Besides surgery, radiation therapy, endocrine therapy or chemotherapy, which were widely used in cancer patients for decades, the 21st century has seen the emergence of "targeted" therapy, resulting from the identification of molecular pathways in cells and their alterations in tumors. An increasing number of compounds targeting specific molecules or cancer cells have been developed and, for some of them, approved by the United States Food and Drug Administration (FDA) as well as other regulators in EU and Japan Additional new and more efficient types of compounds, are still in clinical trials, but are expected to gain future approval. More than eighty FDA-approved targeted therapies are described here, along with about eighty other promising compounds. These drugs are members of various therapy classes, including tyrosine kinase inhibitors; serine/threonine kinase inhibitors; dual specificity kinase inhibitors; lipid kinase inhibitors; poly ADP ribose polymerase inhibitors; monoclonal antibodies; microtubule targeting agents; histone deacetylase inhibitors; proteasome inhibitors; antimetabolites; immunomodulatory agents; DNA methyltransferase inhibitors; hedgehog pathway inhibitors; enzymes; protein translation inhibitors; vaccines, oncolytic viruses; chimeric antigen receptor T-cells (CAR-T); and so on. A series of "companion" diagnostics intended to be used as an indication for specific therapies, and approved to this aim are also mentioned. The book aims to present the broad landscape of compounds and companion diagnostics that are expected to pave the way towards a future of hope for cancer patients.

Since the year 2000, exciting developments in cancer therapy have occurred. For decades in the 20th century, the hallmark of medical treatment for cancer had been cytotoxic chemotherapy, with drugs targeting rapidly dividing cells, including cancer cells but also certain normal tissues. As a result, many patients experienced the "classic" toxicities of alopecia, gastrointestinal symptoms and/or myelosuppression. In the last years, however, clinical research has been strongly occupied with the identification of mutations and aberrations concerning molecular pathways in cancer and their alterations, which has enabled the emergence of a "targeted" (somewhat personalized) medicine approach to treatment. Today, although traditional cytotoxic chemotherapy remains the treatment of choice for many malignancies, notably as first-line agents, targeted therapies are a possible choice for many types of cancer, including breast, prostate, CRC, lung, kidney cancers, as well as lymphoma, leukaemia, and myeloma. Over 60 of these targeted therapies recently approved by the United States Food and Drug Administration (FDA) are detailed in the book, and their intended use in one or more cancer types are shown.

MicroRNAs, or miRNAs, are a recently discovered class of small regulatory RNAs that influence the stability and translational efficiency of target messenger RNAs (mRNAs). Alterations in miRNA expression are associated with an increasing number of biological processes, including breast cancer. The study of miRNAs is a rapidly developing field that could considerably change our vision of breast cancer biology. This book offers an insight into our current knowledge of human miRNAs, with a specific interest for breast cancer.

Breast cancer is the most frequently diagnosed type of cancer and a second leading cause of cancer death in women after lung cancer. Despite their proven efficacy, classical therapies are, however, unable to cure metastatic breast cancer and are often associated with significant toxicity and side-effects, due to a wide spectrum of action. During the last years, our increasing knowledge of the molecular pathways underlying cancer development has led to the introduction of new drugs, of which most are directed towards very specific targets. Rather than to be used as single agents, these "modern" compounds could ultimately be combined with classical molecules. Here are described nearly 150 drugs that are currently used in routine therapy or are in clinical trials in breast cancer patients. From the classical tamoxifen, fluorouracil, cyclophosphamide, doxorubicin, epirubin, docetaxel, paclitaxel..., to the more recently introduced ixabepilone, lapatinib, vorinostat, everolimus, bevacizumab..., they also include capecitabine, gemcitabine, trastuzumab, bevacizumab, fulvestrant, aromatase inhibitors, cancer vaccines, inhibitors of tumour-induced osteolysis, insulin-like growth factor-I receptor inhibitors, poly(ADP-ribose) polymerase (PARP)-1 inhibitors, and many others. This book offers an insight into current developments of breast cancer therapy, when classicism meets modernity.

Breast cancer is the most frequently diagnosed type of cancer and the second leading cause of cancer death in women after lung cancer. It is estimated that breast cancer affects more than 1,000,000 women world-wide each year, and about 450,000 die from the disease. During the last decades, breast cancer has received considerable attention, yet it is a very old disease that was described years and years ago. This book provides a summary of breast cancer history. It covers the ages from the ancient times to the early 2000's, but mainly focuses on the 20th century and its numerous discoveries and inventions in the field of breast cancer detection, analysis and treatment.

Breast cancer is characterised by the accumulation of genetic alterations, including point mutations and loss of entire DNA regions ("loss of heterozygosity" or LOH). Among genes that are affected by such events, the "tumour suppresser genes" (TSGs) have a peculiar interest since they often occupy pivotal positions in regulatory networks that control the cell cycle and/or encompass various signal transduction cascades. While a number of genes have been suggested as candidate TSGs in breast cancer, only a few of them have been confirmed in this status. They include TP53, BRCA1, BRCA2...and are mainly involved in the control of DNA repair, cell proliferation, apoptosis and signalling. Some TSGs are linked to familial (hereditary) forms of breast cancer. The exact definition of what is a TSG is still debated. Recently, genes not affected by mutation or even LOH, but occasionally methylated have been considered as TSGs.

Cancer is characterised by uncontrolled cell division and the potential of the cells to invade surrounding tissues and spread around the body. Most of these changes in cellular behaviour are the result of alterations in the function or levels of the proteins that control these processes. And these alterations are, in turn, usually caused by modifications at the DNA level. Indeed, cancer is now recognised as being essentially a disease caused by mutation, or dysregulated expression, of genes. Of the estimated 30,000 genes in the human genome, currently more than 250 are known to play an important role in the development of cancer, either sporadic or familial. In some cases, their effects result from gene fusion, due to translocation for instance, or from amplification of a chromosomal region. During the last years, attention has largely shifted from the identification of rare high-risk genetic mutations to a hunt for lower risk gene polymorphisms, many of which are likely to be common within the population. Another increasingly investigated field is epigenetics, which relates to abnormal and prolonged changes in the mechanisms that alter gene expression and activity, without involving changes in genetic sequence.