"Aziz Sancar Completely Cured Glioblastoma": The Real Story and the Scientific Facts (84 chars)
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"Aziz Sancar Completely Cured Glioblastoma": The Real Story and the Scientific Facts
In recent days, a story claiming that "Aziz Sancar has completely cured glioblastoma" has been circulating on social media, and many of our patients have been asking us about it. The short answer: no, not a single patient has yet been treated with this method. The study that Nobel laureate Prof. Aziz Sancar and his team published in PNAS in December 2025 did show genuinely impressive results in mice; we covered it in detail in our January 2026 article. According to Sancar's statement in October 2026, human trials could begin in about two years. In this article, we explain what is true, what is exaggerated, and why this achievement still matters.
- The story is wrong: The claim that "glioblastoma has been completely cured" is not accurate. The results were obtained only in mice, in cell cultures, and in surgically removed human tumor tissue. Sancar himself emphasized that results have been obtained "only in mice at this stage."
- What was found: Adding EdU, a compound used in laboratories to label DNA, to the standard drug temozolomide eliminated tumors completely in some mouse models. In the patient-derived GBM8 model, for example, all mice receiving the combination were alive and tumor-free at day 170.
- What deserves credit: The study is an original, well-reasoned idea that grew out of the DNA repair knowledge that earned Sancar his Nobel Prize. It was published in a peer-reviewed journal, its data are open, and the team stated its limitations clearly.
- Realistic expectations: Only about 3–5% of cancer drugs that enter Phase 1 go on to be approved. In glioblastoma, many treatments that were highly successful in mice showed no benefit in humans. For patients today, the right path is standard treatment and appropriate clinical trials.
Why does this matter?
Glioblastoma is the most common and most aggressive primary brain tumor in adults. With standard treatment consisting of surgery, radiation therapy, and temozolomide chemotherapy, median survival is about 15–20 months; the disease recurs in about 80% of patients, and the five-year survival rate is around 5–10%. Very few advances have changed this picture since 2005. That is why every piece of "good news" about glioblastoma raises very strong hopes among patients and their families.
The source of the story amplifies that hope: Aziz Sancar received the 2015 Nobel Prize in Chemistry for his work on DNA repair mechanisms and is, rightly, a deeply admired and trusted scientist in Turkey. But a scientist's standing and the stage a finding has reached are two different things. Accurate information protects patients from needless disappointment and poor decisions, and it ensures that this valuable work is understood as it deserves.
No. In glioblastoma, many treatments looked highly successful in mice but did not deliver the expected benefit in humans; only a few have also succeeded in people:
- Successes: Temozolomide (added to radiation therapy, 2005), tumor treating fields (TTFields, 2015), and vorasidenib for low-grade, IDH-mutant gliomas (FDA approval, August 2024).
- Did not deliver the expected benefit in humans: Bevacizumab delayed disease progression in first-line treatment but did not extend overall survival (2014). The EGFRvIII-targeted vaccine rindopepimut failed in the Phase 3 ACT IV trial (2017).
- Still under investigation: Approaches such as personalized vaccines and CAR-T cell therapies.
Did Aziz Sancar cure glioblastoma?
No, not in humans yet. Sancar and his team showed that adding a molecule called EdU to the standard drug temozolomide eliminated tumors and markedly extended survival in mouse models of glioblastoma. However, the method has not been tested in a single patient. According to Sancar, human trials could begin in about two years; only those trials will show whether it is effective and safe.
Where did the story come from? A brief timeline
As you can see, Sancar's own statements have always been measured. The phrase "completely cured" comes not from the scientist but from news stories that were shortened and reshared on social media.
What exactly did the study find?
The idea: a clever use of Nobel-winning knowledge
Temozolomide, the standard chemotherapy drug for glioblastoma, damages the tumor cell's DNA by attaching methyl groups to it. However, a substantial proportion of tumors repair this damage using a repair enzyme called MGMT and become resistant to the drug; whether MGMT is "silenced" is one of the most important markers assessed in the molecular diagnosis of glioblastoma.
EdU (5-ethynyl-2′-deoxyuridine) is a molecule that closely resembles thymidine, one of the building blocks of DNA, and it is widely used in laboratories to label dividing cells. Rapidly dividing tumor cells take up more EdU into their DNA. The Sancar team's finding is this: once EdU is incorporated into DNA, it is cut out by "nucleotide excision repair," the system behind Sancar's Nobel Prize, but the cell then puts it back into the DNA. This futile cycle exhausts the cell and leads to cell death. Combined with the damage caused by temozolomide, the result is stronger than the sum of the two effects. Sancar sums it up as "one plus one equals three."
The team had previously carried out studies that brought Sancar's expertise in DNA repair and the biological clock into cancer treatment; his work on the right timing of chemotherapy was one of them. This new study is a fine example of the path from basic science to a treatment idea.
