Interrogate the Hallmarks of Cancer
Products for every stage of cancer discovery research—built by experts you can trust.
Discover a range of antibody reagents and kits you can rely on to examine the signaling pathways and hallmarks driving cancer. With over 25 years of experience supporting cancer research innovation, you can trust our antibody products will perform, every time—backed by application-specific data, peer-reviewed citations, and industry-leading technical support.
Immunoassay tools to study the hallmarks of cancer
How do researchers gain new ground when studying the mechanisms driving cancer progression? By understanding the foundational hallmarks that are present across hundreds of cancer types. Innovative methods and technologies are continually emerging, poised to examine the now twelve hallmarks and two enabling characteristics of cancer in new ways.
Expand your toolbox with help from Cell Signaling Technology (CST). See the ways CST can support your cancer research within each Hallmark.
Evading Growth Suppressors
Tumor cells can proliferate uncontrollably due to their ability to evade critical growth-inhibiting checkpoints. This means key tumor suppressors, such as p53 and retinoblastoma (Rb), are often mutated in many cancers, impacting their function.
How can I monitor whether tumor suppressors are contributing to tumor growth?
Nonmutational Epigenetic Reprogramming
Changes in normal epigenetic signatures within a tumor or cancer cells can be driven by epigenetic factors in a non-mutational, heritable way.
How can I identify changes in epigenetic signatures in cancer?
Avoiding Immune Destruction
The ability to evade immunological destruction is an emerging hallmark of cancer, whereby tumor cells disable key immune system mechanisms, enabling their survival.
How can I identify the mechanisms tumors use to evade immune destruction?
Tumor-Promoting Inflammation
Cancer cells can co-opt chronic inflammation to supply growth factors that facilitate invasion and metastasis.
How can I determine whether an inflamed tissue is more likely to be acutely or chronically inflamed?
Activating Invasion & Metastasis
The migration and invasion of tumor cells into other tissues is driven by mechanisms including the Epithelial-to-Mesenchymal Transition (EMT), which facilitates changes in cell-cell and cell-matrix interactions.
How do I determine if the TME is hypoxic and cancer-associated-fibroblast (CAF)-induced tumor cell detachment has been activated?
How can I identify if a pre-metastatic niche has been created for circulating tumor cells to seed and grow, enabling metastasis?
Inducing or Accessing Vasculature (Angiogenesis)
Tumor growth and metastasis are dependent on angiogenesis, a process in which cancer cells secrete growth factors, such as VEGF, to induce a disorganized vascular network for the delivery of nutrients and oxygen.
How can I characterize tumor vascular architecture?
How do I identify which signaling pathways are active in the tumor vasculature?
Senescent Cells
Senescence is a stable and generally irreversible state of cell cycle arrest. Although it was initially thought to act solely as a tumor-suppressing mechanism, preventing malignant cells from dividing, it is now understood that senescent cells can also drive tumorigenesis under certain conditions.
How can I tell if my cells are senescent?
Genome Instability & Mutation
Cancer cells exhibit genomic instability due to defective DNA Damage Response (DDR) pathways. With a high proliferative rate and error-prone DNA repair mechanisms, mutations often accumulate, impacting how cells grow, divide, and regulate or repair DNA, promoting further cancerous adaptations.
How can I determine which DNA repair pathways are active in my experimental model?
Resisting Cell Death
Apoptotic resistance is a key cancer hallmark that promotes tumor cell growth and survival, often achieved through diverse mechanisms, such as the loss of functional p53, increased expression of antiapoptotic regulators, or decreased expression of proapoptotic factors.
How can I determine whether Bcl-2 family members are contributing to cell death resistance?
How can I determine if my cells are undergoing apoptosis?
How can I tell if non-apoptotic cell death pathways are activated or suppressed?
Deregulating Cellular Metabolism
Cancer cells exhibit altered metabolic pathways, such as the Warburg effect and increased glutamine metabolism, to support their rapid growth, increased biomass needs, and survival in oxygen-deprived (hypoxic) tumor microenvironments (TMEs)
How can I monitor changes in metabolic pathways within cancer cells?
How can I monitor metabolic changes in cancer-associated fibroblasts and other cell types in the tumor microenvironment (TME)?
How do I determine if hypoxic conditions are present in tumor cells or other cell types in the TME?
How can I monitor changes in autophagy associated with tumors?
Unlocking Phenotypic Plasticity
The ability to unlock phenotypic plasticity enables cancer cells to reversibly switch between distinct cellular states, such as epithelial and mesenchymal, fueling their capacity to adapt to therapeutic pressure and facilitate metastasis.
How do I assess epigenetic changes associated with dedifferentiation or transdifferentiation of cancer cells?
How can I tell if tumor cells have undergone epithelial-to-mesenchymal transition (EMT)?
Sustaining Proliferative Signaling
Cancer thrives by keeping cell proliferation “on”. Normally, cells wait for signals from cytokines, growth factors, and regulatory checkpoints to proceed with division. But cancer cells bypass typical checks and balances using altered growth signaling, enabling them to ignore proliferation stop-gaps and grow uncontrollably.
How can I investigate activation of the Akt/PI3K/mTOR pathway in native tissue or a single-cell context?
How can I investigate whether the RAS-RAF-MEK-ERK pathway is activated in either native tissue or a single-cell context?