Cancer Biology 101



What is cancer? This video will give you a short and simple introduction to cancer biology. It explains the fundamental principles involved in tumorigenesis and also explores different treatment strategies. It also emphasizes that cancer is a very heterogeneous disease and therefore difficult to understand and to treat.


This animation explains the mechanism of abnormal signal transduction resulting in uncontrolled cell proliferation. It also provides an overview of the potential targets of anticancer therapies. Be sure to visit our signaling page to learn more about cancer signaling.


Another common mechanism of cancer biology is the ability of malignant cells to migrate from their original site to organs throughout the body. This animation provides a closer look at how the EGFR pathway activates and modulates this process of metastasis. Be sure to visit our signaling page to learn more about cancer signaling.


As the tumor grows, it eventually reaches a size where it requires additional vasculature in order to sustain continued growth. To achieve this, tumor cells excrete certain proteins that stimulate blood vessel growth into and around the tumor – a process called angiogenesis. To learn more about angiogenesis and how it can be influenced by certain nutrients, visit our cancer geniuses.


Cancer cells are hungry. To feed their rapid growth and division, their metabolism changes. Moreover, they use sugar (glucose) in a different way to normal cells. This animation, created by Nature Reviews Drug Discovery, explores the key aspects of the altered metabolism in cancer cells and explains how these can be exploited for the development of new anticancer strategies.


Apoptosis or “programmed cell death” is a mechanism by which organisms limit the growth and replication of cells. Loss of apoptosis is one of the key mechanisms behind cancer. This animation reveals the faulty apoptotic pathways that tumor cells often have. To learn more about apoptosis and death receptor signaling, be sure to visit our signaling page.


There are many mutations that can contribute to cancer. Some mutations create more active genes, and others break genes, such as the Tumor Suppressor Gene displayed here. The disruption of the Tumor Supressor Gene expression causes the cancerous cell to divide when it should not. This nucleotide mutation has been observed in a specific type of triple negative breast cancer, presenting this area for further research.


Death receptors are cell surface receptors that transmit apoptotic signals initiated by specific ligands such as Fas ligand, TNF alpha and TRAIL. They play an important role in apoptosis and can activate a caspase cascade within seconds of ligand binding. Induction of apoptosis via this mechanism is therefore very rapid. Targeting death receptor signaling is a promising treatment option for many cancers.


This video shows how the microenvironment of a tumor can influence Hedgehog Signaling. The principal of the activation of Hedgehog Signaling also applies to activation through mutations in different components of this complex pathway. Activation of the Hedgehog pathway leads to an increase in Snail protein expression and a decrease in E-cadherin and Tight Junctions. Hedgehog signaling also appears to be a crucial regulator of angiogenesis and thus metastasis.


The JAK-STAT signaling pathway transmits information from chemical signals outside the cell, through the cell membrane, and into gene promoters on the DNA in the cell nucleus, which causes DNA transcription and activity in the cell. The JAK-STAT system is a major signaling alternative to the second messenger system. Disrupted or dysregulated JAK-STAT functionality (which is usually by inherited or acquired genetic defects) can result in immune deficiency syndromes and cancers.


The MAPK/ERK pathway (also known as the Ras-Raf-MEK-ERK pathway) is a chain of proteins in the cell that communicates a signal from a receptor on the surface of the cell to the DNA in the nucleus of the cell. Components of the MAPK/ERK pathway were discovered when they were found in cancer cells. Drugs that influence this signaling pathway are being investigated as cancer treatments.


Animation depicting the Notch intracellular signaling pathway, which is involved in many important developmental processes determining cell fate. The involvement of Notch signalling in many cancers has led to investigation of notch inhibitors (especially gamma-secretase inhibitors) as cancer treatments. As of 2013 at least 7 notch inhibitors were in clinical trials. MK-0752 has given promising results in an early clinical trial for breast cancer.


This video provides an overview of the PI3K/AKT signaling pathway. In many cancers, this pathway is overactive, thus reducing apoptosis and allowing proliferation. This pathway is necessary, however, to promote growth and proliferation over differentiation of adult stem cells, neural stem cells specifically. It is the difficulty in finding an appropriate amount of proliferation versus differentiation that researchers are trying to determine in order to utilize this balance in the development of various therapies.


The transforming growth factor beta (TGF-β) signaling pathway is involved in many cellular processes in both the adult organism and the developing embryo including cell growth, cell differentiation, apoptosis, cellular homeostasis and other cellular functions.When a cell is transformed into a cancer cell, parts of the TGF-β signaling pathway are mutated, and TGF-β no longer controls the cell. TGF-β acts on the surrounding stromal cells, immune cells, endothelial and smooth-muscle cells. It causes immunosuppression and angiogenesis, which makes the cancer more invasive


Animation showing a simplified version of the canonical Wnt/ β-catenin signaling pathway in normal cells and in tumor cells. Changes in CTNNB1 expression, which is the gene that encodes β-catenin, can be measured in not just breast cancer, but also colorectal cancer, melanoma, prostate cancer, lung cancer, and several other cancer types. Increased expression of Wnt ligand-proteins such as Wnt 1, Wnt2, and Wnt7A have been observed in the development of glioblastoma, oesophageal cancer, and ovarian cancer respectively.

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