The findings: three different mouse models and patient tissue
The researchers implanted human glioblastoma cells into the brains of immunodeficient mice and administered treatment for six weeks. They also tested surgically removed tumor tissue from four patients in the laboratory, together with living brain tissue.
| Model | Number of mice | Key result (temozolomide + EdU) | Interaction |
|---|---|---|---|
| U87 cell line | 40 | Untreated mice did not survive beyond about 30 days. The combination extended survival by more than 130% compared with no treatment and by about 60% compared with temozolomide alone. According to the preprint, tumors returned after treatment was stopped; 1 of 8 mice remained tumor-free. | Synergistic (stronger than the sum) |
| GBM8 (patient-derived) | 42 | All 14 mice receiving the combination were alive and tumor-free at day 170. Tumors returned in about 60% of those receiving temozolomide alone. | Synergistic |
| LN229 cell line | 50 | No tumor recurrence was seen in the combination groups; untreated mice did not survive beyond day 46. | Additive |
| Surgical tissue from 4 patients | - | The combination was effective in all four tumors. | Synergistic in 1, additive in 3 |
Patient-derived GBM8 mouse model: mice alive at day 170
Percent. Mouse experiment; 5–7 mice per group. Colored bars show the combination.
All mice in the combination groups were tumor-free at day 170. Source: the study's bioRxiv preprint. These are results from a mouse experiment and cannot be applied directly to humans.
Side effects in mice were mild and reversible: transient changes were seen in the small intestine, the spleen, and blood counts; no liver damage was detected. The number of cells incorporating EdU into their DNA was about 70–80 times higher in the tumor than in the surrounding normal brain tissue. This selectivity is one of the most striking aspects of the study.
The university's press release states that all mice receiving the combination in the U87 model lived beyond 250 days and were "essentially cured." The preprint of the same study, however, reports that in this model tumors returned after treatment was stopped and only 1 of 8 mice remained tumor-free. This experiment may differ in the final published version of the article; still, this press release is one of the sources of the "completely cured" wording. The strongest and most consistent result is in the patient-derived GBM8 model.
Curing mice versus curing people: why aren't they the same?
Richard Klausner, then director of the US National Cancer Institute, said in 1998: "The history of cancer research has been a history of curing cancer in the mouse. We have cured mice of cancer for decades, and it simply didn't work in humans." He made the remark at a time when news that Judah Folkman's drugs blocking blood vessel formation had eradicated tumors in mice was being presented in the US press as a "cure for cancer." Folkman himself always answered the question "Can you cure cancer?" with "Yes, in mice."
The rest of the story is instructive: those drugs did not have the expected effect in humans; a derivative of endostatin received only a limited approval, in China, for lung cancer. But Folkman's idea was right: another drug targeting blood vessel formation, bevacizumab, was approved in 2004 and is used today in many cancers. In other words, success in mice is not a treatment on its own; but a good idea can eventually reach patients, even if its path changes along the way.
For this study, the most important differences between mice and humans are the following:
- The immune system: The mice used were immunodeficient (nude) mice, so that they would not reject the human tumor. In humans, a tumor has a far more complex relationship with the immune system and brain tissue.
- The tumor itself: Tumors implanted in mice come from cell lines that have been grown in the laboratory for years and are relatively uniform. For example, a 2016 analysis showed that U87, the most widely used cell line, actually differs from the tumor of the patient it was derived from. Real glioblastoma, by contrast, is highly heterogeneous even within the same tumor and infiltrates the brain diffusely.
- How the drug behaves in the body: In mice, EdU has a half-life of about 10 minutes, and its level in the brain is about one-eighth of that in the blood. The authors themselves note that a drug formulation suitable for humans must be developed. The dose used in mice (200 mg/kg) corresponds to about 16 mg per kilogram in humans by standard conversion; whether this dose is safe in humans is unknown.
- Patient characteristics: Real patients have undergone surgery and radiation therapy, are taking corticosteroids, and differ in age and overall health. In mice, treatment begins shortly after the tumor is implanted.
- Numbers: Each group had 5–8 mice. That is typical for a laboratory study but small for a definitive conclusion.
Because of these differences, the drug development and approval process in oncology is a very demanding one. According to a large analysis, only about 3.4% of cancer drugs that enter first-in-human testing (Phase 1) are ultimately approved. In brain tumors, getting drugs across the blood-brain barrier adds a further challenge.
Figure 1 · The path from a laboratory discovery to patients
Simplified; timelines are approximate and vary by drug.
What do proven glioblastoma treatments achieve today?
To understand the value of a new treatment, you need to know where the bar is. Today's standard rests on two large Phase 3 trials: the addition of temozolomide to radiation therapy (2005) and the further addition of tumor treating fields (TTFields) (2017). In both trials, the benefit over the control arm was clear but modest.
