EGF/ErbB Receptor Family in Ovarian Cancer

Maihle, Nita J.; Baron, Andre T.; Barrette, Brigitte A.; Boardman, Cecelia H.; Christensen, Trace; Cora, Elsa M.; Faupel-Badger, Jessica M.; Greenwood, Tammy M.; Juneja, Subhash C.; Lafky, Jacqueline M.; Lee, H.; Reiter, Jill L.; Podratz, Karl C.

doi:10.1007/978-1-4757-3587-1_11

Cited by 79 publications

(81 citation statements)

References 61 publications

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“…Several mechanisms have been suggested for the origin of serum EGFR: proteolytic cleavage of the extracellular domain of the EGFR glycoprotein and/or alternate transcription of primary messenger RNA. 3 Potential explanations for decreased serum EGFR levels in a proportion of patients with metastatic breast cancer include: 1) Increased circulating TGF-a levels, which have been reported in serum from patients with breast cancer, 44 may form complexes with circulating EGFR and, subsequently, may be cleared more rapidly from the circulation; and 2) an internal autocrine mechanism also may occur in which newly synthesized TGF-a binds to and activates EGFR, with the result that less EGFR would be available for proteolysis at the tumor cell surface. With either of these mechanisms, activation of the EGFR pathway may explain the decreased serum EGFR levels and the worse prognosis observed in these patients.…”

Section: Discussionmentioning

confidence: 99%

“…[1][2][3] Similar to other growth factor receptors, 4 EGFR has 3 major domains: an intracellular protein tyrosine kinase, an extracellular glycosylated ligand-binding domain, and a hydrophobic transmembrane anchor that connects the other 2 domains. 5,6 Activation of EGFR ultimately results in cell cycle progression through various mechanisms, including initiation of Src family kinases, phosphatidylinositol-3 kinase (PI3 kinase), and mitogen-activated protein kinase.…”

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confidence: 99%

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Serum epidermal growth factor receptor/HER‐2 predicts poor survival in patients with metastatic breast cancer

Souder

Leitzel

Ali

et al. 2006

Cancer

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BACKGROUND.Epidermal growth factor receptor (EGFR, HER‐1, and erbB1) is overexpressed in primary breast cancer and had been identified as a poor prognostic factor.METHODS.Pretreatment serum EGFR levels were quantified by using an enzyme‐linked immunoadsorbent assay in a Phase III first‐line trial of letrozole and tamoxifen and were correlated with patient outcomes.RESULTS.Serum EGFR levels in a control group of 117 healthy, postmenopausal women measured 64.1 ± 13.3 ng/mL (mean ± standard deviation). Using a cutoff EGFR level of 44.1 ng/mL from the control group (5% nonparametric method), 53 of 535 patients (10%) had decreased serum levels of EGFR. Patients with decreased serum EGFR had no significant difference in objective response rate (ORR), clinical benefit rate (CBR), time to progression (TTP), or time to treatment failure (TTF); however, they did have significantly reduced survival compared with patients who had normal serum EGFR levels (median survival, 23.3 months vs. 30.9 months; P = .007). A combined analysis of pretreatment serum EGFR and HER‐2 yielded no additional predictive information for ORR, CBR, TTP, or TTF compared to serum HER‐2 alone. However, in the current analysis, a subgroup of patients who had decreased serum EGFR and normal serum HER‐2 was identified (n = 39 of 535 patients; 7.3%) that had significantly reduced survival compared with patients who had normal serum levels of both EGFR and HER‐2 (median survival, 23.5 months vs. 37.1 months; P = .005). In multivariate analysis, a decreased serum EGFR level remained a significant independent prognostic factor for decreased survival (hazards ratio, 1.58; P = .007).CONCLUSIONS.In patients who had metastatic breast cancer, decreased serum EGFR/normal serum HER‐2 predicted shorter survival compared with patients who had normal levels of serum EGFR/HER‐2. This patient subgroup deserves further study to assess their response to and selection for anti‐EGFR‐directed therapies. Cancer 2006. © 2006 American Cancer Society.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Serum epidermal growth factor receptor/HER‐2 predicts poor survival in patients with metastatic breast cancer

Souder

Leitzel

Ali

et al. 2006

Cancer

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“…Growth factors are a popular choice for optical imaging agents because, in addition to high-affi nity targeting, the ligand and its fl uorescent label are often internalized by the normal endocytic pathway, amplifying the signal in the tumor cells. Fluorochrome-labeled epidermal growth factor (EGF) has been a versatile tumor imaging agent because the epidermal growth factor receptor (EGFR) is overexpressed on the surface of many types of tumor cells [20], [21], [22], [23], and [24]. In a study measuring the diffusion of small molecules across the extracellular space in rat brains, Thorne et al [25] showed that EGF labeled with Oregon green 514 could be used as a reporter.…”

Section: Tumor Surface Proteinsmentioning

confidence: 99%

A systematic approach to the development of fluorescent contrast agents for optical imaging of mouse cancer models

Kovar

Simpson

Schutz-Geschwender

et al. 2007

Analytical Biochemistry

141

142

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“…As the normal ovaries were not microdissected before RNA extraction and profiling and therefore contain a high proportion of stromal tissue compared to epithelial cells, these genes likely reflect epithelial-specific genes expressed in MOC. Nonetheless, the majority of these genes are common to all subtypes of ovarian cancer, and several have been previously implicated in its pathogenesis, including TACSTD1 (Ep-CAM), CDH1 (E-cadherin), KLF5 (Kruppel-like factor 5) and ERB-B3 (Darai et al, 1997;Balzar et al, 1999;Maihle et al, 2002;Heinzelmann-Schwarz et al, 2004). Combining the two analyses, we identified that 13 of these 40 genes overlap with those that are upregulated in MOC compared to the other subtypes of ovarian cancer (highlighted in Table 3).…”

Section: Moc Exhibit a Gene Expression Profile Distinct From Other Ovmentioning

confidence: 99%

A distinct molecular profile associated with mucinous epithelial ovarian cancer

et al. 2006

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Mucinous epithelial ovarian cancers (MOC) are clinically and morphologically distinct from the other histological subtypes of ovarian cancer. To determine the genetic basis of MOC and to identify potential tumour markers, gene expression profiling of 49 primary ovarian cancers of different histological subtypes was performed using a customised oligonucleotide microarray containing 459 000 probesets. The results show that MOC express a genetic profile that both differs and overlaps with other subtypes of epithelial ovarian cancer. Concordant with its histological phenotype, MOC express genes characteristic of mucinous carcinomas of varying epithelial origin, including intestinal carcinomas. Differences in gene expression between MOC and other histological subtypes of ovarian cancer were confirmed by RT -PCR and/or immunohistochemistry. In particular, galectin 4 (LGALS4) was highly and specifically expressed in MOC, but expressed at lower levels in benign mucinous cysts and borderline (atypical proliferative) tumours, supporting a malignant progression model of MOC. Hence LGALS4 may have application as an early and differential diagnostic marker of MOC.

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EGF/ErbB Receptor Family in Ovarian Cancer

Cited by 79 publications

References 61 publications

Serum epidermal growth factor receptor/HER‐2 predicts poor survival in patients with metastatic breast cancer

Serum epidermal growth factor receptor/HER‐2 predicts poor survival in patients with metastatic breast cancer

A systematic approach to the development of fluorescent contrast agents for optical imaging of mouse cancer models

A distinct molecular profile associated with mucinous epithelial ovarian cancer

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