Functional Profiling · Timing
Surgery Coming Up? It's Your Unique Opportunity for Functional Profiling of Your Tumor
Functional profiling works best when there is plenty of viable tissue. That means at surgery, whether for a new diagnosis or for recurrent disease. Here is the biology and the evidence behind that advice.
The practical takeaway
Do you have surgery coming up, whether for a new diagnosis or for recurrent disease? That operation is the window when your tumor is most testable. It is when fresh, viable tissue can be collected in quantity. But you have to plan for it in advance. Viable tissue must be sent to the laboratory at the time of surgery. By default it goes to pathology in fixative instead. So this conversation needs to happen before the operation, not after. Profiling early does not change your standard frontline treatment. It preserves information that can guide the harder choices later, when a repeat biopsy may not be possible. Talk this over with your treating oncologist. The SAGE Oncotest™ is meant to support that discussion, not replace it.
Ask your care team whether profiling now makes sense, or check eligibility today.
Where the SAGE Oncotest™ fits
The SAGE Oncotest™ is a CLIA-certified functional assay. It measures cytotoxicity and antiproliferation at the same time on a patient's own 3D microtumors. It uses an NCCN-aligned drug panel and returns results in 7 to 10 days. We are careful about what SAGE itself has shown. We have not yet run a randomized outcome trial of the SAGE Oncotest™, and the timing data above rest on a single case. What the broader field has shown is clearer. Functional profiling predicts clinical drug response at the accuracies above. And two recent randomized trials of related assays reported better outcomes when the assay guided chemotherapy instead of physician's choice. These were Ranjan et al. in recurrent glioblastoma (Ranjan 2023) and Herzog et al. in recurrent platinum-resistant ovarian cancer. (Herzog 2025) Those trials used different platforms than the SAGE Oncotest™. We offer them as context for the premise, not as SAGE-specific evidence.
What we found when we tested the assumption directly
To test the "the tumor will be different" concern with real data, we profiled paired specimens from a single HGSOC patient. The first was taken at baseline (ascites). The second was taken after neoadjuvant carboplatin-paclitaxel (solid tissue). We used the SAGE Oncotest™ 3D microtumor platform and compared drug-response profiles across the two timepoints. (Maestri 2026)
[FIGURE 1 — upload PNG here]
Across the tested drug panel, responses before and after treatment matched closely for both readouts. Cytotoxicity was r = 0.82 and antiproliferation was r = 0.89 (R2 = 0.68 and 0.80; both p < 0.001). In other words, neoadjuvant chemotherapy did not broadly reshape how the tumor responded to drugs it had not yet seen. Carboplatin-paclitaxel scored low at both timepoints, which fits the patient's limited clinical response. Meanwhile vincristine-actinomycin-cyclophosphamide (VAC) and irinotecan were active at both timepoints. These are later-line options a baseline test would already have flagged.
[FIGURE 3 — upload PNG here]
In this case, the profile for drugs the tumor had not received was preserved across treatment. That is what the selection model of resistance predicts, and what makes an early test still useful at relapse.
This is a single-patient case study, and we present it that way. It generates a hypothesis; it does not confirm one. To know whether preserved drug-response profiles hold across HGSOC, we will need larger paired-sample cohorts. That is the direction of our ongoing work. The point is narrow and honest. Tumors do change. But the change is concentrated against the drug given. So baseline profiles stay informative for the untested drugs that matter at relapse.
Tissue is most abundant at the start
Timing also sets how much tissue you can test. The best source of viable tissue is surgery. That means primary debulking, or surgery for recurrent disease. In ovarian cancer, large-volume ascites is also a good source. A diagnostic needle or core biopsy is different. It is usually too small, and it goes to pathology in fixative instead of being kept alive for testing. A repeat biopsy at relapse can also be scarred from prior therapy, hard to get, or not possible at all. In high-grade serous ovarian carcinoma (HGSOC), 70 to 80 percent of patients who respond to frontline platinum therapy later relapse. Yet the time of most tissue and the time of hardest decisions rarely line up. (Havasi 2023)
Banking a functional profile while tissue is plentiful keeps an option open that may be gone later. The advice is not to test instead of standard care. It is to test early, while the tumor can still be profiled, so the result is ready when the choices get harder.
Acquired resistance is therapy-driven, not spontaneous
Acquired drug resistance does not make a tumor resist every drug at once. It is mostly a process of selection. Chemotherapy puts pressure on the tumor. That pressure favors resistant subclones that were already present, and they survive and grow. The surviving population is then enriched for resistance to the drug that was given. Platinum resistance in ovarian cancer is the classic example. It arises through specific platinum-related mechanisms, not through broad, random change. (Havasi 2023)
What this means for timing is simple. A tumor cannot become resistant to a drug it never received. So a profile taken before treatment stays useful for later-line drugs the patient has not yet had. Those are exactly the drugs a functional test helps with, because those choices come up when frontline therapy fails. This is the core idea of functional precision medicine. You test a patient's living tumor against candidate drugs. That reveals weak points which gene or tissue tests alone may miss. (Letai 2017)
A common and reasonable objection
Oncologists and gynecologic-oncology surgeons often ask a fair question about timing. A newly diagnosed patient will get standard platinum-based chemotherapy either way. So why test the tumor up front? Two arguments usually follow. First, the frontline regimen is already set, so the result will not change the first treatment. Second, by the time it matters, at relapse, the tumor will have changed under therapy. A baseline profile would then be out of date.
Both points deserve a direct answer. The first is true but incomplete. The second rests on an assumption about how tumors change under treatment. The biology does not fully support that assumption, and our own data did not bear it out.
Figure 1. Patient-derived ex vivo 3D microtumors from baseline ascites and post-treatment solid tissue. Hoechst 33342 (nuclei, blue), EdU (proliferating cells, green), EpCAM (epithelial tumor marker, red), and merged. The platform recovers viable, proliferating tumor cells from both specimen types. Scale bar 100 um.
Figure 2. Pre- versus post-neoadjuvant drug-response correlation across the tested panel, shown separately for the cytotoxicity (r = 0.82) and antiproliferation (r = 0.89) readouts; both p < 0.001 (figure labels show the corresponding R2 = 0.68 and 0.80). Points clustering on the diagonal indicate preserved drug-response profiles across treatment.