Proven treatments in glioblastoma: median survival
Months. Colored bar: experimental arm; gray bar: control arm of the same trial.
Absolute gain: about 2.5 months with the addition of temozolomide (about a 37% relative reduction in the risk of loss of life); about 4.9 months with the addition of TTFields (about a 37% relative reduction). In EF-14, patients were enrolled after completing radiation therapy, so survival times are longer. Comparisons across different studies are indirect; patient populations, prior treatments and follow-up differ.
Proven treatments in glioblastoma: five-year survival rate
Percent. Colored bar: experimental arm; gray bar: control arm of the same trial.
In relative terms, the five-year survival rate increased about 2.5- to 5-fold; in absolute terms, however, about 8 more patients out of every 100 live five years. The progress is real, but glioblastoma remains a very difficult disease. Comparisons across different studies are indirect; patient populations, prior treatments and follow-up differ.
These figures show both why glioblastoma so urgently needs new treatments and why the phrase "completely cured" must be used with great care. We summarized the new treatment approaches of 2026 in this field in a separate article.
What should glioblastoma patients and their families do now?
- Do not interrupt standard treatment: Surgery, radiation therapy, and temozolomide are the treatments proven today to extend survival. Tumor treating fields can also be added for suitable patients. Stopping or delaying treatment because of a news story can cause serious harm.
- Do not try to obtain EdU: EdU is a laboratory chemical; it is not a drug approved for human use, and its safe dose in humans is unknown. Any product or treatment sold online as a "Sancar treatment" has nothing to do with this study; our warnings about alternative practices without evidence apply here as well.
- Ask about clinical trials: In glioblastoma, one of the best options is to take part in an appropriate clinical trial. When a trial of the temozolomide and EdU combination opens, eligibility criteria will be announced through official channels; no such trial is currently enrolling patients.
- Complete your molecular diagnosis: IDH, MGMT, and other markers determine both the treatment plan and which clinical trials are suitable. Getting a second opinion on this is also valuable.
- Do not neglect supportive care: Controlling brain edema, preventing seizures, and rehabilitation directly affect quality of life.
According to Sancar's statements, the Turkish Ministry of Health and TÜSEB have shown interest in the clinical research; in October 2026 the project was transferred to TÜBİTAK, and human trials are expected to begin in about two years. Press reports also indicate that a patent application has been filed for the method. This is an important opportunity for an early-phase cancer drug trial to be conducted in Turkey. However, there is as yet no published study protocol, named center, or patient enrollment process. The standard treatments for glioblastoma, namely surgery, radiation therapy, and temozolomide, are available in Turkey; experimental options such as new cell therapies are available only within clinical trials.
Frequently asked questions
- Did Aziz Sancar cure glioblastoma?
- No, not in humans yet. Sancar and his team showed that the combination of temozolomide and EdU eliminated tumors and extended survival in mouse models of glioblastoma. The method has not yet been tested in any patient; according to Sancar, human trials could begin in about two years.
- What is EdU, and can I get it from a pharmacy?
- EdU is a thymidine-like molecule used in laboratories to label dividing cells. It is not a drug approved for human use, and its safe dose in humans is unknown. Obtaining and using it on your own could be dangerous.
- How can I join temozolomide and EdU treatment?
- No clinical trial is currently enrolling patients. When human trials are planned, eligibility criteria will be announced through official channels. In the meantime, the best course is to continue standard treatment and talk with your oncologist about suitable clinical trials.
- Does a treatment that works in mice also work in humans?
- Not always. Only about 3–5% of cancer drugs that enter first-in-human testing go on to be approved. Mouse models do not fully reflect the human immune system, tumor diversity, or how a drug behaves in the body.
Glossary
- Glioblastoma
- The most common and most aggressive primary brain tumor in adults, arising from the brain's supportive cells.
- Temozolomide
- An oral chemotherapy drug used during and after radiation therapy as part of standard glioblastoma treatment.
- EdU
- 5-ethynyl-2′-deoxyuridine; a molecule resembling thymidine, a building block of DNA, used in laboratories to label dividing cells.
- Nucleotide excision repair
- A system that repairs DNA by cutting out the damaged segment; Aziz Sancar received the 2015 Nobel Prize in Chemistry for work elucidating this mechanism.
- Xenograft
- An experimental model created by implanting human tumor cells into animals, usually immunodeficient ones.
- Synergy
- When two treatments given together have a stronger effect than the sum of their separate effects.
DROZDOGAN Academy Commentary
The Sancar team's study is a fine example of an original treatment idea, born of basic science, backed by well-conducted laboratory work. The problem lies not in the finding but in how it has been reported.
