Colorectal cancer (CRC) represents the third type of cancer in incidence and second in mortality worldwide, with the newly diagnosed case number on the rise. Among the diagnosed patients, approximately 70% have no hereditary germ-line mutations or family history of pathology, thus being termed sporadic CRC. Diet and environmental factors are to date considered solely responsible for the development of sporadic CRC; therefore; attention should be directed towards the discovery of preventative actions to combat the CRC initiation, promotion, and progression. Quercetin is a polyphenolic flavonoid plant secondary metabolite with a well-characterized antioxidant activity. It has been extensively reported as an anti-carcinogenic agent in the scientific literature, and the modulated targets of quercetin have been also characterized in the context of CRC, mainly in original research publications. In this fairly comprehensive review, we summarize the molecular targets of quercetin reported to date in in vivo and in vitro CRC models, while also giving background information about the signal transduction pathways that it up- and downregulates. Among the most relevant modulated pathways, the Wnt/β-catenin, PI3K/AKT, MAPK/Erk, JNK, or p38, p53, and NF-κB have been described. With this work, we hope to encourage further quests in the elucidation of quercetin anti-carcinogenic activity as single agent, as dietary component, or as pharmaconutrient delivered in the form of plant extracts.

The standard treatment for breast cancer typically includes surgery, often followed by systemic therapy and individualized treatment regimens. However, there is growing interest in identifying pre-therapeutic biomarkers that can predict tumor response to neoadjuvant chemotherapy (NACT). This study systematically evaluated various analytical parameters, including age, TNM stage, histological type, molecular subtype, and several biomarker ratios, such as the platelet-to-lymphocyte ratio (PLR), neutrophil-to-lymphocyte ratio (NLR), lymphocyte-to-monocyte ratio (LMR), systemic immune-inflammatory index (SII), and prognostic nutritional index (PNI). We aimed to assess the predictive value of these parameters regarding the tumor’s response rate to NACT. The analysis revealed a statistically significant association between the pathological complete response—pCR (absence of any detectable cancer cells in the tissue following neoadjuvant chemotherapy (NACT))—rate and NLR in the subgroup with values between 1 and 3 (p = 0.001). The optimal cut-off for PLR was determined to be 120.45, with 80.55% of patients achieving pCR showing PLR values below this threshold (p = 0.000). Similarly, the LMR cut-off was found to be 12.34, with 77.77% of patients with pCR having LMR values below this threshold (p = 0.002). Additionally, lower pre-therapeutic values of NLR (p < 0.001), PLR (p = 0.002), SII (p = 0.001), and LMR (p = 0.001) were significantly correlated with pCR compared to the non-pCR subgroup (p < 0.005). These findings highlight the predictive potential of these biomarkers for achieving pCR following NACT. Our study supports the hypothesis that pre-therapeutic values of NLR, PLR, SII, and LMR can serve as predictive biomarkers for pCR in breast cancer patients undergoing NACT. However, the PNI did not demonstrate predictive potential in relation to pCR. These biomarkers may provide valuable insights into patient prognosis and guide personalized treatment strategies.

Chlorogenic acids are plant secondary metabolites, chemically—polyphenols with similar biological activity, formed through the esterification of quinic acid and hydrocinnamic acid moieties. They are best known for their high concentration in coffee and other dietary sources and the antioxidant properties that they exhibit. Both chlorogenic acids and plant extracts containing significant amounts of the compounds show promising in vitro activity against colorectal cancer. With coffee being the most popular drink in the world, and colorectal cancer at an unfortunate peak in incidence and mortality, the mechanisms through which the anti-tumorigenic effect of chlorogenic acids could be functionalized for CRC prevention seem appealing to study. Therefore, this review aims to enable a better understanding of the modes of action of chlorogenic acids in combating carcinogenesis, with a focus on cell cycle arrest, the induction of apoptosis, and the modulation of Wnt, Pi3K/Akt, and MAPK signal transduction pathways, alongside the reduction in the number of inflammatory cytokines and chemokines and the counterintuitive beneficial elevation of oxidative stress.

Type 2 diabetes mellitus (DM) is a chronic metabolic disorder posing multifaceted challenges to global public health. Among its numerous complications, infected diabetic foot ulcers (IDFUs) represent a particularly debilitating consequence. Beyond cardiovascular implications, there is an emerging understanding of the interconnectedness among IDFUs, neuropathy, atherosclerosis, and dyslipidemia. IDFUs, peripheral neuropathy, and atherosclerosis share common risk factors and mechanistic pathways. The primary objective of this study was to characterize the lipid profiles in DM patients with IDFUs, comparing them with DM patients without foot ulcers, and with a control group of healthy subjects. The secondary objectives included evaluating apolipoprotein E (ApoE) levels across these study groups and comparing lipid profiles within IDFU subgroups. A total of 160 patients were assessed for this study. After applying exclusion criteria, 140 participants were included, divided into three groups: Group IDFU (80 patients with IDFUs), Group DM (32 patients with DM but no foot ulcers), and Group Controls (28 healthy controls). Compared to Group DM, Group IDFU demonstrated lower levels of high-density lipoprotein cholesterol (HDL-C) (30.9 ± 12.6 mg/dL vs. 40.8 ± 16.6 mg/dL, p = 0.002), but improved levels of ApoE (160.9 ± 68.4 mg/dL vs. 197.2 ± 69.6 mg/dL, p = 0.01), triglycerides (TG) (126.9 ± 56.2 mg/dL vs. 165.8 ± 79.0 mg/dL, p = 0.004), low-density lipoprotein cholesterol (LDL-C) (84.2 ± 32.3 mg/dL vs. 92.3 ± 39.3 mg/dL, p = 0.1), and total cholesterol (133.6 ± 43 mg/dL vs. 164.6 ± 44.4 mg/dL, p = 0.002). The IDFU patients exhibit improved lipid profiles, excepting HDL-C, which is unusual because IDFU follows complications related to dyslipidemia for DM patients. Anemia, impaired renal function, and elevated TG levels were identified as biomarkers for mortality among patients with IDFUs. The data suggest that a lower level of HDL-C and an improved lipid profile may indicate a systemic end-stage disease manifestation in DM patients with IDFUs.

