalam mengklasifikasikan keparahan efek samping kulit ini dimana tingkat III (berat) dapat diberikan antibiotik secara oral seperti klindamisin 300mg/12 jam. Kesimpulan: Reaksi kulit berupa erupsi akneiformis dapat muncul pada pasien yang mendapatkan obat selain EGFR inhibitor dan antibodi monoclonal yaitu daunorubisin dan atau sitarabin. Perlu dilakukan penelitian lebih lanjut untuk mengetahui agen spesifik yang menjadi penyebab, serta mekanisme terjadinya reaksi tersebut.

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Tetracycline Limits Severity of EGFR Inhibitor Rash

Skin & Allergy News ◽

10.1016/s0037-6337(07)70625-3 ◽

2007 ◽

Vol 38 (8) ◽

pp. 23

Author(s):

KERRI WACHTER

Keyword(s):

Egfr Inhibitor

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UJI KOMPARASI KADAR TESTOSTERON SERUM PADA BERBAGAI DERAJAT KEPARAHAN AKNE VULGARIS LAKI-LAKI

Media Dermato Venereologica Indonesiana ◽

10.33820/mdvi.v46i2.56 ◽

2019 ◽

Vol 46 (2) ◽

Author(s):

Firmina Kus Setianingrum ◽

Tantari SHW ◽

Arif Widiatmoko

Keyword(s):

Post Hoc ◽

Akne Vulgaris

Hormon testosteron merupakan prekursor adrenal poten yang menyebabkan peningkatan ukuran, sekresi, serta fungsi kelenjar sebasea dengan mengikat reseptor adrenal, peningkatan proliferasi keratinosit folikuler yang dapat menyumbat kanal pilosebasea dan mengakibatkan obstruksi aliran sebum, sehingga terjadi pembentukan mikrokomedo, sebagai lesi awal akne vulgaris (AV).Tujuan penelitian menentukan kadar testosteron serum dan uji beda kadar testosteron serum pada berbagai derajat keparahan AV. Metode penelitian secara potong lintang. Subyek penelitian adalah pasien AV laki-laki umur 13-30 tahun di instalasi rawat jalan (IRJ) Kulit dan Kelamin RSUD dr. Saiful Anwar, Malang, yang memenuhi kriteria penerimaan dan penolakan. Jumlah subyek 63 orang, terdiri dari AV derajat ringan, sedang, dan berat masing-masing berjumlah 21 orang.Hasil penelitian didapatkan rerata kadar testosteron serum AV ringan 6,66 ng/mL, AV sedang 8,11 ng/mL, dan AV berat 8,97 ng.mL. Komparasi rerata kadar testosteron serum ketiga derajat keparahan AV tidak menunjukkan perbedaan bermakna (p>0,05). Demikian pula hasil uji post hoc untuk mengetahui perbedaan kadar testosteron serum pada masing-masing derajat keparahan AV, yaitu AV ringan dengan sedang, ringan dengan berat dan sedang dengan berat menunjukkan hasil perbedaan tidak bermakna (p>0,05), walaupun nilai rerata pada masing-masing derajat keparahan AV lebih tinggi dibandingkan nilai normal.Disimpulkan tidak ada perbedaan bermakna kadar testosteron serum pada berbagai derajat keparahan AV.Kata kunci: hormon testosteron, akne vulgaris, laki-laki

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

Neuro-Oncology ◽

10.1093/neuonc/noz175.300 ◽

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.

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

Translational Oncology ◽

10.1016/j.tranon.2020.100961 ◽

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

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

Cancer Cell International ◽

10.1186/s12935-021-01801-6 ◽

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.

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Third‐generation EGFR inhibitor HS ‐10296 in combination with famitinib, a multi‐targeted tyrosine kinase inhibitor, exerts synergistic antitumor effects through enhanced inhibition of downstream signaling in EGFR ‐mutant non‐small cell lung cancer cells

Thoracic Cancer ◽

10.1111/1759-7714.13902 ◽

2021 ◽

Author(s):

Mi Zhang ◽

Haitian Quan ◽

Li Fu ◽

Yun Li ◽

Haoyu Fu ◽

...

