Bøger i SpringerBriefs in Cancer Research serien

Obesity is a risk factor for breast cancer in older women. A number of adipose-derived and obesity-related factors have been shown to affect tumour cell growth. These include adipokines, insulin, IGF-1 and oestrogens. The majority of obesity-related postmenopausal breast cancers are oestrogen-dependent. Since the ovaries no longer produce oestrogens after menopause, and that circulating levels are negligible, it is evident that it is the oestrogens produced locally within the breast adipose that are responsible for the increased growth of breast cancer cells. Aromatase is the enzyme that converts androgens into oestrogens and its regulation is dependent on the activity of a number of tissue-specific promoters. Targeting oestrogen biosynthesis in obesity may be useful for the prevention of breast cancer. Aromatase inhibitors are efficacious at treating postmenopausal breast cancer and recent studies suggest that they may also be useful in the prevention setting. However, these compounds inhibit the catalytic activity of aromatase and as a consequence lead to a number of undesirable side-effects, including arthralgia and possible cognitive defects due to inhibition of aromatase in the bone and brain, respectively. Novel therapies, such as those employed to treat obesity-associated disease, including anti-diabetics, may prove successful at inhibiting aromatase specifically within the breast. This SpringerBrief will explore all of these issues in depth and the authors are in a unique position to write about this topic, having extensive experience in the field of aromatase research.

Abnormal expression of MHC class I molecules in malignant cells is a frequent occurrence that ranges from total loss of all class I antigens to partial loss of MHC specific haplotypes or alleles. Different mechanisms are described to be responsible for these alterations, requiring different therapeutic approaches. A complete characterization of these molecular defects is important for improvement of the strategies for the selection and follow-up of patients undergoing T-cell based cancer immunotherapy. Precise identification of the mechanism leading to MHC class I defects will help to develop new personalized patient-tailored treatment protocols. There is significant new research on the prevalence of various patterns of MHC class I defects and the underlying molecular mechanisms in different types of cancer. In contrast, few data is available on the changes in MHC class I expression during the course of cancer immunotherapy, but the authors have recently made discoveries that show the progression or regression of a tumor lesion in cancer patients undergoing immunotherapy depends on the molecular mechanism responsible for the MHC class I alteration and not on the type of immunotherapy used. According to this notion, the nature of the preexisting MHC class I lesion in the cancer cell has a crucial impact on determining the final outcome of cancer immunotherapy. This SpringerBrief will present how MHC class 1 is expressed, explain its role in tumor progression, and its role in resistance to immunotherapy.

This SpringerBrief is comprehensive account of the functions and effects of the Epstein-Barr virus (EBV) EBNA1 protein that relate to EBV-associated cancers and evidence for EBNA1 contributions to these cancers. EBNA1 was the first EBV protein detected and the most critical for EBV latent infection. EBNA1 fulfills multiple functions at EBV genomes which have been described in many (sometimes confusing) reports over the last 28 years. While these were initially thought to be the only roles of EBNA1, many reports in recent years have shown that EBNA1 also directly affects cellular processes in ways that would be expected to contribute to oncogenesis. However, the degree to which EBNA1 promotes cell survival and oncogenesis in various types of human tumours is not entirely clear and a matter of debate. This book offers a current synopsis of EBNA1 functions in EBV latency, including functions in DNA replication, mitotic segregation and transcription. Mechanisms of these EBNA1 functions is also discussed as well as implications for tumourigenesis. In addition, the cellular effects of EBNA1 will be reviewed, including how EBNA1 manipulates specific cellular proteins and relationships to EBV-associated lymphomas and carcinomas.

This exciting SpringerBrief presents evidence for new ideas that will challenge several theories of how cancer biology is understood. However, this text combines the complex levels studying cancer at the molecular biology level, endocrinology level, and transcriptomics level.

This book provides up-to-date information on the development and progression of hepatocellular carcinoma (HCC) with a review of the cellular and molecular mechanisms involved in the disease process.