Abstract: Inhibitor peptides for combinatorial inactivation of ErbB1, ErbB2, and ErbB3 featuring an EGFR-based peptide and a cell penetrating component such as a protein transduction domain (e.g., PTD4) for enhancing penetration of the EGFR-based peptide into a cell. The EGFR peptide may be from 8 to 30 amino acids in length. The inhibitor peptides can inhibit tumor growth, reduce metastasis, activate apoptosis, activate necrosis, disrupt calcium signaling, and/or increase ROS. In some embodiments, the EGFR-based peptide is at least 50% identical to at least 8 consecutive residues of SEQ ID NO: 1.

Abstract: Observations regarding the role of MUC1 in promoting the nuclear accumulation of EGFR led us to propose the development of peptides to block nuclear accumulation of EGFR as a means to block breast cancer progression. One exemplary peptide, the ENLS1 peptide, promotes cell death in breast cancer cell lines. Studies in the MMTV-pyMT mouse model of breast cancer demonstrate significant anti-tumor activity.

Abstract: Inhibitor peptides for combinatorial inactivation of ErbB1, ErbB2, and ErbB3 featuring an EGFR-based peptide and a cell penetrating component such as a protein transduction domain (e.g., PTD4) for enhancing penetration of the EGFR-based peptide into a cell. The EGFR peptide may be from 8 to 30 amino acids in length. The inhibitor peptides can inhibit tumor growth, reduce metastasis, activate apoptosis, activate necrosis, disrupt calcium signaling, and/or increase ROS. In some embodiments, the EGFR-based peptide is at least 50% identical to at least 8 consecutive residues of SEQ ID NO: 1.

Abstract: MUC1 (DF3, CD227, episialin, PEM) is a heavily O-glycosylated heterodimeric protein of >300 kDa, normally expressed abundantly on the apical surface of glandular epithelia. MUC1 mimetic peptides are selectively retained in mammary gland tumors, colon and skin after systemic administration. Moreover, MUC1 mimetic peptides reduce tumor initiation. In addition, MUC1 mimetic peptides can be used in conjunction with other anti-EGFR treatments in the adjuvant context, i.e., after surgery.

Abstract: Cystatin C (CysC) and Galectin 3 (Gal-3) are biomarkers for pulmonary arterial hypertension (PAH), wherein elevated levels of one or other or both CysC and Gal-3 indicates a likelihood of PAH. Also provided are methods for identifying candidates for pulmonary arterial hypertension treatment and methods for monitoring therapeutic treatments of pulmonary arterial hypertension by monitoring levels of CysC and Gal-3 in the subject undergoing therapy.

Abstract: Observations regarding the role of MUC1 in promoting the nuclear accumulation of EGFR led us to propose the development of peptides to block nuclear accumulation of EGFR as a means to block breast cancer progression. One exemplary peptide, the ENLS1 peptide, promotes cell death in breast cancer cell lines. Studies in the MMTV-pyMT mouse model of breast cancer demonstrate significant anti-tumor activity.

Abstract: Interaction between MUC1 and ?-catenin can be interrupted using polypeptides or antibodies that specifically bind to the binding site on MUC1. Interruption provides the beneficial effect of inhibiting, reducing, and/or retarding invasiveness and metastasis. Fusion polypeptides and antibodies are provided to achieve a therapeutic effect.

Abstract: MUC1 (DF3, CD227, episialin, PEM) is a heavily O-glycosylated heterodimeric protein of >300 kDa, normally expressed abundantly on the apical surface of glandular epithelia. MUC1 mimetic peptides are selectively retained in mammary gland tumors, colon and skin after systemic administration. Moreover, MUC1 mimetic peptides reduce tumor initiation. In addition, MUC1 mimetic peptides can be used in conjunction with other anti-EGFR treatments in the adjuvant context, i.e., after surgery.

Abstract: Interaction between MUC1 and ?-catenin can be interrupted using polypeptides or antibodies that specifically bind to the binding site on MUC1. Interruption provides the beneficial effect of inhibiting, reducing, and/or retarding invasiveness and metastasis. Fusion polypeptides and antibodies are provided to achieve a therapeutic effect.

Abstract: Interaction between MUC1 and ?-catenin can be interrupted using polypeptides or antibodies that specifically bind to the binding site on MUC1. Interruption provides the beneficial effect of inhibiting, reducing, and/or retarding invasiveness and metastasis. Fusion polypeptides and antibodies are provided to achieve a therapeutic effect.

Abstract: Interaction between MUC1 and ?-catenin can be interrupted using polypeptides or antibodies that specifically bind to the binding site on MUC1. Interruption provides the beneficial effect of inhibiting, reducing, and/or retarding invasiveness and metastasis. Fusion polypeptides and antibodies are provided to achieve a therapeutic effect.