Bladder cancer (BCa) progression is closely linked to the immune microenvironment. However, the key molecules that regulate this microenvironment and their specific mechanisms remain poorly understood. This study aims to identify a key molecule and elucidate its mechanisms, providing a theoretical basis for identifying novel therapeutic targets.

ADP-ribosyltransferases (ARTs) regulate key processes in cancer, including DNA repair, transcription, immune responses, and treatment resistance. The clostridial toxin-like ADP-ribosyltransferase (ARTC) family and the diphtheria toxin-like ADP-ribosyltransferase (ARTD) family play a crucial role in genomic stability by modification of proteins either with mono(ADP-ribosyl)ation (MARylation) or poly(ADP-ribosyl)ation (PARylation). These ARTs are promising therapeutic targets and could serve as biomarkers in cancer management. This review explores the roles of these enzymes and current knowledge on specific inhibitors. A literature search was conducted in PubMed and Google Scholar to identify studies published between 1992 and 2025 on ADP-ribosyltransferases and their roles in cancer. Among ARTC family, ART1 and ART3 modulate the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) pathway, influencing angiogenesis, tumor growth, and immune evasion via cluster of differentiation 8+ (CD8+) T-cell apoptosis. Within the ARTD family, poly(ADP-ribose)polymerase (PARP)1 and PARP2 are activated by DNA single-strand breaks and are clinically validated targets in cancers with homologous recombination deficiency, such as breast cancer susceptibility genes 1/2 (BRCA1/2)-mutated breast cancer. Their inhibition exemplifies synthetic lethality and has shown clinical efficacy. Four PARP inhibitors, olaparib, niraparib, rucaparib, are approved by the Food and Drug Administration (FDA) approved. Despite these advances, selective inhibitors for ARTs remain underexplored. Ongoing research focuses on overcoming PARP inhibitor resistance, improving biomarker-driven patient selection, and expanding therapeutic strategies that target ART-related pathways.

The progression of prostate cancer cells to metastasis is supported by their tumor microenvironment. Within this microenvironment, infiltrating immune cells, such as B cells, can be either anti-tumorigenic or pro-tumorigenic. Our preliminary data showed that a higher density of the infiltrating B cells was found near prostate cancer cells in human cancer tissues, as compared to the benign prostate tissue regions, thus suggesting that infiltrating B cells would promote the progression of prostate cancer cells. In this study, we aim to investigate the role of infiltrating B cells in enhancing the migratory ability of human prostate cancer cells.

Long non-coding RNAs have been found to play a pivotal role in breast cancer, yet the majority of these lncRNAs remain to be thoroughly investigated. This study aimed to explore the role of differentially expressed long non-coding RNAs (lncRNAs) in breast cancer stemness and drug sensitivity.

The management of renal neoplasms in adolescent patients poses unique clinical challenges due to their transitional position between paediatric and adult populations. This age group exhibits marked heterogeneity in tumour histology, ranging from entities commonly observed in paediatric oncology to tumours typical of adult age, as well as rare histological subtypes that exceptionally affect the kidney. Given the substantial differences in clinical protocols between paediatric and adult populations, rigorous multidisciplinary evaluation is essential to determine optimal diagnostic and therapeutic strategies for adolescent patients.

Glioblastoma (GB) therapy is challenged by tumor heterogeneity and multidrug resistance (MDR), highlighting the need for effective therapies. This study aimed to explore the combined anticancer effects of Sunitinib (SNB) and Fenofibrate (FEN) on U87 cells.

Lung adenocarcinoma (LUAD), the most prevalent histological subtype of lung cancer, remains a leading cause of cancer-related mortality due to late diagnosis, metastasis, and therapy resistance. The aim of the study is to investigate the role of Kinetochore Scaffold 1 (KNL1) in promoting LUAD progression and its underlying molecular regulatory mechanisms.

Tumor recurrence is a major determinant of poor prognosis in hepatocellular carcinoma (HCC), yet its cellular and molecular basis remains incompletely understood. This study aimed to identify recurrence-associated genes at single-cell resolution and to develop a prognostic model for predicting survival outcomes and immunotherapy responsiveness in HCC.

