Neutrophils are recognized active participants in inflammatory responses and are intricately linked to cancer progression. In response to inflammatory stimuli, neutrophils become activated, releasing neutrophils extracellular traps (NETs) for the capture and eradication of pathogens, a phenomenon termed NETosis. With a deeper understanding of NETs, there is growing evidence supporting their role in cancer progression and their involvement in conferring resistance to various cancer therapies, especially concerning tumor reactions to chemotherapy, radiation therapy (RT), and immunotherapy. This review summarizes the roles of NETs in the tumor microenvironment (TME) and their mechanisms of neutrophil involvement in the host defense. Additionally, it elucidates the mechanisms through which NETs promote tumor progression and their role in cancer treatment resistance, highlighting their potential as promising therapeutic targets in cancer treatment and their clinical applicability.

By the beginning of the year 2021, the estimated number of new cancer cases worldwide was about 19.3 million and there were 10.0 million cancer-related deaths. Cancer is one of the deadliest diseases worldwide that can be attributed to genetic and environmental factors, including nutrition. The good nutrition concept focuses on the dietary requirements to sustain life. There is a substantial amount of evidence suggesting that a healthy diet can modulate cancer risk, particularly the risk of colorectal and breast cancers. Many studies have evaluated the correlation between our diet and the risk of cancer development, prevention, and treatment. The effect of diet on cancer development is likely to happen through intertwining mechanisms including inflammation and immune responses. For instance, a greater intake of red and processed meat along with low consumption of fruits and vegetables has been associated with increased levels of inflammatory biomarkers that are implicated in cancer development. On the other hand, the consumption of phytosterols, vitamins, and minerals, which exert antioxidant and anti-inflammatory roles have been linked to lower cancer risk, or even its occurrence prevention. In this book, we aim to summarize the current knowledge on the role of nutrition in cancer to provide the best scientific advice in this regard.

RNA modifications play a crucial role in cancer development, profoundly influencing various stages of the RNA lifecycle. These stages encompass nuclear processing, nuclear export, splicing, and translation in the cytoplasm. Among RNA modifications, the ac4C RNA modification, also known as N4-acetylcytidine, stands out for its unique role in acetylation processes. Specific proteins regulate ac4C RNA modification, maintaining the dynamic and reversible nature of these changes. This review explores the molecular mechanisms and biological functions of ac4C RNA modification. It examines the intricate ways in which ac4C RNA modification influences the pathogenesis and progression of cancer. Additionally, the review provides an integrated overview of the current methodologies for detecting ac4C RNA modification. Exploring the potential applications of manipulating this modification suggests avenues for novel therapeutic strategies, potentially leading to more effective cancer treatments in the future.

Angiogenesis is recognized as a hallmark of cancer, and vascular endothelial growth factor (VEGF) is a key regulator of the angiogenic process and is related to cancer progression. Anti-VEGF therapy has been tried but with limited success and without useful stratification for angiogenesis markers. Further, the landscape of VEGF single nucleotide polymorphisms (SNPs) in breast cancer and their clinical relevance is not well studied, and their relation to tissue-based angiogenesis markers has not been explored. Here, we studied a selection of VEGFA SNPs in nontumor lymph nodes from a population-based breast cancer cohort (n = 544), and their relation to clinicopathologic variables, vascular tissue metrics, and breast cancer-specific survival. Two of the SNP candidates (rs833068GA genotype and rs25648CC genotype) showed associations with angiogenesis tissue markers, and the VEGFA rs833068GA genotype was associated with breast cancer-specific survival among ER-negative cases. We also found trends of association between the rs699947CA genotype and large tumor diameter and ER-negative tumors, and between the rs3025039CC genotype and large tumor diameter. Our findings indicate some associations between certain VEGF SNPs, in particular the rs833068GA genotype, and both vascular metrics and patient survival. These findings and their potential implications need to be validated by independent studies.

Long noncoding RNAs (lncRNAs) constitute a distinctive subset of RNA molecules with limited protein-coding potential, which exert crucial impacts on various biological activities. In the context of cancer, dysregulated lncRNAs function as essential regulators that affect tumor initiation and malignant progression. These lncRNAs serve as competitive endogenous RNAs (ceRNAs) through sponging microRNAs and regulating the expression of targeted genes. Moreover, they also directly bind to RNA-binding proteins, which can be integrated into a complex mechanistic network. E2F1, an extensively studied transcription factor, mediates multiple malignant behaviors by regulating cell cycle progression, tumor metastasis, and therapeutic response. Emerging evidence suggests that lncRNAs play a pivotal role in regulating the E2F1 pathway. This review aims to elucidate the intricate gene regulatory programs between lncRNAs and E2F1 in cancer progression. We elaborate on distinct mechanistic networks involved in cancer progression, emphasizing the potential of the lncRNAs/E2F1 axes as promising targets for cancer therapy. Additionally, we provide novel perspectives on current evidence, limitations, and future directions for targeting lncRNAs in human cancers. Fully deciphering the intricate network of lncRNA/E2F1-mediated regulatory mechanisms in cancer could facilitate the translation of current findings into clinical course, such efforts ultimately significantly improve the clinical prognosis of cancer patients.

