Publications by authors named "A M Nappi"

Obesity exacerbates the risk and aggressiveness of many types of cancer. Adipose tissue (AT) represents a prevalent component of the tumor microenvironment (TME) and contributes to cancer development and progression. Reciprocal communication between cancer and adipose cells leads to the generation of cancer-associated adipocytes (CAAs), which in turn foster tumor invasiveness by producing paracrine metabolites, adipocytokines, and growth factors.

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Adipose tissue, particularly white adipose tissue (WAT), plays a central role in energy storage and metabolic regulation. Excess WAT, especially visceral fat, is strongly linked to metabolic disorders such as obesity and type 2 diabetes. The browning of WAT, whereby white fat cells acquire characteristics of brown adipose tissue (BAT) with enhanced thermogenic capacity, represents a promising strategy to enhance metabolic health.

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Muscle and adipose tissue (AT) are in mutual interaction through the integration of endocrine and biochemical signals, thus regulating whole-body function and physiology. Besides a traditional view of endocrine relationships that imply the release of cytokines and growth factors, it is becoming increasingly clear that a metabolic network involving metabolites as signal molecules also exists between the two tissues. By elevating the number and functionality of mitochondria, a key role in muscle metabolism is played by the master regulator of mitochondrial biogenesis peroxisome-proliferator-activated receptor-γ coactivator-1α (PGC-1α), that induces a fiber type shift from glycolytic to oxidative myofibers.

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Purpose: To investigate whether intermittent treatment after an induction phase of first-line schedule of fluorouracil, leucovorin, and irinotecan (FOLFIRI) plus panitumumab (PAN) prevents or delays the onset of resistance and improves safety and compliance with treatment in patients with unresectable / wild-type (wt) metastatic colorectal cancer (mCRC).

Patients And Methods: IMPROVE (ClinicalTrials.gov identifier: NCT04425239) was an open-label, multicenter, randomized phase II noncomparative trial.

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Article Synopsis
  • * Thyroid dysfunctions, such as hyperthyroidism and hypothyroidism, can lead to various muscle issues, including weakness, fatigue, and myopathies, due to imbalances in muscle protein synthesis and degradation.
  • * Understanding the molecular mechanisms behind THs' effects on muscle can help develop strategies to manage muscle problems in individuals with thyroid diseases.
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