Pathobiology of Cancer Regimen-Related Toxicities

Sonis, Stephen T.; Keefe, Dorothy

doi:10.1007/978-1-4614-5438-0

Cited by 6 publications

(2 citation statements)

References 816 publications

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“…Data outlining molecular mechanisms by which treatment-related fibrosis develops has largely been captured from animal models that accurately replicate chemotherapy or radiotherapy regimens routinely used in patients (Sonis and Keefe, 2013). Immediately following insult due to chemotherapy and radiation, there is a large cellular response that involves cell type specific programs occurring in three general phases ( Figure 1 ).…”

Section: Mechanisms Of Fibrosismentioning

confidence: 99%

“…These regimen-related toxicities are not only associated with poor health outcomes, but they often become dose-limiting for patients and impair patients’ quality of life (QoL) and recovery in both the short and the long term (Elting et al, 2008). Hematological disorders such as anemia, thrombocytopenia, and neutropenia are among the most common complications associated with radiation and chemotherapy; however, cancer patients are also at risk for a wide range of non-hematological toxicities (Sonis and Keefe, 2013). The overall incidence of some form of cancer treatment-related toxicity is almost 100% and can occur both during cancer treatment (acute toxicities), or will develop well after the completion of treatment (≥100 days, late toxicities).…”

Section: Introductionmentioning

confidence: 99%

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Mechanisms of cellular fibrosis associated with cancer regimen-related toxicities

Mancini¹,

Sonis²

2014

Front. Pharmacol.

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Fibrosis is a common, persistent and potentially debilitating complication of chemotherapy and radiation regimens used for the treatment of cancer. The molecular mechanisms underlying fibrosis have been well studied and reveal overall processes that are largely ubiquitous. However, it is important to note that although the processes are similar, they result in cellular phenotypes that are highly tissue specific. These tissue specific differences may present opportunities for therapeutic interventions to prevent or treat this often irreversible condition. Data generated from animal models of cancer therapy-related tissue toxicities have revealed that the signaling pathways involved in fibrosis are the same as those involved in the normal injury response and include the transforming growth factor β superfamily and a range of pro-inflammatory cytokines. The critical difference between normal wound healing and fibrosis development appears to be, that in fibrosis, these signaling pathways escape normal cellular regulation. As a result, an injury state is maintained and processes involved in normal healing are usurped. There are a few, if any, therapeutics that effectively prevent or treat fibrosis in patients. Consequently, cancer survivors may be chronically plagued with a variety of life-altering fibrosis-related symptoms. Uncovering the signaling pathways that drive cellular fibrosis is paramount to the development of specific therapeutics that will mitigate this potentially devastating condition.

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Section: Mechanisms Of Fibrosismentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Mechanisms of cellular fibrosis associated with cancer regimen-related toxicities

Mancini¹,

Sonis²

2014

Front. Pharmacol.

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Matrix metalloproteinase expression is altered in the small and large intestine following fractionated radiation in vivo

Stansborough

Al‐Dasooqi

Bateman

et al. 2018

Support Care Cancer

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PPIA rs6850: A > G single-nucleotide polymorphism is associated with raised plasma cyclophilin A levels in patients with coronary artery disease

Vinitha

Kutty²,

Vivekanand

et al. 2015

Mol Cell Biochem

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Plasma level of cyclophilin A is a promising marker of vascular disease in patients with type 2 diabetes. Genetic variants in the peptidylprolyl isomerase A gene, encoding human cyclophilin may alter protein synthesis thus affecting its activity, function, and circulating plasma levels. We examined the effect of single-nucleotide polymorphisms (SNPs) within the PPIA gene on plasma levels of cyclophilin A and coupled this with status of vascular disease in patients with and without type 2 diabetes in 212 South Indian subjects. The regulatory region of PPIA gene was sequenced for SNPs. The association of SNPs with known blood markers of type 2 diabetes and coronary artery disease such as HbA1c, low- and high-density lipoproteins, triglycerides, fasting and postprandial blood sugar levels, and cyclophilin A were probed. We identified three SNPs namely, rs6850: A > G; (AG/-) c.*227_*228delAG and (-/T) c.*318_*319insT. Welchs two-sample t test indicated an association of SNP rs6850: A > G, located at the 5' UTR region with increased plasma levels of cyclophilin A in patients with coronary artery disease and with coronary artery disease associated with diabetes. The presence of rs6850: A > G variant was significantly associated with coronary artery disease irrespective of whether the patients had diabetes or not. In silico analysis of the sequence using different tools and matrix libraries did not predict any significant differential binding sites for rs6850: A > G, c.*227_*228delAG and c.*318_*319insT. Our results indicate that the SNP rs6850: A > G is associated with increased risk for elevated plasma levels of cyclophilin A and coronary artery disease in patients with and without type 2 diabetes.

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Pathobiology of Cancer Regimen-Related Toxicities

Cited by 6 publications

References 816 publications

Mechanisms of cellular fibrosis associated with cancer regimen-related toxicities

Mechanisms of cellular fibrosis associated with cancer regimen-related toxicities

Matrix metalloproteinase expression is altered in the small and large intestine following fractionated radiation in vivo

PPIA rs6850: A > G single-nucleotide polymorphism is associated with raised plasma cyclophilin A levels in patients with coronary artery disease

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