Epidermal Growth Factor-Related Peptides in Endocrine Neoplasias

Salomon, David; Bianco, Caterina; Santis, Marta De; Martínez-Lacaci, Isabel; Wechselberger, Christian; Ebert, Andreas D.

doi:10.1007/978-1-59259-223-4_9

Cited by 2 publications

(3 citation statements)

References 346 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…58 EGFR and ER␣ also are inversely related in human breast tumors. [15][16][17] In our model, transgenic TGF␣ reduced ER␣ expression in Figure 8. PRL and TGF␣ together prolong ERK1/2 phosphorylation.…”

Section: Discussionmentioning

confidence: 99%

“…Elevated TGF␣, EGFR, and ErbB2 are associated with ER loss and antiestrogen resistance in breast tumors. [15][16][17] TGF␣ is also a potent, well-characterized oncogene in transgenic mice. 18 Transgenic mammary TGF␣ overexpression driven by several promoters, including whey acidic protein (WAP), MT, and mouse mammary tumor virus (MMTV), result in premature alveolar development, delayed involution after lactation, increased number of preneoplastic lesions, and eventually tumors.…”

Section: Prolactin Influences Mammary Development and Carcinogenesis mentioning

confidence: 99%

“…9 -13 TGF␣ is overexpressed in 50 to 70% of human breast tumors. 14,15 It binds to epidermal growth factor receptor (EGFR, ErbB1) and activates both EGFR homodimers and EGFR/ErbB2 heterodimers. Elevated TGF␣, EGFR, and ErbB2 are associated with ER loss and antiestrogen resistance in breast tumors.…”

mentioning

confidence: 99%

See 2 more Smart Citations

Prolactin Potentiates Transforming Growth Factor α Induction of Mammary Neoplasia in Transgenic Mice

Arendt

Rose-Hellekant

Sandgren

et al. 2006

The American Journal of Pathology

View full text Add to dashboard Cite

Prolactin influences mammary development and carcinogenesis through endocrine and autocrine/paracrine mechanisms. In virgin female mice, pro-lactin overexpression under control of a mammary selective nonhormonally responsive promoter, neu-related lipocalin, results in estrogen receptor alpha (ERalpha)-positive and ERalpha-negative adenocarcinomas. However, disease in vivo occurs in the context of dysregulation of multiple pathways. In this study, we investigated the ability of prolactin to modulate carcinogenesis when co-expressed with the potent oncogene transforming growth factor alpha (TGFalpha) in bitransgenic mice. Prolactin and TGFalpha cooperated to reduce dramatically the latency of mammary macrocyst development, the principal lesion type induced by TGFalpha. In combination, prolactin and TGFalpha also increased the incidence and reduced the latency of other preneoplastic lesions and increased cellular turnover in structurally normal alveoli and ducts compared with single transgenic females. Bitransgenic glands contained higher levels of phosphorylated ERK1/2 compared with single TGFalpha transgenic glands, suggesting that this kinase may be a point of signaling crosstalk. Furthermore, transgenic prolactin also reversed the decrease in ERalpha induced by neu-related lipocalin-TGFalpha. Our findings demonstrate that locally produced prolactin can strikingly potentiate the carcinogenic actions of another oncogene and modify ovarian hormone responsiveness, suggesting that prolactin signaling may be a potential therapeutic target.

show abstract

Section: Discussionmentioning

confidence: 99%