Lecture

Hallmarks of Cancer: Complexity and Capabilities

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In course

BIO-392: Oncology

This course provides a comprehensive overview of the biology of cancer, including common mechanisms that cancer cells use to grow and disseminate in humans and in animal models. ...

Description

This lecture introduces the hallmarks of cancer, highlighting the extraordinary complexity of the disease at genetic, histological, and prognostic levels. It explores the rationalization of cancer complexity, proposing that seemingly disparate cancers may share fundamental capabilities. The hallmarks, such as sustained proliferative signaling and evading growth suppressors, are discussed in detail, along with emerging hallmarks like deregulating cellular energetics. The lecture also covers the role of enabling characteristics and the reprogramming of signaling circuits within cancer cells. Additionally, it delves into the interactions between cancer cells and their microenvironment, emphasizing the importance of understanding tumor heterogeneity and the tumor microenvironment in cancer progression.

Instructors (2)

Daniel Constam

Daniel Constam received his doctoral degree in Natural Sciences from ETH Zürich in the neuroimmunology group of Adriano Fontana (1993). For postdoctoral studies, he joined the laboratory of Elizabeth Robertson as an EMBO fellow at Harvard University to characterize proprotein convertase (PC) functions in mouse models of early embryogenesis (1994-1999). As an ISREC group leader (>2000) and Associate Professor at EPFL (>2007), he initially continued to study pluripotency and lineage differentiation during development and found that several secreted PCs jointly regulate cell-cell adhesion and TGFβ signaling pathways at the cross-roads of stem cell and cancer biology. To map the proteolytic activity of PCs and their relative distribution in exocytic or endocytic vesicles, his lab developed PC-specific FRET sensors for high resolution live imaging in normal cells and in tumour-host interactions. His studies on TGFβ signaling also identified the RNA-binding protein Bicc1 and its self-polymerization in membrane-less organelles as regulators of mRNA translation and cell metabolism that cooperate with primary cilia to prevent cystic growth in renal tubules and in pancreatic and bile ducts.

Michele De Palma

Official source

Ontological neighbourhood

Biology

Cell biology: Cancer

Related concepts (31)

Somatic evolution in cancer

Somatic evolution is the accumulation of mutations and epimutations in somatic cells (the cells of a body, as opposed to germ plasm and stem cells) during a lifetime, and the effects of those mutations and epimutations on the fitness of those cells. This evolutionary process has first been shown by the studies of Bert Vogelstein in colon cancer. Somatic evolution is important in the process of aging as well as the development of some diseases, including cancer. Cells in pre-malignant and malignant neoplasms (tumors) evolve by natural selection.

Tumor marker

A tumor marker is a biomarker found in blood, urine, or body tissues that can be elevated by the presence of one or more types of cancer. There are many different tumor markers, each indicative of a particular disease process, and they are used in oncology to help detect the presence of cancer. An elevated level of a tumor marker can indicate cancer; however, there can also be other causes of the elevation (false positive values). Tumor markers can be produced directly by the tumor or by non-tumor cells as a response to the presence of a tumor.

Breast cancer

Breast cancer is cancer that develops from breast tissue. Signs of breast cancer may include a lump in the breast, a change in breast shape, dimpling of the skin, milk rejection, fluid coming from the nipple, a newly inverted nipple, or a red or scaly patch of skin. In those with distant spread of the disease, there may be bone pain, swollen lymph nodes, shortness of breath, or yellow skin.

Benign tumor

A benign tumor is a mass of cells (tumor) that does not invade neighboring tissue or metastasize (spread throughout the body). Compared to malignant (cancerous) tumors, benign tumors generally have a slower growth rate. Benign tumors have relatively well differentiated cells. They are often surrounded by an outer surface (fibrous sheath of connective tissue) or stay contained within the epithelium. Common examples of benign tumors include moles and uterine fibroids. Some forms of benign tumors may be harmful to health.

Neuroendocrine tumor

Neuroendocrine tumors (NETs) are neoplasms that arise from cells of the endocrine (hormonal) and nervous systems. They most commonly occur in the intestine, where they are often called carcinoid tumors, but they are also found in the pancreas, lung, and the rest of the body. Although there are many kinds of NETs, they are treated as a group of tissue because the cells of these neoplasms share common features, including a similar histological appearance, having special secretory granules, and often producing biogenic amines and polypeptide hormones.

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