Julita Kulbacka

The Impact of Chronic Stress on Treatment Outcomes of Cancer Patients with Divergent Survival Rates: A Systematic Review

This systematic review investigates the impact of chronic stress on treatment outcomes among cancer patients with divergent survival rates, focusing on breast, prostate, pancreatic, and ovarian cancers. The analysis explores how chronic stress influences molecular pathways and tumor progression while comparing cancers with five-year survival rates above and below 50%. A comprehensive literature search was conducted in PubMed and Scopus for studies published between 2014 and 2025 using combinations of keywords related to “chronic stress,” “psychological stress,” “psychotherapy,” and selected cancer types. All studies met the inclusion criteria according to the PRISMA 2020 guidelines. Evidence suggests that chronic stress is associated with the activation of neuroendocrine and immune mechanisms, including β-adrenergic and glucocorticoid signaling. These multifactorial processes are associated with disease progression and survival, particularly in pancreatic and ovarian cancers; however, these links remain primarily associative rather than causative. Conversely, psychotherapeutic interventions alleviate stress-related biological responses, improve quality of life, and may indirectly enhance therapeutic efficacy. By structuring the evidence around cancers with higher versus lower five-year survival, our review provides a survival informed synthesis of cancer type specific stress biology and stress-mitigating interventions, highlighting potentially targetable pathways and clear evidence gaps for future trials. The findings underscore the need to integrate psychological care into oncological practice to improve overall outcomes.

Recent Therapies and Biomarkers in Mucinous Ovarian Carcinoma

Mucinous ovarian carcinoma (MOC) represents a rare and biologically distinct subtype of ovarian cancer, characterized by poor response to standard platinum-based chemotherapy and a unique molecular profile, including frequent KRAS mutations and HER2 amplifications. Recent advancements in targeted therapy, such as HER2 inhibitors and KRASG12C inhibitors, offer promising avenues for personalized treatment. Immunotherapy, particularly checkpoint inhibitors, shows potential in tumors with high PD-L1 expression or tumor mutational burden. Novel strategies, including antibody–drug conjugates, synthetic lethality approaches, and Wnt/β-catenin pathway inhibitors, are reshaping the therapeutic landscape. Despite these developments, challenges such as intratumoral heterogeneity and therapy resistance persist, underscoring the need for innovative clinical trial designs and combination regimens. This review synthesizes the latest advancements in MOC therapies, highlighting opportunities for improved outcomes in this challenging malignancy.

The additive effect of 17β-estradiol on the modulation of electrochemotherapy with calcium ions or cisplatin in human clear carcinoma cells

Calcium electroporation (CaEP) is an efficient approach for ovarian cancer treatment. It causes cell death by introducing elevated levels of calcium into cells. In this work, the research focused on two types of cell lines: CHO-K1, representing normal ovary cells, and OvBH-1, representing ovarian clear carcinoma cells. Those cell lines exhibited distinct reactions to calcium electroporation (CaEP). Also, we have evaluated the effects of 17β-estradiol following CaEP and electrochemotherapy (ECT) with cisplatin (CPP). The combination of ECT with CPP and CaEP with prior E

Cytotoxic Activity of Curcumin- and Resveratrol-Loaded Core–Shell Systems in Resistant and Sensitive Human Ovarian Cancer Cells

Due to the high mortality rate of ovarian cancer, there is a need to find novel strategies to improve current treatment modalities. Natural compounds offer great potential in this field but also require the careful design of systems for their delivery to cancer cells. Our study explored the anticancer effects of novel resveratrol (RSV)- and curcumin (CUR)-loaded core–shell nanoparticles in human ovarian cancer cells. We evaluated the in vitro cytotoxicity of various nanocarriers (CUR 1-3, RSV I-III) delivered to MDAH-2774 and SKOV-3 cells in comparison to free RVS and CUR after 24 h and 72 h treatment. A two-way ANOVA was applied to compare the results of the MTT assay. Confocal laser scanning microscopy was employed to visualize cellular uptake and mitochondrial localization. Our findings revealed that the cytotoxicity of the core–shell nanoparticles with RSV was not significant, but the systems loaded with CUR effectively decreased the viability of cells. The MDAH-2774 cell line was more sensitive to the treatment than SKOV-3. The enhanced cellular uptake of CUR delivered by core–shell systems and its colocalization with mitochondria were demonstrated. Further research focused on the detailed biological effects of the most effective systems (CUR 2 and CUR 3) should be conducted to provide detailed insights. These findings highlight the promising role of CUR-loaded nanoparticles in ovarian cancer treatment.

