Therapeutic interventions for advanced prostate cancer (PCa) center on inhibiting androgen receptor (AR) and downstream signaling pathways. Resistance to androgen deprivation therapy and/or AR antagonists is inevitable and molecular mechanisms driving castration-resistant PCa (CR-PCa) primarily involve alterations in AR expression and activity.
The urgent need for castration-resistant prostate cancer molecular characterization to guide treatment has been constrained by the disease's predilection to metastasize primarily to bone. We hypothesized that the use of clinical and imaging criteria could maximize tissue acquisition from bone marrow biopsies (BMBs).
Bladder cancer is a real health problem due to its increased incidence, high recurrence rate and the fact that usually it is detected in advanced stages with limited number of diagnostic tools and different therapy response rates to current therapeutic strategies.
Human papillomavirus (HPV) infection is associated with several cancers such as cancer in the cervix, vagina, and vulva and oropharyngeal, anal, penile, and cutaneous carcinomas, which is regarded as a great public health concern.
Receptor tyrosine kinase (RTK) co-expression facilitates tumor resistance due to redundancies in the PI3K-AKT and KRAS-ERK signaling pathways, among others. Crosstalk between the oncogenic RTKs hepatocyte growth factor receptor (MET), epidermal growth factor receptor (EGFR), and human epidermal growth factor receptor 2 (HER2) are involved in tumor resistance to RTK-targeted therapies.
Systemic chemotherapy is integral to the management of muscle-invasive and metastatic bladder cancer (BCa). Neoadjuvant chemotherapy has been increasingly utilized for muscle-invasive BCa over the past several years, and several options for cisplatin-based regimens have emerged.
Castration-resistant prostate cancer was subjected to a paradigm switch from hormone resistance to androgen deprivation therapy resistance during the last decade.
Prostate cancer is an androgen-dependent disease subject to interactions between the tumor epithelia and its microenvironment. Here, we found epigenetic changes in cancer-associated prostatic fibroblasts (CAF) initiated a cascade of stromal-epithelial interactions.
Urothelial carcinoma of the bladder (UCB) is a common malignancy with limited systemic treatment options in advanced stages. Despite recent advances in immunotherapy, the majority of patients do not respond to these treatments.
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