⚡ Why it matters
Resistance to temozolomide is one of the biggest problems in glioblastoma. The idea of overcoming this resistance with an inexpensive small molecule is an approach that, if it works, could reach many patients. That the study was led by Turkish researchers, and the possibility of clinical research in Turkey, add further value.
✅ Strengths
An original, mechanism-based idea grounded in Nobel-level expertise in DNA repair. Three different mouse models, testing in patient tissue, pharmacokinetic and toxicity data, and publication in a peer-reviewed journal. The team stated its limitations openly, and Sancar informed the public in a measured way.
⚠️ Limitations
All data come from mice, cells, and tissue in the laboratory. The mice were immunodeficient and the groups were small. EdU has a very short half-life in mice and no formulation suitable for humans. Its safe dose in humans is unknown. The press release and the preprint differ in their results for the U87 model.
🩺 In practice
Patients should be told plainly: this method is not a treatment option today, and standard treatment should continue. Talking with patients about how news stories can become misleading is the best protection against the exploitation of hope, as we have also seen with "cancer vaccine discovered" headlines.
❓ Open questions
Will EdU reach the tumor in sufficient amounts at a dose that is safe in humans? Which patients will respond; for example, will MGMT status or EGFR alterations affect response? At which institution, with what design, and when will the Phase 1 trial begin?
Bottom line: Aziz Sancar has not cured glioblastoma; but he has put forward a clever, promising idea for glioblastoma treatment that is worth testing in humans. The best way to appreciate this achievement is without exaggeration, waiting patiently for the results of clinical trials. That is exactly what evidence-based medicine is about.
- This article was prepared in October 2026.
- Numerical data from the mouse studies were taken from the study's bioRxiv preprint and the University of North Carolina press release. We were unable to access the full final text published in PNAS; the results for the U87 model differ between the two sources, as noted in the text.
- Sancar's statements are quoted from reports in the Turkish press. The human equivalent dose is an approximate value we calculated using standard body surface area conversion.
- Comparisons in the charts are indirect; the diagram is derived from the text and contains no new data. The Academy commentary is our own.
References
- Kaanoglu H, Akyel YK, Adefolaju A, et al. Combinatorial treatment of glioblastoma with temozolomide (TMZ) plus 5-ethynyl-2′-deoxyuridine (EdU). Proc Natl Acad Sci U S A 2026;123(1):e2532187123. doi:10.1073/pnas.2532187123
- Preprint of the same study (October 2025). bioRxiv
- UNC Health. UNC researchers show combination therapy effective for brain cancer (January 2, 2026). news.unchealthcare.org
- UNC Department of Biochemistry. Kaanoglu and Akyel, first authors of the Sancar lab's glioblastoma study. med.unc.edu
- Habertürk. Aziz Sancar beyin tümörü tedavisine yönelik çalışmasına gösterilen ilgi için teşekkür etti [Aziz Sancar thanks the public for its interest in his brain tumor treatment study] (January 13, 2026). haberturk.com
- T24. Prof. Dr. Aziz Sancar'dan yeni açıklamalar [New statements from Prof. Aziz Sancar] (February 5, 2026). t24.com.tr
- Yeni Başkent. Prof. Dr. Aziz Sancar'ın beyin kanseri çalışması Türkiye'ye geliyor [Prof. Aziz Sancar's brain cancer study is coming to Turkey] (TRT Haber interview, October 7, 2026). yenibaskentgazetesi.com
- Cumhuriyet, Orhan Bursalı. Sancar müjde verdi: Beyin kanseri klinik deneylerini Türkiye'de yapacağız [Sancar shares good news: we will conduct the brain cancer clinical trials in Turkey]. cumhuriyet.com.tr
- TIME. Cancer: How to tell the hope from the hype (May 18, 1998). csts.ua.edu
- Stupp R, et al. Radiotherapy plus concomitant and adjuvant temozolomide for glioblastoma. N Engl J Med 2005;352:987–996. PubMed 15758009
- Stupp R, et al. Effects of radiotherapy with concomitant and adjuvant temozolomide versus radiotherapy alone on survival in glioblastoma: 5-year analysis of the EORTC-NCIC trial. Lancet Oncol 2009;10:459–466. PubMed
- Stupp R, et al. Effect of tumor-treating fields plus maintenance temozolomide vs maintenance temozolomide alone on survival in patients with glioblastoma (EF-14). JAMA 2017;318:2306–2316. PubMed 29260225
- Wong CH, Siah KW, Lo AW. Estimation of clinical trial success rates and related parameters. Biostatistics 2019;20:273–286. PubMed 29394327
- Allen M, et al. Origin of the U87MG glioma cell line: good news and bad news for the development of glioma therapies. Sci Transl Med 2016;8:354re3. PubMed
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