Dyslipidemia is a component of metabolic syndrome, having an important role in the carcinogenesis of different tumor types, such as prostate, ovarian, or renal cancer. The number of studies on the predictive potential of the different components of the lipid profile with a predictive potential in breast cancer is quite low. The evaluation of the lipid profile was carried out for the 142 patients who benefited from neoadjuvant therapy (NAC) in order to identify a potential predictive biomarker. The serological sample collection was performed sequentially according to a standardized protocol, pre-NAC, post-NAC and 6 months post-NAC after a 6-h pre-collection fast. We also investigated in the general group the presence or absence of the p53 mutation (TP53) and of the mitotic index ki-67, respectively, in relation to the molecular subtypes. The menopausal status, tumor size, family history, grading, Ki-67, p53 and LN metastases have a predictive nature regarding overall survival (OS) (p < 0.05), while for disease free survival (DFS), only tumor size, tumor grading, Ki-67 > 14, and p53+ are of predictive nature. The genetic and molecular analysis carried out in our group indicates that 71.67% have a Ki-67 score higher than 14%, and 39% of the patients have the positive P53 mutation. The multivariate analysis in the case of patients included in the TNBC subtype showed that the increased tumor volume (p = 0.002) and increased level of HDL (p = 0.004) represent predictive factors for the tumor response rate to NAC. High HDL-C levels before NAC and increased LDL-C levels after NAC were associated with the better treatment response in ER-positive and HER2+ breast cancer patients. Increased HDL-C values and tumor volume represent predictive factors as to the response rate to NAC in the case of patients included in the TNBC subtype. Regarding the ER+ and HER2+ subtypes, increased levels of HDL-C pre-NAC and increased levels of LDL-C post-NAC were associated with a better therapeutic response rate. Tumor grading, Ki-67, p53, and LN metastases have a predictive nature for OS, while tumor size, tumor grading, and Ki-67 > 14, and p53+ are predictive for DFS.

Introduction: Lipid metabolism plays a crucial role in breast cancer’s progression, treatment response, and prognosis. Alterations in triglycerides (TGs), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C) have been implicated in tumor aggressiveness and chemotherapy outcomes. This review examines the relationship between dyslipidemia and breast cancer, with a focus on chemotherapy-induced lipid alterations and their prognostic significance. Methods: A comprehensive literature search was conducted in PUBMED, Web of Science, and Google Scholar, identifying 108 unique studies. After applying the inclusion criteria, 21 studies were selected for analysis, covering lipid profile changes before, during, and after chemotherapy, as well as their impact on treatment response and clinical outcomes. Results: Breast cancer patients exhibited lower baseline TC, TG, and LDL-C levels compared to healthy controls; however, chemotherapy significantly increased these markers while decreasing HDL-C from 1.1 to 0.9 mmol/L. The incidence of dyslipidemia rose from 42.98% pre-treatment to 58.28% post-treatment. Chemotherapy-induced lipid alterations were most pronounced in anthracycline- and taxane-based regimens, leading to a 38% increase in TGs and a 23% reduction in HDL-C. While some studies reported that lipid levels normalized post-treatment, others indicated persistent dyslipidemia up to 12 months later. High baseline HDL-C was associated with a better chemotherapy response, whereas elevated TGs and LDL-C correlated with increased tumor aggressiveness, lower pathological complete response rates, and a higher relapse risk. Patients with persistently high post-treatment TGs had significantly worse disease-free survival, with a 30% relapse rate compared to 18% in those with normal TG. Preliminary evidence suggests that lipid-lowering therapies, such as statins, may offer therapeutic benefits in breast cancer by targeting the cholesterol synthesis pathways involved in tumor growth, though further clinical trials are required. Conclusions: Dyslipidemia is a key metabolic factor influencing breast cancer’s progression, treatment response, and long-term prognosis. Chemotherapy-induced lipid alterations may persist, increasing cardiovascular risk and potentially affecting therapeutic efficacy. Routine lipid monitoring and metabolic interventions could enhance treatment outcomes and survivorship. Future research should focus on developing lipid-targeted strategies to optimize breast cancer management.