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Glioblastoma (GBM) are the most prevalent type of primary malignant brain tumor in adults that can develop in the brain stem, cerebellum, or spinal cord. Temozolomide (TMZ) is an alkylating agent that is used to treat adults with newly diagnosed GBM and resistant anaplastic astrocytoma who have progressed on a nitrosourea and procarbazine-containing therapy regimen. Ferroptosis, a novel form of programmed cell death, plays a crucial role in glioblastoma therapy. Cell membrane damage produced by mechanisms such as intracellular iron build-up, reactive oxygen species (ROS), lipid peroxidation, glutathione peroxidase (GPX) activity failure, and x-catenin (xCT) causes ferroptosis (iron dependent programmed cell death). This blog discusses the molecular mechanisms of ferroptosis, its application, and challenges in the development and treatment of glioblastoma. GBM invasiveness and treatment resistance may increase if ferroptosis is avoided due to changes in glucose, lipid, glutamine, and iron metabolism. Targeting ferroptosis, which involves fatal phospholipid peroxidation due to dysregulated redox homeostasis and cellular metabolism, could be a promising treatment for GBM, as it is essential for tumor cell viability.

Breast cancer is a diverse disease with varying clinical presentations, morphologic features, and molecular characteristics. It is influenced by various genetic pathways and is a major trend in breast cancer care. Neoadjuvant chemotherapy is a major trend, requiring integrated multidisciplinary care from pathologists, radiologists, surgeons, and oncologists. Anti-HER2 therapy has improved clinical results for HER2-positive breast cancer patients.

Pertuzumab, a humanized monoclonal antibody, targets the extracellular dimerization domain of HER2, inhibiting downstream signaling and cell survival pathways. It is used in conjunction with trastuzumab and docetaxel to treat HER2-positive metastatic breast cancer. In addition to directly encouraging the death of cancer cells, monoclonal antibodies also trigger immunological activation, which is deadly to tumour cells.

Pertuzumab possesses the capability to elicit immune effector responses, including cell-mediated cytotoxicity that is dependent on antibodies. The antibody targets the PI3K/AKT and RAS/MEK/ERK pathways, protecting normal cells from suicide. It can activate immunological effector mechanisms, such as antibody-dependent cell-mediated cytotoxicity. Trastuzumab and pertuzumab function in complementary ways, highlighting the importance of understanding the biology of this devastating disease. This blog focuses on the mechanism of pertuzumab in patients with early-stage HER2-positive breast cancer receiving neoadjuvant treatment.