Predictors of inflammation in response to anthracycline-based chemotherapy for breast cancer

Abstract

Although chemotherapy for breast cancer can increase inflammation, few studies have examined predictors of this phenomenon. This study examined potential contributions of demographics, disease characteristics, and treatment regimens to markers of inflammation in response to chemotherapy for breast cancer. Thirty-five women with stage I -III-A breast cancer (mean age 50 years) were studied prior to cycle 1 and prior to cycle 4 of anthracycline-based chemotherapy. Circulating levels of inflammatory markers with high relevance to breast cancer were examined, including C-reactive protein (CRP), tumor necrosis factor-α (TNF-α), Interleukin-1 receptor antagonist (IL1-RA), vascular endothelial growth factor (VEGF), soluble intercellular adhesion molecule-1 (sICAM-1), Interleukin-(IL-6), soluble P-selectin (sP-selectin), and von Willebrand factor (vWf). Chemotherapy was associated with elevations in VEGF (p≤0.01), sICAM-1 (p≤0.01), sP-selectin (p≤0.02) and vWf (p≤0.05). Multiple regression analysis controlling for age and body mass index (BMI) showed that higher post-chemotherapy levels of inflammation were consistently related to higher prechemotherapy levels of inflammation (p's ≤0.05) as well as to certain disease characteristics. Postchemotherapy IL-6 levels were higher in patients who had larger tumors (p≤0.05) while postchemotherapy VEGF levels were higher in patients who had smaller tumors (p≤0.05). Postchemotherapy sP-selectin levels were highest in women who had received epirubicin, cytoxan, 5fluorouracil chemotherapy (p≤0.01). These findings indicate that chemotherapy treatment can be associated with elevations in certain markers of inflammation, particularly markers of endothelial and platelet activation. Inflammation in response to chemotherapy is most significantly related to inflammation that existed prior to chemotherapy but also potentially to treatment regimen and to certain disease characteristics.

The α-Lipoic acid derivative sodium zinc dihydrolipoylhistidinate reduces chemotherapy-induced alopecia in a rat model: A pilot study

“…14 Some of the toxic effects of chemotherapy drugs are caused by the increased production of infl ammatory mediators. 15,16 Consistent with previous studies, we demonstrated that AraC caused infl ammatory cell Fig. 1A-D. The effect of sodium zinc dihydrolipoylhistidinate against cytosine arabinoside-induced alopecia.…”

Circadian rhythms measured by actigraphy during oncological treatments: a systematic review

“…Chemotherapy can induce the release of vascular endothelial growth factor, interleukin-6 (IL-6), and other cytokines (Mills et al 2008;. Increased level of circulating pro-inflammatory cytokines is highly associated with fatigue (Rich et al 2005;Schubert et al 2007;Mills et al 2008;.…”

Optical imaging of breast cancer oxyhemoglobin flare correlates with neoadjuvant chemotherapy response one day after starting treatment

“…Previous studies have shown that clinical outcome in breast cancer patients is associated with elevations of proinflammatory serum biomarkers after taxane treatment (47)(48)(49)(50). Tumor cell exposure to anthracyclines and some platin drugs has been shown to induce immunostimulatory apoptosis and presentation of damage-associated molecular patterns, including calreticulin, heat-shock proteins, and high-mobility group box 1 proteins, before, during, or after apoptosis (51)(52)(53)(54).…”