Growth suppression of colorectal cancer expressing S492R EGFR by monoclonal antibody CH12

Dong, Qian; Shi, Bizhi; Zhou, Min; Gao, Huile; Luo, Xiaoying; Li, Zonghai; Jiang, Hua

doi:10.1007/s11684-019-0682-z

Cited by 3 publications

(2 citation statements)

References 40 publications

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“…L688F and E690K were in exon 18 and K754E in exon 19, which is in contrast to others responsive to lapatinib treatment (Leslie et al, 2013;Reyes et al, 2014) Colorectal cancer: EGFR mutation status of 13 patients among 35 male and 23 female patients at different stages of colorectal cancer showed exon 20 mutation but not exons 18,19 and 21 mutations (Oh et al, 2011). S492R EGFR ectodomain mutation also increases the mutation rate and mABCH12 was suggested to prevent the effect of mutated EGFR (Dong et al, 2019).…”

Section: Homologymentioning

confidence: 82%

EGFR (Epidermal Growth Factor Receptor)

Hatil¹,

Çiçek²,

Oyken³

et al. 2020

Atlas of Genetics and Cytogenetics in Oncology and Haematology

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ERBB family member epidermal receptor tyrosine kinase (EGFR) is composed of 28 exons and 27 introns. EGFR codes for 11 transcripts and 8 of them are protein coding. EGFR is a transmembrane glycoprotein that can be activated by several different ligands such as epidermal growth factor (EGF), transforming growth factor-alpha (TGFA), heparin-binding EGF-like growth factor (HBEGF), betacellulin (BTC), amphiregulin (AREG), epiregulin (EREG), and epigen (EPGN) (Singh, 2016). Ligand binding induces the dimerization of EGFR and autophosphorylation followed by a cascade of downstream phosphorylation events (Capuani et al., 2015). EGFR activation plays a key role in cell survival, proliferation, migration and differentiation (Purba, 2017).

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Section: Homologymentioning

confidence: 82%

EGFR (Epidermal Growth Factor Receptor)

Hatil¹,

Çiçek²,

Oyken³

et al. 2020

Atlas of Genetics and Cytogenetics in Oncology and Haematology

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“…42 Amplifications are notably more prevalent in Chinese populations; around 14% of patients with KRAS/BRAF WT mCRC and 4.4% with RAS mutant disease. 43 An analysis of patients from the "FOCUS" and "PICCOLO" studies (n=1342) in mCRC demonstrated that Her2 amplification confers resistance to anti-EGFR treatment. 42,44 Her2 activating mutations, which are also rare in breast and gastric cancer, are found in around 2% of mCRC; these will not be identified by immunohistochemistry.…”

Section: Targeting Her2mentioning

confidence: 99%

<p>Refractory Metastatic Colorectal Cancer: Current Challenges and Future Prospects</p>

Lam¹,

Lum²,

Latham³

et al. 2020

CMAR

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Despite advances, patients with metastatic colorectal cancer (mCRC) still have poor long-term survival. Identification of molecular subtypes is important to guide therapy through standard treatment pathways and holds promise for the development of new treatments. Following standard firstand second-line chemotherapy plus targeted agents, many patients retain a reasonable performance status, and thus are seeking further effective treatment to extend life and maintain symptom control. The challenge lies in selecting the most appropriate therapy in the third-and fourth-line settings, from a range of options including the relatively new oral agents TAS-102 and regorafenib, or rechallenge with previous chemotherapy or anti-epidermal growth factor receptor (anti-EGFR) monoclonal antibodies (mAB). Beyond this, therapy consists of trials involving novel agents and new combinations of treatments with theoretical synergy and/or non-overlapping toxicity. There is a great focus on enhancing immunogenicity in mCRC, to reflect the impressive results of immunotherapy drugs in the small cohort with mismatch repair deficient (dMMR) mCRC. Rare molecular subtypes of mCRC are increasingly being identified, including Her2-positive disease, NTRK fusions and others. Clinical trials exploring the efficacy of immunomodulatory and precision agents are plentiful and will hopefully yield clinically meaningful results that can be rapidly translated into routine care.

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BRAF and KRAS mutations in metastatic colorectal cancer: future perspectives for personalized therapy

Zhao

et al. 2020

Gastroenterology Report

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Abstract Colorectal cancer (CRC) is one of the most commonly diagnosed cancers worldwide and 30% of patients with CRC experience metastasis. Patients with metastatic colorectal cancer (mCRC) have a 5-year overall survival rate of <10%. V-raf murine sarcoma viral oncogene homolog B1 (BRAF) and V-Ki-ras2 Kirsten ratsarcoma viral oncogene homolog (KRAS) mutations are mostly studied in mCRC, as clinical trials found that first-line chemotherapy with anti-epidermal growth factor receptor agent confers limited efficacy for mCRC. Treatment decisions for early-stage mCRC do not consider BRAF or KRAS mutations, given the dramatically poor prognosis conferred by these mutations in clinical trials. Thus, it is necessary to identify patients with mCRC harboring BRAF or KRAS mutations to formulate rational therapeutic strategies to improve prognosis and survival. BRAF and KRAS mutations occur in ∼10% and ∼44% of patients with mCRC, respectively. Although the survival rate of patients with mCRC has improved in recent years, the response and prognosis of patients with the aforementioned mutations are still poor. There is a substantial unmet need for prospective personalized therapies for patients with BRAF- or KRAS-mutant mCRC. In this review, we focus on BRAF and KRAS mutations to understand the mechanisms underlying resistance and improving the response rate, outcomes, and prognosis of patients with mCRC bearing these mutations and to discuss prospective personalized therapies for BRAF- and KRAS-mutant mCRC.

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Growth suppression of colorectal cancer expressing S492R EGFR by monoclonal antibody CH12

Cited by 3 publications

References 40 publications

EGFR (Epidermal Growth Factor Receptor)

EGFR (Epidermal Growth Factor Receptor)

<p>Refractory Metastatic Colorectal Cancer: Current Challenges and Future Prospects</p>

BRAF and KRAS mutations in metastatic colorectal cancer: future perspectives for personalized therapy

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