Breast cancer is one of the leading causes of cancer deaths in women worldwide. Neoadjuvant chemotherapy (NACT) has increased rates of breast-conserving procedures and enabled the identification of patients with a particularly poor prognosis. Achieving a pathological complete response (pCR), an indicator of NACT efficacy, contrasts with residual disease (RD), which identifies patients at higher risk of recurrence. This review provides an overview of current evidence on the clinical and prognostic significance of pCR and RD in patients receiving NACT for breast cancer. The analysis is based on data from randomized clinical trials, meta-analyses, and current clinical guidelines for contemporary systemic treatment. Pathological complete response varies according to tumor subtype, with the highest rates observed in triple-negative and non-luminal HER2-positive breast cancer. In HER2-positive disease, the combination of chemotherapy with HER2-targeted therapies increases pCR rates, while the presence of RD supports escalation of postoperative treatment with antibody–drug conjugates. In triple-negative breast cancer (TNBC), the inclusion of platinum agents and immune checkpoint inhibitors improves treatment efficacy. In HER2-negative breast cancer and germline BRCA1/2 mutations, adjuvant PARP inhibitors improve survival independently of pCR, highlighting the complex relationship between pathological response and prognosis. Immunotherapy and targeted therapies are used alongside standard chemotherapy and hormone therapy in perioperative treatment. Further research is required to refine response assessment, integrate new biomarkers such as circulating tumor DNA (ctDNA), and optimize treatment selection, while clarifying the significance of reassessing hormone receptor and HER2 status in residual disease and its impact on subsequent treatment decisions.

Pancreatic adenocarcinoma is one of the most aggressive malignancies, with a steadily increasing incidence rate. Due to the asymptomatic nature of early cancer and frequent late diagnosis, only 10–20% of patients are considered for radical treatment. In approximately 40% of patients, local advancement precludes primary surgical treatment, and in approximately half of patients, the cancer is diagnosed at the metastatic stage. Treatment of advanced pancreatic cancer is based on systemic therapy, while a growing number of studies are focusing on the potential use of molecularly targeted agents. The median survival time for metastatic patients treated with FOLFIRINOX chemotherapy is 11 months, compared to 8.5 months for patients treated with gemcitabine and nab-paclitaxel-based chemotherapy. Olaparib in the maintenance treatment of patients with advanced pancreatic cancer prolongs the time to progression compared to placebo but does not affect median overall survival. Immunotherapy and targeted therapy have so far been used in a narrow group of patients with a specific molecular profile, but further research on this cancer offers a real opportunity to develop new treatment approaches. This review article is based on the NCCN (National Comprehensive Cancer Network) guidelines and publications available in the PubMed database.

Ovarian cancer, particularly high-grade serous ovarian cancer (HGSOC), remains one of the most lethal gynecological malignancies due to late diagnosis and the development of chemoresistance. The tumor microenvironment (TME) plays an important role in disease progression, with chemokines influencing cell recruitment, angiogenesis, metastasis, and immune modification. This review synthesizes current evidence on key chemokine axes in ovarian cancer, highlighting their dual roles as prognostic biomarkers and therapeutic targets. The most important axes include CXCL12/CXCR4 (which drives tumor proliferation, angiogenesis and chemoresistance via epithelial–mesenchymal transition), CCL2/CCR2 (promoting immunosuppressive tumor-associated macrophages and resistance), and CCL5/CCR5 (enhancing pro-oncogenic signaling and Treg/MDSC infiltration). Pro-angiogenic ELR+CXC chemokines like CXCL8 induce vascularization and inflammation. On the contrary, effector chemokines (CXCL9/10/11/13) correlate with “hot” immune subtypes and improved survival in several studies. High expression of immunosuppressive chemokines predicts poorer prognosis and therapy resistance, while immune-attracting profiles associate with better outcomes and chemotherapy responsiveness. Therapeutically, inhibitors like plerixafor (CXCR4), PF-04136309 (CCR2), and maraviroc (CCR5) show preclinical promise, synergizing with chemotherapy, anti-VEGF, and checkpoint inhibitors. Chemokines also represent actionable molecular targets to overcome ovarian cancer’s “cold” immune phenotype. Future research should validate multi-chemokine signatures for patient stratification and advanced clinical trials toward personalized therapies.

Pancreatic cancer (PC) is considered one of the deadliest cancers worldwide, and the number of PC-related deaths is expected to increase. Early diagnosis of PC is crucial for improving treatment outcomes. Despite improvements in overall survival (OS) in metastatic and unresectable PC due to systemic therapy, there is still a need to search for novel therapies and factors predictive of response to treatment. Cancer profiling based on genome sequencing can be used to develop targeted therapies and improve prognostics and treatment outcomes. Therefore, this review was conducted to evaluate the clinical value of molecular subtyping in pancreatic cancer as a prognostic and predictive factor in pancreatic cancer. Due to its limitations, including the lack of a registered protocol and risk of bias assessment for the included studies and those whose results were not included, this study should be considered a narrative review with a structured search strategy rather than a systematic review.