Cancer Research Products and Resources
Cancers are often named after the primary tumor site. Each primary tumor site has characteristic features and markers that can be targeted in research. For more information about each cancer type by primary tumor site please browse by cancer disease product areas, you can also search by cancer target or product type. You can browse below or search in the search bar above.
Table of Contents
Cancer Disease Types
Browse research products by Cancer disease Type
Breast Cancer | Leukemia | Lung Cancer | Prostate Cancer |
Colorectal Cancer (at tocris.com) | Liver Cancer (at tocris.com) | Pancreatic Cancer (at tocris.com) |
Cancer Research Areas
Browse research products by cancer research type:
Angiogenesis | Apoptosis | Cancer Biomarker | Cancer Metabolism |
Cancer Stem Cells | Cell Cycle | Cytokines | DNA Repair |
Epigenetics | Exosomes in Cancer | Growth Factors | Hypoxia |
Targeted Protein Degradation |
Cancer Research Tools and Resources
View All Tools and Resources
View All Cancer Literature
View All Cancer Signal Pathways
- mTOR Pathway
- MAPK/ERK Pathway
- p38 MAPK Pathway
- JNK Pathway
- AKT Pathway
- Apoptosis Pathway
- Autophagy Pathway
View All Cancer Articles & Blogs
- The ERK Signal Transduction Pathway: Its Role in Growth Factor Signaling and Cancer
- A Simple Flow Cytometry-Based Assay for CAR Detection Using Fluorokines™
- Tired T cells: Hypoxia Drives T cell Exhaustion in the Tumor Microenvironment
- Harnessing Natural Killer Cell Activity for Anti-Tumor Immunotherapy
Cancer Background and FAQs
Tumor Suppressors | Oncogenes | References & Further Reading
Cancer encompasses a wide range of diseases where cellular proliferation goes unchecked leading to increased cell growth and decreased cell death. Genetic alterations, which may be inherited or result from environmental influence, represent the main basic underlying mechanism for disease onset and progression. Accelerated growth, programmed cell death evasion, immune checkpoint evasion and ability to invade distant tissues are all hallmark properties of cancerous cells. These abnormal cellular properties are brought about by mutations in genes involved in the regulation of cell proliferation and growth, including proto-oncogenes and tumor suppressor genes. Additionally, mutations in genes involved in DNA repair further undermine the integrity of DNA sequences facilitating the accumulation of multiple DNA lesions in cancer cells.
Traditionally, cancer types have been identified based on the site of origin and afflicted organ or tissue. In the US, prostate and breast cancer represent the most prevalent cancer types afflicting males and females, respectively. It is also noteworthy that lung cancer causes ~25% of cancer-related deaths in both males and females. Lung cancer causes more deaths annually than breast, prostate, and colon cancer combined.
Tumor suppressors are genes that protect cells from cancerous transformations. But, occasionally, these genes mutate and a loss in function leads to cancer. This is in contrast to oncogenes, which cause cancer through a mutation resulting in a gain of function. Tumor suppressor genes are often grouped into three categories: Caretakers, gatekeepers, and landscapers. Gatekeepers are those genes which prevent abnormal cell proliferation, caretakers provide genomic stability (through assessing and correcting DNA damage/mismatches/chromosomal abnormalities), and landscapers control the microenvironment in which cells grow.
p53 is often referred to as the “master” tumor suppressor gene because it is involved in the broadest of cancers. It can act as caretaker or gatekeeper and plays a role in apoptosis, genomic stability, and angiogenesis inhibition. There have been hundreds of other tumor suppressors reported and there continues to be new targets discovered through the field of oncogenomics. Bio-Techne has an extensive catalog of tumor suppressor antibodies to suit most researchers needs.
Oncogenes are genes that are critical to the cause and proliferation of cancer. Normal, non-mutated forms of these genes (proto-oncogenes) code for proteins that regulate cell growth and differentiation. In contrast to tumor suppressors, they are involved in cancer through a gain of function, not loss of function (caused by a mutation, increased expression, or chromosome rearrangement). Many current cancer therapies focus on targeting proteins that are encoded by oncogenes.
There are many known and proposed mechanisms of oncogenesis, which can lead to abnormal cell growth. Some well-studied drivers of malignancy include mutation of proteins involved in intracellular signaling (such as MAPK/ERK and PI3K/AKT/MTOR pathways), mutation of growth factor receptors (ex. PDGF), and excess expression of growth factors (ex. ErbB2/HER2).
Select References for further reading
Aoki, K., & Taketo, M. M. (2007). Adenomatous polyposis coli (APC): a multi-functional tumor suppressor gene. Journal of Cell Science. https://doi.org/10.1242/jcs.03485
Fuhrman-Luck, R. A., Loessner, D., & Clements, J. A. (2014). Kallikrein-Related Peptidases in Prostate Cancer: From Molecular Function to Clinical Application. EJIFCC. PMCID: PMC4975200
Goldar, S., Khaniani, M. S., Derakhshan, S. M., & Baradaran, B. (2015). Molecular mechanisms of apoptosis and roles in cancer development and treatment. Asian Pacific Journal of Cancer Prevention. https://doi.org/10.7314/APJCP.2015.16.6.2129
Hassanpour, S. H., & Dehghani, M. (2017). Review of cancer from perspective of molecular. Journal of Cancer Research and Practice. https://doi.org/10.1016/j.jcrpr.2017.07.001
Jaiswal, P. K., Goel, A., & Mittal, R. D. (2015). Survivin: A molecular biomarker in cancer. Indian Journal of Medical Research. https://doi.org/10.1002/stem.592
Maguer-Satta, V., Besançon, R., & Bachelard-Cascales, E. (2011). Concise review: Neutral endopeptidase (CD10): A multifaceted environment actor in stem cells, physiological mechanisms, and cancer. Stem Cells. https://doi.org/10.1002/stem.592
Sau, A., Lau, R., Cabrita, M. A., Nolan, E., Crooks, P. A., Visvader, J. E., & Pratt, M. A. C. (2016). Persistent Activation of NF-κB in BRCA1-Deficient Mammary Progenitors Drives Aberrant Proliferation and Accumulation of DNA Damage. Cell Stem Cell. https://doi.org/10.1016/j.stem.2016.05.003
Yang, D., Wu, Z., Duan, H., Luo, Y., Lu, D., Li, W., … Yan, X. (2011). CD146, an epithelial-mesenchymal transition inducer, is associated with triple-negative breast cancer. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.1111053108
Zamay, T. N., Zamay, G. S., Kolovskaya, O. S., Zukov, R. A., Petrova, M. M., Gargaun, A., … Kichkailo, A. S. (2017). Current and prospective protein biomarkers of lung cancer. Cancers. https://doi.org/10.3390/cancers9110155