Decisions regarding CT after nCCRT for locally advanced rectal cancer (LARC) are challenging due to limited evidence guiding treatment. This study aimed to (i) evaluate the predictive performance of machine learning (ML) models in patients treated with neoadjuvant concurrent chemoradiotherapy (nCCRT) alone vs. those receiving nCCRT plus chemotherapy (CT), (ii) identify features associated with treatment improvement, and (iii) derive ML-based thresholds for treatment response.

Hepatocellular carcinoma (HCC) has limited systemic options with substantial toxicity. G-quadruplex (G4) structures in oncogene promoters are attractive but challenging drug targets. This study aimed to determine whether glutamic acid-chelated cobalt (GACC) is a G4-active scaffold with anti-HCC efficacy and favorable in vivo safety, and whether an AI-guided phenotypic response surface (PRS) can optimize less toxic combinations.

-Synovial sarcoma is a rare soft tissue sarcoma. Treatment of synovial sarcoma includes surgery, radiation, pazopanib, and chemotherapy. Targeted therapies, such as B-Raf proto-oncogene, serine/threonine kinase (BRAF) inhibitors, are emerging as a potential treatment option. We describe the sixth case of a BRAFV600E synovial sarcoma, the first extra-thoracic case. This case is the first to show a complete pathological response to BRAF & mitogen-activated protein kinase kinase (MEK) inhibitors.

Breast cancer remains the primary cause of cancer-related mortality for women globally; therefore, further breakthroughs in treatment approaches are crucial. Palbociclib, ribociclib, and abemaciclib are among the Cyclin-dependent kinase 4 and 6 (CDK4/6) inhibitors that have become an innovative family of targeted therapy for hormone receptor-positive, Human Epidermal Growth factor receptor 2 (HR+/HER2-) breast cancer. These inhibitors work by preventing the action of CDK4/6, which are crucial in the regulation of the cell cycle. Leading cancer cells to cell cycle arrest and undergo apoptosis. When these inhibitors are used with endocrine medicines like letrozole and fulvestrant, clinical trials lead positive impact in progression-free survival and, in a few cases, complete survival. However, despite their effectiveness, resistance mechanisms are primary and current acquired problems, requiring combined approaches with additional targeted medicines and continuous investigation into innovative therapeutic plans. To maintain patient compliance and quality of life, common side effects such as tiredness, gastrointestinal problems, and neutropenia need to be effectively managed. There is hopefulness for wider oncological applications as next-generation CDK inhibitor development and adaptive clinical trials continue to test their potential beyond breast cancer. CDK4/6 inhibitors continue to be a key part of breast cancer treatment as cancer biology advances, marking a major advancement towards more potent and customized cancer medicines. This review aims to provide current evidence on CDK4/6 inhibitors in HR+/HER2- breast cancer, highlighting their mechanisms, interaction with endocrine resistance, combination strategies, and emerging biomarkers guiding personalized therapy.

Combined chemotherapy and photothermal therapy (PTT) represents a promising approach for enhancing cancer treatment efficacy. This study aimed to develop arsenic trioxide (ATO) and poly(cyclopentadithiophene-alt-benzothiadiazole) (PCPDTBT)-loaded nanoparticles (ATO/PCPDTBT@NPs) to evaluate their synergistic efficacy in inhibiting lung cancer growth and metastasis.

Progesterone (P4) is believed to inhibit breast cancer growth, but its role in counteracting estrogen (E2)-driven progression remains unclear. This study aimed to investigate the inhibitory effect of P4 on E2-induced cell proliferation, migration, and invasion in Estrogen receptor (ER)+/progesterone receptor (PR)+ breast cancer cells by examining its regulatory role in the epithelial-mesenchymal transition (EMT).

Breast cancer metastasis remains the leading cause of mortality and frequently targets the bone. Breast cancer cells release soluble factors and extracellular vesicles that disrupt bone marrow (BM)/bone homeostasis, promoting osteoclastogenesis and the accumulation of senescent cells. In line with updated cancer hallmarks, senescent mesenchymal stem/ stromal cells (MSCs), osteoblasts, and osteocytes contribute to remodeling of the BM microenvironment, thereby favoring pre-metastatic niche (PMN) formation and subsequent bone metastasis. We previously demonstrated that untreated stage III-B breast cancer patients (BCPs) exhibit increased oxidative stress and elevated reactive oxygen species (ROS) levels, accompanied by senescent and functionally impaired BM-MSCs-key regulators of BM/bone homeostasis. In the present study, we sought to identify the molecular targets affected by oxidative stress that drive MSC senescence in these patients.

