Ovarian cancer is a silent cancer which rate survival mainly relays in early stage detection. The discovery of reliable ovarian cancer biomarkers plays a crucial role in the disease management and strongly impact in patient's prognosis and survival. Although having many limitations CA125 is a classical ovarian cancer biomarker, but current research using proteomic or metabolomic methodologies struggles to find alternative biomarkers, using non-invasive our relatively non-invasive sources such as urine, serum, plasma, tissue, ascites or exosomes. Metabolism and metabolites are key players in cancer biology and its importance in biomarkers discovery cannot be neglected. In this chapter we overview the state of art and the challenges facing the use and discovery of biomarkers and focus on ovarian cancer early detection.Hydrogen sulfide (H2S), while historically perceived merely as a toxicant, has progressively emerged as a key regulator of numerous processes in mammalian physiology, exerting its signaling function essentially through interaction with and/or modification of proteins, targeting mainly cysteine residues and metal centers. As a gaseous signaling molecule that freely diffuses across aqueous and hydrophobic biological milieu, it has been designated the third 'gasotransmitter' in mammalian physiology. H2S is synthesized and detoxified by specialized endogenous enzymes that operate under a tight regulation, ensuring homeostatic levels of this otherwise toxic molecule. Indeed, imbalances in H2S levels associated with dysfunctional H2S metabolism have been growingly correlated with various human pathologies, from cardiovascular and neurodegenerative diseases to cancer. Several cancer cell lines and specimens have been shown to naturally overexpress one or more of the H2S-synthesizing enzymes.  https://www.selleckchem.com/products/ziftomenib.html  The resulting increased H2S levels have been proposed to promote cancer development through the regulation of various cancer-related processes, which led to the interest in pharmacological targeting of H2S metabolism. Herein are summarized some of the key observations that place H2S metabolism and signaling pathways at the forefront of the cellular mechanisms that support the establishment and development of a tumor within its complex and challenging microenvironment. Special emphasis is given to the mechanisms whereby H2S helps shaping cancer cell bioenergetic metabolism and affords resistance and adaptive mechanisms to hypoxia.Lung cancer is the leading cause of cancer-related deaths worldwide in both men and women. Conventional chemotherapy has failed to provide long-term benefits for many patients and in the past decade, important advances were made to understand the underlying molecular/genetic mechanisms of lung cancer, allowing the unfolding of several other pathological entities. Considering these molecular subtypes, and the appearance of promising targeted therapies, an effective personalized control of the disease has emerged, nonetheless benefiting a small proportion of patients. Although immunotherapy has also appeared as a new hope, it is still not accessible to the majority of patients with lung cancer.The metabolism of energy and biomass is the basis of cellular survival. This is true for normal cells under physiological conditions and it is also true for pathophysiologically altered cells, such as cancer cells. Thus, knowledge of the metabolic remodelling that occurs in cancer cells in the sense of, on one hand, surviving in the microenvironment of the organ in which the tumour develops and, on the other hand, escaping from drugs conditioned microenvironment, is essential to understand the disease and to develop new therapeutic approaches.Despite all the progresses developed in prevention and new treatment approaches, cancer is the second leading cause of death worldwide, being chemoresistance a pivotal barrier in cancer management. Cancer cells present several mechanisms of drug resistance/tolerance and recently, growing evidence have been supporting a role of metabolism reprograming per se as a driver of chemoresistance. In fact, cancer cells display several adaptive mechanisms that allow the emergency of chemoresistance, revealing cancer as a disease that adapts and evolve along with the treatment. Therefore, clinical protocols that take into account the adaptive potential of cancer cells should be more effective than the current traditional standard protocols on the fighting against cancer.In here, some of the recent findings on the role of metabolism reprograming in cancer chemoresistance emergence will be discussed, as the potential evolutionary strategies that could unable these adaptations, hence allowing to prevent the emergency of treatment resistance, changing cancer outcome.The human body requires a constant delivery of fresh blood cells that are needed to maintain body homeostasis. Hematopoiesis is the process that drives the formation of new blood cells from a single stem cell. This is a complex, orchestrated and tightly regulated process that occurs within the bone marrow. When such process is faulty or deregulated, leukemia arises, develops and thrives by subverting normal hematopoiesis and availing the supplies of this rich milieu.In this book chapter we will describe and characterize the bone marrow microenvironment and its key importance for leukemia expansion. The several components of the bone marrow niche, their interaction with the leukemic cells and the cellular pathways activated within the malignant cells will be emphasized. Finally, novel therapeutic strategies to target this sibling interaction will also be discussed.The relationship between inflammation and cancer has been long recognized by the medical and scientific community. In the last decades, it has returned to the forefront of clinical oncology since a wealth of knowledge has been gathered about the cells, cytokines and physiological processes that are central to both inflammation and cancer. It is now robustly established that chronic inflammation can induce certain cancers but also that solid tumors, in turn, can initiate and perpetuate local inflammatory processes that foster tumor growth and dissemination. Inflammation is the hallmark of the innate immune response to tissue damage or infection, but also mediates the activation, expansion and recruitment to the tissues of cells and antibodies of the adaptive immune system. The functional integration of both components of the immune response is crucial to identify and subdue tumor development, progression and dissemination. When this tight control goes awry, altered cells can avoid the immune surveillance and even subvert the innate immunity to promote their full oncogenic transformation.