Keyword(s):

Lung Cancer ◽

Cancer Cells ◽

Kinase Inhibitor ◽

Small Cell ◽

Third Generation ◽

Egfr Inhibitor ◽

Small Cell Lung ◽

Antitumor Effects ◽

Downstream Signaling ◽

Egfr Mutant

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cSCC: EGFR-Inhibitor bei immunkompromittierten Patienten

Im Focus Onkologie ◽

10.1007/s15015-020-2493-0 ◽

2020 ◽

Vol 23 (4) ◽

pp. 59-59

Author(s):

Friederike Klein

Keyword(s):

Egfr Inhibitor

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Refinement of Covalent EGFR Inhibitor AZD9291 to Eliminate Off-target Activity

Tetrahedron Letters ◽

10.1016/j.tetlet.2021.153178 ◽

2021 ◽

pp. 153178

Author(s):

Elise Bouffard ◽

Balyn W Zaro ◽

Melissa M Dix ◽

Benjamin Cravatt ◽

Chi-Huey Wong

Keyword(s):

Egfr Inhibitor ◽

Target Activity

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Incidence of Adverse Cutaneous Reactions to Epidermal Growth Factor Receptor Inhibitors in Patients with Non-Small-Cell Lung Cancer

Dermatology ◽

10.1159/000513233 ◽

2021 ◽

pp. 1-5

Author(s):

Paolo Gisondi ◽

Davide Geat ◽

Alessandra Mattiucci ◽

Fiorella Lombardo ◽

Antonio Santo ◽

...

Keyword(s):

Lung Cancer ◽

Epidermal Growth Factor Receptor ◽

Growth Factor Receptor ◽

Small Cell ◽

Egfr Inhibitor ◽

Small Cell Lung ◽

Nail Changes ◽

Cutaneous Reactions ◽

Epidermal Growth ◽

Oncologic Treatment

Background: Epidermal growth factor receptor (EGFR) inhibitors are routinely used in advanced non-small-cell lung cancer (NSCLC) harboring EGFR mutations. However, their use is associated with gastrointestinal and cutaneous toxicities, including acneiform eruptions, pruritus, xerosis, nail and hair changes. Aside from reducing patients’ quality of life, such cutaneous reactions have a considerable impact on the oncologic treatment given that dose reduction or even drug discontinuation may be necessary, especially for the severe forms. Objectives: To assess the incidence, impact on treatment and management of EGFR inhibitor-related cutaneous reactions in patients with NSCLC. Methods: We conducted a prospective observational study on 87 consecutive patients with advanced NSCLC treated with EGFR-tyrosine kinase inhibitors from January to December 2019. Patients who developed mucocutaneous reactions were evaluated and treated by both oncologists and dermatologists, and underwent dermatologic follow-up until resolution of the cutaneous reaction. Demographic and clinical data were collected for each patient, and the severity of the cutaneous reaction was graded using the Common Terminology Criteria for Adverse Events. Results: Seventy-one patients (81.6%) developed cutaneous reactions. The number of cutaneous reactions per patient was 1 in 37%, 2 in 41% and 3 or more in 22%. The most common cutaneous reactions included acneiform eruptions (56.3%), xerosis ± asteatotic eczema (48.3%), nail changes (39.1%), mucositis (29.9%), pruritus (24.1%) and hair changes (12.6%). Afatinib was associated with a higher rate of nail changes and mucositis (p < 0.01 and p < 0.005, respectively) compared to other agents, while no patient-related predictive factors were identified. Dose reduction was performed in 18% of patients. Multidisciplinary management involving dermatologists allowed to resume the drug in all patients who had discontinued it due to the cutaneous reactions. Conclusions: A multidisciplinary approach to EGFR inhibitor-related cutaneous reactions is advantageous and can reduce the need to discontinue oncologic treatment.

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