Objective: In most countries of the world, breast cancer ranks first in the structure of oncological morbidity in women. The etiology of this disease remains largely unclear, although it is known that disturbances in the elemental homeostasis of somatic cells play a certain role in oncogenesis. The purpose of this study was to identify changes in the content of chemical elements during malignant transformation of breast tissue.
Methods: For this purpose, we used the previously developed method of sample preparation, which allows determining the content of Al, Ba, Ca, Cu, Fe, K, Mg, Mn, Na, P, S, Si, Sr, Ti, and Zn in micro samples of breast tissue by using atomic emission spectrometry with inductively coupled plasma. Samples of cancerous and visually unchanged breast tissue adjacent to the tumor were examined using the developed technique.
Results: A significantly higher content of all the chemical elements studied, except for Si, was found in cancerous tissue compared to their content in intact tissue.
Conclusions: The detected multiple increase in the content of many minor and trace elements in cancer tissue compared to adjacent intact breast tissue can be used to develop new methods for in vitro and in vivo cancer diagnostics, in which the ratios of chemical elements levels in these tissues will act as tumor markers. Further, more in-depth study and understanding of the discovered phenomenon will allow the development of new methods for the prevention and treatment of breast cancer.

Hypoxia, a characteristic of the tumor microenvironment caused by abnormal blood vessels and rapid cellular growth, enhances tumor aggressiveness and leads to resistance against conventional therapies. Unlike normal cells, hypoxic tumor cells activate adaptive survival mechanisms, prominently mediated by hypoxia-inducible factors (HIFs). HIF-1α is the most studied member of the HIF family, and the stability of its alpha subunit (HIF-1α) is a crucial determinant of the overall activity of the HIF-1α complex. HIF-1α stabilization under low oxygen occurs via oxygen-dependent and oxygen-independent pathways: in the oxygen-dependent pathway, HIf-1α is normally degraded by the von Hippel-Lindau protein (pVHL) when oxygen is present. Under hypoxia, hydroxylation is inhibited, allowing HIF-1α to accumulate. In the oxygen-independent pathway, growth factor signals activate cascades like PI3K/Akt/mTOR and MAPK/ERK, stabilizing HIF-1α regardless of oxygen levels. Stabilized HIF-1α translocates to the nucleus, promoting transcription of proangiogenic genes such as vascular endothelial growth factor (VEGF), thereby facilitating angiogenesis, tumor invasion, and progression. Dysregulation of these signaling pathways underpins the pathogenesis of many cancers, making HIF and its associated cascades critical targets for innovative cancer therapies. This review focuses on the pivotal role of HIF in tumor angiogenesis and emphasizes the therapeutic potential of targeting HIF signaling in cancer treatment.

Objective: Glioblastoma (GBM) is the most common and malignant brain tumor, with a ~14.5 months median survival rate without disease-modifying curative treatment. After surgical resection, radiation, and adjuvant temozolomide (TMZ) chemotherapy is the first-line treatment of GBM with adverse effects, including bone marrow suppression, genotoxicity, and teratogenicity. Here, we report a synthetic quinazoline derivative that inhibits the growth of GBM cells as a new therapeutic approach.
Methods: A potent quinazoline derivative (6-Pyridin-2-yl-5,6-dihydro-benzo[4,5] imidazo[1,2-c] quinazoline) was synthesized by one chemical step with 90% yield, followed by in vitro testing in GBM and neuroblastoma cells.
Results: The in vitro studies showed that the quinazoline derivative is highly specific by decreasing GBM cell invasion while inducing cell death and inhibiting the cellular invasion in the three-dimensional Matrigel matrix. This compound is highly specific to GBM cell death compared with other cells. Synthetic quinazoline derivative is non-toxic to normal non-tumorigenic cells but toxic to cancerous cells. Under these experimental conditions, quinazoline derivatives caused inhibition of beta-1 integrin, which is an important cell adhesion molecule required for tumor cell invasion and metastasis, with extracellular matrix-mediated interactions. Furthermore, a synthetic quinazoline derivative decreases oncogenic PKC-epsilon activity in neuroblastoma cells.
Conclusions: These studies suggest that a synthetic quinazoline derivative may treat GBM effectively alone or combined with other chemotherapeutic/immunotherapeutic agents.

Chimeric antigen receptor-T (CAR-T) therapy has been an effective treatment for leukemia and lymphoma. Unlike hematological cancers, solid tumors like prostate cancer utilize a dynamic microenvironment to evade the host immune defenses. We aimed to systematically review preclinical and clinical studies to evaluate how CAR-T therapies in prostate cancer modify the tumor microenvironment and influence patient outcomes. PubMed, Embase, and Scopus were screened for published, peer reviewed preclinical and clinical studies in accordance with Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. The CAR-T antigen, tumor eradication rates, change in prostate-specific antigen (PSA) expression, and tumor tissue infiltration were compared across studies. Nineteen preclinical trials examining xenograft mice models and 3 phase I clinical trials with 32 total patients were included in this review. Tumor eradication rates in mice treated with armored CAR-T therapy were significantly greater than that of mice treated with unarmored CAR-T cells (p-value <.05). Ten of 32 clinical trial patients had a minimum of 30% PSA decline. Patients receiving higher doses of lymphocyte depletion (LD) therapy had higher peaks of CAR-T expansion, and those receiving LD therapy before CAR-T infusion experienced reduced dose-limiting toxicities. Immunohistochemistry staining of biopsied tumor tissue suggests CAR-T increased T cell proliferation markers and upregulated cytokines. CAR-T cells can modify the tumor microenvironment when armored or paired with LD therapy. Future studies should include expanded clinical investigations, particularly using armored CAR-T cells with LD regimens, to determine its safety and efficacy profiles in prostate cancer.