The influence of asymmetrical bipolar pulses and interphase intervals on the bipolar cancellation phenomenon in the ovarian cancer cell line

The application of negative polarity electrical pulse (↓) following positive polarity pulses (↑) may induce bipolar cancellation (BPC), a unique physiological response believed to be specific to nanosecond electroporation (nsEP). The literature lacks analysis of bipolar electroporation (BP EP) involving asymmetrical sequences composed of nanosecond and microsecond pulses. Moreover, the impact of interphase interval on BPC caused by such asymmetrical pulse needs consideration. In this study, the authors utilized the ovarian clear carcinoma cell line (OvBH-1) model to investigate the BPC with asymmetrical sequences. Cells were exposed to pulses delivered in 10-pulse bursts but as uni- or bipolar, symmetrical, or asymmetrical sequences with a duration of 600 ns or 10 µs and electric field strength equal to 7.0 or 1.8 kV/cm, respectively. It was shown that the asymmetry of pulses influences BPC. The obtained results have also been investigated in the context of calcium electrochemotherapy. The reduction of cell membrane poration, and cell survival have been observed following Ca

Effect of Interaction between 17β-Estradiol, 2-Methoxyestradiol and 16α-Hydroxyestrone with Chromium (VI) on Ovary Cancer Line SKOV-3: Preliminary Study

Ovarian cancer is the leading cause of death from gynecologic malignancies. Some estrogens, as well as xenoestrogens, such as chromium (VI) (Cr(VI)), are indicated as important pathogenic agents. The objective of this study was to evaluate the role of estradiol and some its metabolites upon exposure to the metalloestrogen Cr(VI) in an in vitro model. The changes in cell viability of malignant ovarian cancer cells (SKOV-3 resistant to cisplatin) exposed to 17β-estradiol (E2) and its two metabolites, 2-methoxyestradiol (2-MeOE2) and 16α-hydroxyestrone (16α-OHE1), upon exposure to potassium chromate (VI) and its interactions were examined. The single and mixed models of action, during short and long times of incubation with estrogens, were applied. The different effects (synergism and antagonism) of estrogens on cell viability in the presence of Cr(VI) was observed. E2 and 16α-OHE1 caused a synergistic effect after exposure to Cr(VI). 2-MeOE2 showed an antagonistic effect on Cr(VI). The examined estrogens could be ranked according to the most protective effect or least toxicity in the order: 2-MeOE2 > E2 > 16α-OHE1. Early pre-incubation (24 h or 7 days) of cells with estrogens caused mostly an antagonistic effect—protective against the toxic action of Cr(VI). The beneficial action of estrogens on the toxic effect of Cr(VI), in the context of the risk of ovarian cancer, seems to be important and further studies are needed.

The Influence of Interaction between Cadmium with 17β-Estradiol, 2-Methoxyestradiol and 16α-Hydroxyestrone on Viability and p-Glycoprotein in Ovarian Cancer Cell Line

Occupational and environmental exposure to xenoestrogens, a subgroup of endocrine disruptors (EDCs), can affect the endocrine system and increase the risk of cancer, primarily the hormone-dependent kind. This type of cancer includes ovarian cancer, which is the leading cause of death from gynecological tumors. The aim of this study was to assess the role of 17β-estradiol and its metabolites: 2-MeOE2, 16α-OHE1 in exposure to the metalloestrogen cadmium. The effect of interactions of cadmium with estrogens on the viability of cells in malignant ovarian cancer cells SKOV-3 was investigated, both in simultaneous action and in the pre-incubation model. There are no known interactions between estrogens and cadmium in ovarian cancer cells. Due to the frequent occurrence of multidrug resistance (MDR) in ovarian cancer, the effects of estrogens and cadmium on MDR in SKOV-3, measured as P-glycoprotein (P-gp), were assessed. An interaction study showed that E2 had an antagonistic effect on cadmium-induced cell damage, while 2-MeOE2 showed less of a protective effect in combination with CdCl2 than E2. There were two types of interaction: toxic synergism and beneficial antagonism. E2 and cadmium increased P-gp expression in SKOV-3 cells, while 2-MeOE2 decreased P-gp expression to a potentially beneficial effect on MDR prevention. The obtained results constitute an interesting starting point for further research in the field of interactions between estrogens and xenoestrogens in ovarian cancer.