Background/Objectives: Cell viability assays play a crucial role in cancer research and the development of effective treatments. Evaluating the efficacy of conventional treatments across different tumor profiles is essential for understanding patient resistance to chemotherapy and relapse. The IC50 index has been commonly used as a guide in these assays. The idea behind the IC50 index is to compare cell proliferation under treatment with respect to a control population exposed to the same treatment. The index requires normalization to a control and is time dependent. These aspects are disadvantages, as small variations yield different results. In this article, we propose a new method to analyze cell viability assays. Methods: This method involves calculating the effective growth rate for both control (untreated) cells and cells exposed to a range of drug doses for short times, during which exponential proliferation can be assumed. The concentration dependence of the effective growth rate gives a real estimate of the treatment on cell proliferation. A curve fit of the effective growth rate related to concentration yields the concentration corresponding to a given effective growth rate. Results: We use this estimation to calculate the IC50 index and introduce two new parameters (ICr0 and ICrmed) to compare treatment efficacy under different culture conditions or cell lines. Conclusions: In summary, this study presents a new method to analyze cell viability assays and introduces two more precise parameters, improving the comparison and evaluation of efficacy under different conditions.

Gold nanorods are the most commonly used nanoparticles in photothermal therapy for cancer treatment due to their high efficiency in converting light into heat. This study aimed to investigate the efficacy of gold nanorods of different sizes (large and small) in eliminating two types of cancer cell: melanoma and glioblastoma cells. After establishing the optimal concentration of nanoparticles and determining the appropriate time and power of laser irradiation, photothermal therapy was applied to melanoma and glioblastoma cells, resulting in the highly efficient elimination of both cell types. The efficiency of the PTT was evaluated using several methods, including biochemical analysis, fluorescence microscopy, and flow cytometry. The dehydrogenase activity, as well as calcein-propidium iodide and Annexin V staining, were employed to determine the cell viability and the type of cell death triggered by the PTT. The melanoma cells exhibited greater resistance to photothermal therapy, but this resistance was overcome by irradiating cells at physiological temperatures. Our findings revealed that the predominant cell-death pathway activated by the photothermal therapy mediated by gold nanorods was apoptosis. This is advantageous as the presence of apoptotic cells can stimulate antitumoral immunity in vivo. Considering the high efficacy of these gold nanorods in photothermal therapy, large nanoparticles could be useful for biofunctionalization purposes. Large nanorods offer a greater surface area for attaching biomolecules, thereby promoting high sensitivity and specificity in recognizing target cancer cells. Additionally, large nanoparticles could also be beneficial for theranostic applications, involving both therapy and diagnosis, due to their superior detection sensitivity.

Protein expression profiles are directly related to the different properties of cells and are conditioned by the cellular niche. As an example, they are the cause of the characteristic cell plasticity, epithelium–mesenchymal transition (EMT), and drug resistance of cancer cells. This article characterizes ten biomarkers related to these features in three human colorectal cancer cell lines: SW-480, SW-620, and DLD-1, evaluated by flow cytometry; and in turn, resistance to oxaliplatin is studied through dose–response trials. The main biomarkers present in the three studied lines correspond to EpCAM, CD-133, and AC-133, with the latter two in low proportions in the DLD-1 line. The biomarker CD166 is present in greater amounts in SW-620 and DLD-1 compared to SW-480. Finally, DLD-1 shows high values of Trop2, which may explain the aggressiveness and resistance of these cells to oxaliplatin treatments, as EpCAM is also highly expressed. Exposure to oxaliplatin slows cell growth but also helps generate resistance to the treatment. In conclusion, the response of the cell lines is variable, due to their genetic variability, which will condition protein expression and cell growth. Further analyses in this area will provide important information for better understanding of patients’ cellular response and how to prevent resistance.

Breast cancer is the leading cause of death among females in developed countries. Although the implementation of screening tests and the development of new therapies have increased the probability of remission, relapse rates remain high. Numerous studies have indicated the connection between cancer-initiating cells and slow cellular cycle cells, identified by their capacity to retain long labeling (LT+). In this study, we perform new assays showing how stem cell self-renewal modulating proteins, such as PEDF, can modify the properties, percentage of biomarker-expressing cells, and carcinogenicity of cancer stem cells. The PEDF signaling pathway could be a useful tool for controlling cancer stem cells’ self-renewal and therefore control patient relapse, as PEDF enhances resistance in breast cancer patient cells’ in vitro culture. We have designed a peptide consisting of the C-terminal part of this protein, which acts by blocking endogenous PEDF in cell culture assays. We demonstrate that it is possible to interfere with the self-renewal capacity of cancer stem cells, induce anoikis in vivo, and reduce resistance against docetaxel treatment in cancer patient cells in in vitro culture. We have also demonstrated that this modified PEDF protein produces a significant decrease in the percentage of expressed cancer stem cell markers.

Polyphenols, recognized for their antioxidant capacity, have shown potential in improving the response treatment of various diseases, including cancer. In this context, polyphenols have the ability to induce cytotoxicity in tumor cells, making them possible complementary agents to current treatments. The present study aims to evaluate the effect of the aqueous extract of Synsepalum dulcificum, using the commercial product DMB^®, on the proliferation of colorectal tumor cells. An aqueous extract of DMB^® was obtained, and 12 compounds were identified through high-performance liquid chromatography (HPLC), with protocatechuic acid, gallic acid, and catechin being the most prominent. Regarding cytotoxicity, the extracts reduced cell viability in the DLD-1, HT29, SW480, and SW620 cell lines, with IC₅₀ values of 7, 11, 13, and 15 mg/mL, respectively. The combination of oxaliplatin with the DMB^® extract reduced the resistant population by up to 50% in the DLD-1 and SW620 cell lines, affecting the G₂/M and S phases of the cell cycle, respectively. Additionally, treatment with the DMB^® extract induced an increase in the expression of BCL2, CASP3, and CASP9, suggesting a mechanism of action associated with apoptosis. The aqueous extract of Synsepalum dulcificum (DMB^®) exhibited cytotoxicity in colorectal cancer cells, enhancing the effect of oxaliplatin and activating apoptotic pathways, suggesting its potential as an adjuvant in anticancer therapies.

Summary: Peanut allergies are one of the food allergies with the highest prevalence and mortality due to anaphylaxis, drastically reducing the quality of life of people who suffer from it. In the case of Novel Foods, such as the miracle berry from Synsepalum dulcificum, there is insufficient evidence regarding their allergenic potential. An exhaustive analysis was carried out to study potential cross‐allergy effects between miracle berries and peanuts. First, both an in silico allergenicity prediction model based on sequence homology and an in silico structure homology test were designed to evaluate miraculin cross‐reactivity against Ara h allergens. Second, an in vitro ELISA assay using blood sera from peanut‐allergic patients was executed to discard the possibility of cross‐reaction with total protein content from the berry. The obtained results ruled out the presence of cross‐allergy, leading to the conclusion that consumption of this berry presents no risk for patients with this allergy.