@article {VESELY5693, author = {DAVID L. VESELY}, title = {Heart Peptide Hormones: Adjunct and Primary Treatments of Cancer}, volume = {36}, number = {11}, pages = {5693--5700}, year = {2016}, publisher = {International Institute of Anticancer Research}, abstract = {Four heart hormones, namely atrial natriuretic peptide (ANP), long-acting natriuretic peptide (LANP), vessel dilator and kaliuretic peptide reduce up to 97\% of cancer cells in vitro. These four cardiac hormones eliminate up to 80\% of human pancreatic adenocarcinomas, two-thirds of human breast carcinomas and up to 86\% of human small-cell lung carcinomas growing in athymic mice. ANP given intravenously for 3 hours after {\textquoteleft}curative{\textquoteright} lung surgery as an adjunct to surgery results in a 2-year relapse-free survival of 91\% compared to 75\% for those treated with surgery alone. The anticancer mechanisms of action of these peptides involve binding to receptors on the cancer cells, followed by 95\% inhibition of the conversion of inactive to active rat sarcoma-bound guanosine triphosphate (RAS)-mitogen-activated protein kinase (MAPK) kinases 1/2 (MEK 1/2) (98\% inhibition)-extracellular signal-related kinases 1/2 (ERK1/2) (96\% inhibition) cascade in cancer cells. They are dual inhibitors of vascular endothelial growth factor (VEGF) and its VEGF2 receptor (up to 89\%). They also inhibit MAPK9, i.e. c-JUN-N-terminal kinase 2. One of the downstream targets of VEGF is β-catenin, which these peptides inhibit by up to 88\%. These four peptide hormones inhibit the Wingless-related integration site (WNT) pathway 68\% and WNT secreted-Frizzled protein is reduced by up to 84\%. Signal transducer and activator of transcription 3 (STAT3), a final {\textquoteleft}switch{\textquoteright} that activates gene expression that leads to malignancy, is specifically reduced up to 88\% by these peptides but they do not affect STAT1. There is crosstalk between the RAS-MEK 1/2-ERK 1/2 kinase cascade, VEGF, β-catenin, JNK, WNT, and STAT pathways and each of these pathways and their crosstalk is inhibited by these peptide hormones. They enter the nucleus of cancer cells where they inhibit the proto-oncogenes c-FOS (by up to 82\%) and c-JUN (by up to 61\%). Conclusion: These multiple kinase inhibitors have both adjunct and primary anticancer effects.}, issn = {0250-7005}, URL = {https://ar.iiarjournals.org/content/36/11/5693}, eprint = {https://ar.iiarjournals.org/content/36/11/5693.full.pdf}, journal = {Anticancer Research} }