The traditional view of cancer emphasizes a genes-first process. Novel cancer traits arise by genetic mutations that spread to drive phenotypic change. However, recent data support a phenotypes-first process in which nonheritable cellular variability creates novel traits that later become heritably stabilized by genetic and epigenetic changes. Single-cell measurements reinforce the idea that phenotypes lead genotypes, showing how cancer evolution follows normal developmental plasticity and creates novel traits by recombining parts of different cellular developmental programs. In parallel, studies in evolutionary biology also support a phenotypes-first process driven by developmental plasticity and developmental recombination. These advances in cancer research and evolutionary biology mutually reinforce a revolution in our understanding of how cells and organisms evolve novel traits in response to environmental challenges.

OBJECTIVE: Most patients with colorectal cancer (CRC) show no early symptoms, and tumor markers have low sensitivity and specificity. We therefore investigated the ability of serum fibrin degradation complex DR-70 plus traditional tumor markers to diagnose CRC.
METHODS: We retrospectively screened patients with CRC or non-malignant colorectal diseases, as well as healthy individuals, for inclusion in this study. The individuals\' clinical characteristics were recorded, and serum samples were collected. Expression levels of DR-70 and conventional tumor markers were measured by enzyme-linked immunosorbent assay and electrochemiluminescence.
RESULTS: DR-70 levels differed significantly among patients with CRC, patients with benign colorectal diseases, and healthy individuals. Receiver operating characteristic curve analysis identified DR-70 as a conventional tumor marker with the highest sensitivity and the second-highest specificity after carcinoembryonic antigen.
CONCLUSIONS: This study identified DR-70 as a reliable marker for the detection, differentiation, and progression of CRC, with good sensitivity and specificity. DR-70 measurement could greatly improve the efficacy of CRC diagnosis when used together with other tumor markers.

Cancer cells are generally exposed to numerous extrinsic stimulations in the tumor microenvironment. In this environment, cancer cells change their expression profiles to fight against circumstantial stresses, allowing their progression in the challenging tissue space. Technological advancements of spatial omics have had substantial influence on cancer genomics. This technical progress, especially that occurring in the spatial transcriptome, has been drastic and rapid. Here, we describe the latest spatial analytical technologies that have allowed omics feature characterization to retain their spatial and histopathological information in cancer tissues. Several spatial omics platforms have been launched, and the latest platforms finally attained single-cell level or even higher subcellular level resolution. We discuss several key papers elucidating the initial utility of the spatial analysis. In fact, spatial transcriptome analyses reveal comprehensive omics characteristics not only in cancer cells but also their surrounding cells, such as tumor infiltrating immune cells and cancer-associated fibroblasts. We also introduce several spatial omics platforms. We describe our own attempts to investigate molecular events associated with cancer progression. Furthermore, we discuss the next challenges in analyzing the multiomics status of cells, including their morphology and location. These novel technologies, in conjunction with spatial transcriptome analysis and, more importantly, with histopathology, will elucidate even novel key aspects of the intratumor heterogeneity of cancers. Such enhanced knowledge is expected to open a new path for overcoming therapeutic resistance and eventually to precisely stratify patients.

The endocannabinoid system is composed by a complex and ubiquitous network of endogenous lipid ligands, enzymes for their synthesis and degradation, and receptors, which can also be stimulated by exogenous compounds, such as those derived from the Cannabis sativa. Cannabis and its bioactive compounds, including cannabinoids and non-cannabinoids, have been extensively studied in different conditions. Recent data have shown that the endocannabinoid system is responsible for maintaining the homeostasis of various skin functions such as proliferation, differentiation and release of inflammatory mediators. Because of their role in regulating these key processes, cannabinoids have been studied for the treatment of skin cancers and melanoma; their anti-tumour effects regulate skin cancer progression and are mainly related to the inhibition of tumour growth, proliferation, invasion and angiogenesis, through apoptosis and autophagy induction. This review aims at summarising the current field of research on the potential uses of cannabinoids in the melanoma field.

The nuclear pore complexes are essential for cellular and molecular processes such as trafficking between the cytoplasm and the nucleus, chromatin, transcriptional outputs, and DNA damage repair. Nucleoporins, components of nuclear pore complexes, have been linked to cancer through nucleo-cytoplasmic cargo trafficking, cell division, signalling pathways, chromatin-related processes, and protein stability and degradation. This study aims to understand how nucleoporins specifically contribute to cancer proliferation and progression across various cancer types. Accordingly, angles such as nuclear trafficking, fusion proteins, tumour suppressors, signalling pathways, tumour microenvironment, nucleosomes, and chromatin processes were found to bridge the function of nucleoporins and cancer progression, and the underlying mechanisms have been analysed in this study. A deep understanding of the function of nucleoporins in cancer progression will pave the way for the effective targeting of these molecules for therapeutic gain. Improved treatment responses can enhance the quality of life of cancer patients.