THIS HALLOWEEN, KNOCK OUT THE BAD GENES
Behind every cancer phenotype is a question worth testing. Pick the gene and cell background that match your study, then use a defined KO model to ask what changes when that gene is lost. This Halloween, assemble a Cancer Discovery Package around the questions you actually need to answer.
Halloween Offers at a Glance
Choose One Model
Save 10% on one eligible cancer-related KO cell model.
Build Your Combination
Choose 2–3 eligible models and save 20% on your selected models.
Expand Your Study
Choose 4 or more eligible models and save 25% on your selected models.
Choose from the featured genes. There is no requirement to purchase all six.
Meet Cancer’s Usual Suspects
Meet six familiar names hiding very different mechanisms. A knockout can help test gene function, but the answer depends on the starting genotype, cell background, and readout. Open a gene page to explore its biology, then confirm the right model for your experiment.
KRAS | RAS signaling and gene dependency
Investigate how KRAS loss affects signaling, cellular fitness, and drug response.
If your question is whether a particular cancer model depends on KRAS, compare proliferation and pathway readouts after perturbation in a suitable genetic background. KO and hotspot-mutation models address different questions; choose by hypothesis.
Explore KRASEGFR | Receptor signaling and target dependency
Investigate EGFR function and downstream signaling in a defined cellular background.
If inhibitor response differs between models, ask whether EGFR dependency or downstream alterations explain the difference. KO models support receptor-function studies; mutation-specific drug questions may need a separate variant model.
Explore EGFRTP53 | Cell cycle and stress response
Study the effects of p53 loss on cell-cycle control, apoptosis, and treatment response.
A common problem is interpreting a treatment phenotype without knowing whether p53 is functional at baseline. Check parental TP53 status, then use matched controls to examine stress response and cell-fate readouts.
Explore TP53BRAF | MAPK signaling
Study BRAF function in pathway signaling, proliferation, and treatment response.
For MAPK-focused studies, distinguish BRAF loss from the effect of an activating BRAF variant. Select the appropriate genotype and compare downstream signaling, fitness, or treatment response with a suitable control.
Explore BRAFPTEN | PI3K pathway regulation
Explore the effects of PTEN loss on survival signaling, growth, and drug response.
If PI3K pathway activation complicates a drug-response result, a PTEN-loss model can help probe the contribution of this tumor suppressor. Check the parental genotype and measure the relevant signaling and phenotype readouts.
Explore PTENAPC | Wnt pathway regulation
Examine APC loss and its effects on Wnt signaling and cancer-related phenotypes.
When Wnt readouts shift, APC status may be part of the explanation. Choose a cell background with a known APC and CTNNB1 context, then compare pathway activity and growth rather than assuming every colorectal line starts from the same state.
Explore APCBuild Your Cancer Discovery Package
A long list of cancer genes is easy to collect; a useful experiment starts with one decision. Are you testing whether a candidate target is required for growth, whether tumor-suppressor loss changes a phenotype, or whether a pathway affects drug response? Pick an appropriate background and control before adding models. You can combine eligible products without buying all six genes.
Study a priority target
Select a KO model for your target gene and identify an appropriate parental control. Plan the comparison around your intended phenotype and assay.
Compare related signaling genes
Consider models involving KRAS, EGFR, or BRAF when investigating signaling relationships. Choose a cell background and assay design that fit the hypothesis.
Investigate tumor suppressor loss
Explore TP53, APC, or PTEN loss to study distinct aspects of cancer biology, including cell-fate control and pathway regulation.
Model selection should account for the parental genotype, editing strategy, control requirements, and downstream readout. Sharing a cell-line name alone does not establish that separately sourced models form an isogenic panel.
Looking beyond a single gene? The Oncology research page connects mutation analysis, tumor dependency, and target validation. Use it to frame the next experiment; package eligibility and the exact model configuration still need confirmation.
Explore Oncology ResearchWhich Cancer Gene Will You Unmask Next?
Tell us which gene or pathway you are studying, the cell background you prefer, and the question your assay must answer. We can help identify relevant models and confirm the eligible products, controls, and quotation for your Cancer Discovery Package.
- The offer applies to selected KO cell models associated with KRAS, TP53, APC, PTEN, EGFR, and BRAF. Eligible products are subject to confirmation by EDITGENE. Products displayed on linked gene or research pages are not automatically included.
- Package discounts are based on the number of eligible models purchased. Final pricing and package configuration will be confirmed in the quotation.
- Availability and lead times vary by product. Custom cell line engineering is quoted separately.
- Shipping, taxes, and import-related charges are not included in the stated product discounts.
- This offer cannot be combined with distributor pricing, contract pricing, or other promotions unless confirmed in writing.
- For research use only. Not for diagnostic or therapeutic use.