Mucoepidermoid carcinoma (MEC) of the larynx is an extremely rare malignancy, accounting for less than 1% of primary laryngeal tumors. The optimal role of adjuvant therapy, particularly radiotherapy (RT), remains unclear due to limited evidence. This systematic review aimed to evaluate oncologic outcomes and the impact of adjuvant treatment in patients with early- and advanced-stage laryngeal MEC.

MicroRNAs (miRNAs) are small, non-coding RNAs that play a key role in the development of chemoresistance in various cancer types, including colorectal cancer (CRC). In this study, we aimed to study the underlying mechanisms of miRNA in chemotherapy-resistant CRC.

After about 20 years of exciting improvements in treatment efficacy outcomes of advanced epidermal growth factor receptor (EGFR) mutant and anaplastic lymphoma kinase (ALK) rearranged non-small cell lung cancer (NSCLC), also combined with a progressively better safety profile, from chemotherapy to new generation tyrosine kinase inhibitors (TKIs) (osimertinib, alectinib, brigatinib), the recent MARIPOSA and CROWN trials have changed this trend. For the first time in the history of EGFR and ALK treatments, we must face the issue of being a step behind in terms of toxicity profile. The combination of amivantamab plus lazertinib in EGFR mutant NSCLC, and lorlatinib in ALK rearranged NSCLC, has improved efficacy outcomes as never before. The story would be easy and totally positive if these two innovative, amazing treatments were not associated with new peculiar features in safety profiles that must be discussed with patients, because they potentially affect their quality of life. When treating these patient populations, the peculiar safety profiles of amivantamab plu lazertinib and lorlatinib require a well-structured shared decision making, "where and when", both the high probability of a longer survival and the risk of worse quality of life must be well announced and explained to our patients before the shared final treatment choice.

Cholecystokinin A receptor (CCKAR) has been linked to poor prognosis in colon cancer patients, but the role of CCKAR in colon cancer cell invasiveness and the underlying mechanisms remain elusive. This study aimed to explore the effect of CCKAR on the invasive potential of colon cancer cells.

Lung cancer remains the leading cause of cancer-related mortality worldwide, primarily driven by metabolic reprogramming and immune evasion mechanisms within tumor cells. To adapt to the nutrient-deprived tumor microenvironment (TME), lung cancer cells undergo profound metabolic reprogramming, characterized by enhanced glycolysis (the Warburg effect), increased glutamine dependency (mediated by GLS1), and accelerated lipid synthesis (involving enzymes such as FASN). These metabolic alterations not only remodel the TME but also dampen antitumor immune responses by promoting immunosuppressive cell populations (e.g., Tregs and M2 macrophages) and inhibiting effector functions of CD8+ T cells and natural killer (NK) cells. Critically, a bidirectional crosstalk operates between tumor cell metabolism and the immunosuppressive TME: metabolic reprogramming drives immune suppression through metabolite accumulation, whereas the immunosuppressive TME, in turn, promotes tumor cell adaptability-thus forming a positive feedback loop that reinforces immune evasion and therapy resistance. This review elucidates key molecular pathways governing metabolic reprogramming in lung cancer-spanning glucose, amino acid, and lipid metabolism-and their dynamic crosstalk with immune regulation, including epigenetic modifications and non-coding RNA-mediated mechanisms. Additionally, it evaluates emerging therapeutic strategies targeting the metabolic-immune axis, such as inhibitors of HK2 or GLS1 combined with anti-PD-1/PD-L1 agents, which aim to reverse immunosuppression and improve clinical outcomes. By synthesizing recent advances, this work provides a theoretical framework for precision oncology interventions, highlighting the potential of metabolic immunotherapies and future directions integrating AI and multi-omics data to overcome resistance in lung cancer.