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Adipocyte-Derived Adipokines and Other Obesity-Associated Molecules in Feline Mammary Cancer

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BIOMEDICINES
卷 11, 期 8, 页码 -

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MDPI
DOI: 10.3390/biomedicines11082309

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feline mammary cancer; obesity; leptin; adiponectin; estrogen; prolactin; serum amyloid A

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Obesity has been identified as a serious health concern in domestic cats, and Feline Mammary Cancer (FMC) is highly prevalent and aggressive. This review investigated the association between adipokines and other obesity-associated molecules and FMC, and identified research gaps for future studies. The findings suggest a positive correlation between leptin, serum amyloid A, and estrogen with FMC, while a negative correlation between leptin and FMC. The roles of adiponectin and prolactin in FMC development require further investigation.
Obesity has been identified as a serious health concern in domestic cats. Feline mammary cancer (FMC) is also a concern, as it is highly prevalent and aggressive. Considering the identified connection between obesity and breast cancer, it is worthwhile to investigate the potential obesity-cancer relationship in FMC. This review investigated the association between adipokines and other obesity-associated molecules and FMC, with the aim of identifying gaps in the current literature for future research. Based on the reports to date, it was found that tissue concentrations of leptin, serum concentrations of leptin receptor, serum amyloid A, and estrogen correlate positively with FMC, and serum concentrations of leptin correlate negatively with FMC. The roles of adiponectin and prolactin in FMC development were also investigated, but the reports are either lacking or insufficient to suggest an association. Numerous research gaps were identified and could be used as opportunities for future research. These include the need for studies on additional cohorts to confirm the association of leptin/leptin receptor and serum amyloid A with FMC, and to address the role of adiponectin and prolactin in FMC. It is also important to investigate the genetic determinants of FMC, evaluate the use of molecular-targeted therapies in FMC, and exploit the enrichment of the triple-negative immunophenotype in FMC to address current clinical needs for both human triple-negative breast cancer and FMC. Finally, mechanistic studies with any of the molecules reviewed are scarce and are important to generate hypotheses and ultimately advance our knowledge and the outcome of FMC.

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