The main difference between the available magnetic resonance imaging-transrectal ultrasound (MRI-TRUS) fusion platforms for prostate biopsy is the method of image registration being either rigid or elastic. As elastic registration compensates for possible deformation caused by the introduction of an ultrasound probe for example, it is expected that it would perform better than rigid registration.

The benefit of adjuvant chemotherapy (AC) for muscle-invasive urothelial carcinoma of the bladder (UCB) after radical cystectomy (RC) is controversial.

To effectively manage patients with advanced prostate cancer (APC), it is essential to have accurate, reproducible, and validated methods for detecting and quantifying the burden of bone and soft tissue metastases and for assessing their response to therapy. Current standard of care imaging with bone and computed tomography (CT) scans have significant limitations for the assessment of bone metastases in particular.

Analyses of associations between clinicopathologic outcomes and recurrent somatic mutations in clear cell renal cell carcinoma (ccRCC) have been limited to individual cohorts.

We examined a national data set to determine if workers employed in specific occupations develop distinct bladder cancer (BCa) phenotypes.

Smoking is considered an important risk factor for bladder cancer (BC), yet molecular characterization of BC in nonsmokers has not been extensively studied. Here, we compare molecular differences between smokers and nonsmokers with BC. BC specimens (676) profiled at a Clinical Laboratory Improvement Amendments-certified laboratory from 2006 to 2014 were retrospectively evaluated for molecular differences between smokers and nonsmokers. Protein expression was determined with immunohistochemistry. In situ hybridization was used for ERBB2 (HER2/neu) and EGFR evaluation. Genes were evaluated using Sanger or next-generation sequencing. Thirty patients were confirmed lifetime nonsmokers (NS) and 39 were reformed or current smokers (RCS). There was a trend for increased PIK3CA mutations in NS versus RCS (43% vs 11%, p=0.1760), whereas TP53 alterations were higher in RCS versus NS (63% vs 53%, p=0.6699). EGFR amplification was observed more in NS versus RCS (22% vs 11%, p=0.5815), while HER2 was amplified only in RCS (23% vs 0%, p=0.05). The molecular differences between RCS and NS with BC suggest a different oncogenesis with potentially different treatment options.

Human epidermal growth factor receptor 2 (HER2) protein overexpression or gene amplification has been shown in urothelial bladder cancer. This could be helpful when using targeted anti-HER2 therapy on these tumors.

Active surveillance (AS) is increasingly recognized as a recommended treatment option for prostate cancer (PCa) patients with clinically localized, low-risk disease; however, previous studies suggested that its utilization is uncommon in the United States.

Gleason scoring represents the standard for diagnosis of prostate cancer (PCa) and assessment of prognosis following radical prostatectomy (RP), but it does not account for patterns in neighboring normal-appearing benign fields that may be predictive of disease recurrence.

Decision making in T1 high-grade bladder cancer patients remains a challenging issue in urologic practice.

Reciprocal interactions between malignant and stromal cells create a local microenvironment that fosters tumor growth. Extracellular vesicles (EVs) such as exosomes, microvesicles, and large oncosomes are involved in tumor-stroma communication by shuttling signaling cargo and other molecules. Here we discuss how EVs released by cancer or stromal cells impact the proliferation, differentiation, and metabolism of tumors.

Hypoxia is a potent microenvironmental factor that promotes tumor metastasis. Recent studies have revealed mechanisms by which hypoxia and activation of hypoxia inducible factor (HIF)-dependent signaling promotes metastasis through the regulation of metabolic reprogramming, the stem cell phenotype, invasion, angiogenesis, immune suppression, the premetastatic niche, intravasation and/or extravasation, and resistance to apoptosis. These discoveries suggest novel paradigms in tumor metastasis and identify new opportunities for therapeutic intervention in the prevention and treatment of metastatic disease. Here, we review the impact of hypoxia and hypoxic signaling pathways in tumor and stromal cells on each step of the metastatic cascade.

The relation between fibrosis and cancer has long been debated, specifically whether desmoplasia precedes, accompanies, or succeeds tumourigenesis, progression, and metastasis. Recent reports have published opposing data, adding to the perplexity. However, what is emerging is that it is likely the specific properties of the extracellular matrix (ECM) that determine the paradoxical nature of cancer-associated fibrosis.

The interplay between cancer cells and stromal cells is increasingly recognized as a main driver of tumor progression and metastasis. This Forum article highlights the role of cancer-associated stromal fibroblasts (CAFs) in tumorigenesis and discusses the potential for developing specific stromal cancer therapies.

Intratumoral hypoxia (reduced O2 availability) is a common finding in human cancer and leads to increased activity of hypoxia-inducible factors (HIFs), which regulate the expression of genes that contribute to angiogenesis, metabolic reprogramming, extracellular matrix remodeling, epithelial-mesenchymal transition, motility, invasion, metastasis, cancer stem cell maintenance, immune evasion, and resistance to chemotherapy and radiation therapy. Conventional anticancer therapies target well-oxygenated and proliferating cancer cells, whereas there are no approved therapies that target hypoxic cancer cells, despite growing clinical and experimental evidence indicating that intratumoral hypoxia is a critical microenvironmental factor driving cancer progression. In this review, our current understanding of the consequences of HIF activity and the translational potential of targeting HIFs for cancer therapy are discussed.

Caveolin-1 (CAV1) has emerged as a promoter of proliferation, metastasis, and chemoresistance in hepatoma cells, as well as a marker of poor prognosis in liver cancer. We discuss here current knowledge and future approaches to elucidating the molecular mechanisms underlying CAV1 action during hepatocarcinogenesis and evaluate its potential use in clinical therapies.

Cellular senescence is a permanent growth arrest in cells with damage or stress that could lead to transformation. Some tumor cells also undergo senescence in response to chemotherapy. Senescent cells secrete cytokines and other factors of the senescence-associated secretory phenotype (SASP) that contribute to tumor suppression by enforcing arrest and recruiting immune cells that remove these damaged or oncogene-expressing cells from organisms. However, some cells can develop a SASP comprising factors that are immunosuppressive and protumorigenic by paracrine mechanisms. Likewise, the SASP in treated cancers can either contribute to durable responses or drive relapse. Here, we discuss the studies that have demonstrated a complex and often conflicting role for the SASP in tumorigenesis and treatment response.

Human cancers harbor great numbers of genomic alterations. One of the most common alterations is aneuploidy, an imbalance at the chromosome level. Some aneuploid cancer cell populations show varying chromosome copy number alterations over time, a phenotype known as 'chromosomal instability' (CIN). Chromosome segregation errors in mitosis are the most common cause for CIN in vitro, and these are also thought to underlie the aneuploidies seen in clinical cancer samples. However, CIN and aneuploidy are different traits and they are likely to have distinct impacts on tumor evolution and clinical tumor behavior. In this opinion article, we discuss these differences and describe scenarios in which distinguishing them can be clinically relevant.

Lymphatic vessels facilitate fluid homeostasis, immune cell trafficking, and lipid transport, and contribute to solid tumor progression as routes of metastasis. Given new evidence that lymphatic vessels both correlate with intratumoral lymphocytes and directly suppress immune function, I reevaluate the passive lymphatic vessel paradigm and discuss its relevance to antitumor immunity.