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vasoactive intestinal peptide/cancer mamar

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ArticoleStudii cliniceBrevete
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Vasoactive intestinal peptide (VIP) induces transactivation of EGFR and HER2 in human breast cancer cells.

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We analyzed the cross-talk between receptors for vasoactive intestinal peptide (VIP) and the human epidermal growth factor family of tyrosine kinase receptors (HER) in oestrogen-dependent (T47D) and oestrogen-independent (MDA-MB-468) human breast cancer cells. VIP treatment slowly increased the
High-performance liquid chromatography-purified 125I-vasoactive intestinal peptide (VIP) bound to T-47D human breast cancer cells in a specific, saturable, and reversible manner. Scatchard plots were compatible with the presence of one class of VIP receptors with high affinity (Kd = 4.5 X 10(-10) M
Vasoactive intestinal peptide and pituitary adenylate cyclase activating peptide have high affinity for VPAC1, VPAC2 and PAC1 receptors overexpressed on human cancer cells. Four potent analogues of these peptides, TP3939, TP3982, TP4200 and TP3805 were labeled with (64)Cu and evaluated ex vivo and
Previous studies have shown that vasoactive intestinal peptide (VIP) and its receptors (VPAC(1) and VPAC(2) receptors) are involved in promotion and growth of many human tumours including breast cancer. Here we investigated whether VIP regulates the expression of the main angiogenic factor, vascular
OBJECTIVE A 18fluorine-labeled derivative of vasoactive intestinal peptide [18F- Arg,Arg VIP(18F-dVIP)] was evaluated as a potential imaging agent for breast cancer by comparison with 2-deoxy-2-[18F]fluoro-D-glucose (FDG) using standard ex vivo determinations and small animal position emission

Breast cancer growth is inhibited by vasoactive intestinal peptide (VIP) hybrid, a synthetic VIP receptor antagonist.

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Breast cancer vasoactive intestinal peptide (VIP) receptors were characterized. Using in vitro autoradiographic techniques, 125I-labeled VIP bound with high affinity to breast biopsy sections. 125I-labeled VIP bound specifically to give breast cancer cell lines examined using receptor-binding

Vasoactive intestinal peptide-camptothecin conjugates inhibit the proliferation of breast cancer cells.

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The effects of vasoactive intestinal peptide-camptothecin (VIP-CPT) conjugates were investigated on breast cancer cells and cells transfected with VIP receptors (R). (Ala(2,8,9,19,24.25.27), Nle(17), Lys(28))VIP, (A-NL-K)VIP, was synthesized and Lys(28) was coupled to a linker,
Vasoactive intestinal peptide (VIP) and pituitary adenylate cyclase-activating peptide (PACAP) bind similarly to VPAC1 and VPAC2 receptors, whereas PACAP binds with higher affinity than VIP to PAC1 receptors. Here we demonstrate by different approaches the expression of the three subclasses of

Nuclear localization of vasoactive intestinal peptide (VIP) receptors in human breast cancer.

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Vasoactive intestinal peptide (VIP) and its receptors (VPACs) are involved in proliferation, survival, and differentiation in human breast cancer cells. Its mechanism of action is traditionally thought to be through specific plasma membrane receptors. There is compelling evidence for a novel

Detection of VIP receptors in MNU-induced breast cancer in rats: implications for breast cancer targeting.

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Vasoactive intestinal peptide (VIP) is a 28 amino acid neuropeptide with a wide range of biological activities. Receptors for VIP (VIP-R) are overexpressed in breast cancer, where they may have diagnostic and therapeutic implications. Although N-methyl nitrosourea (MNU)-induced breast cancer in rats

In vitro identification of vasoactive intestinal peptide receptors in human tumors: implications for tumor imaging.

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In vitro receptor measurements in tumors were performed to evaluate the potential of the vasoactive intestinal peptide receptor (VIP-R) as an imaging tool in human cancer. METHODS Three hundred thirty-nine human tumors were investigated for their VIP-R content by in vitro receptor autoradiography on

VIP receptors as molecular targets of breast cancer: implications for targeted imaging and drug delivery.

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Receptors for vasoactive intestinal peptide (VIP-R) are overexpressed in human breast cancer. This phenomenon may have important diagnostic and therapeutic implications because carrier systems loaded with imaging or therapeutic agents, and with surface ligands to VIP-R could potentially be actively
Breast cancer is a leading cause of cancer deaths among women in the US, with 40 % chance of relapse after treatment. Recent studies outline the role of cancer stem cells (CSCs) in tumor initiation, propagation, and regeneration of cancer. Moreover, it has been established that breast CSCs reside in

PET imaging of oncogene overexpression using 64Cu-vasoactive intestinal peptide (VIP) analog: comparison with 99mTc-VIP analog.

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The purpose of this study was to assess the feasibility of PET imaging of oncogene VPAC1 receptors overexpressed in human breast cancer cells. METHODS Vasoactive intestinal peptide (VIP) analog (TP3982) was synthesized to harbor a carboxy-terminus lysine (Lys) residue separated from VIP-asparagine

Intracellular delivery of VIP-grafted sterically stabilized phospholipid mixed nanomicelles in human breast cancer cells.

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The purpose of this study was to determine whether biocompatible and biodegradable vasoactive intestinal peptide-grafted sterically stabilized phospholipid mixed nanomicelles (VIP-SSMM; size, approximately 15 nm), a novel nanosized actively targeted drug delivery platform for breast cancer,
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