HOUSTON, October 19, 2026 — Researchers at MD Anderson Cancer Center have reported new findings showing how immunotherapy is changing cancer care by working with the body’s defenses instead of directly attacking cells.
The shift from chemotherapy to immunotherapy marks a change in how cancer is treated. Chemotherapy works by killing fast-growing cells, which can include healthy ones, leading to side effects like fatigue, nausea, and lowered blood counts. Immunotherapy, in contrast, aims to stimulate or restore the immune system so it can recognize and destroy cancer cells more precisely. This approach is designed to reduce harm to normal tissue while targeting tumors. According to the Wikipedia entry on immunotherapy, it encompasses both passive methods, such as monoclonal antibodies that mark abnormal cells for immune destruction, and active methods like cancer vaccines, immune checkpoint inhibitors, and adoptive cell transfer. These strategies harness the body’s natural defenses rather than introducing toxic chemicals that affect the whole system.
One example of this new approach is the bispecific antibody ivonescimab, tested in the Phase 3 HARMONi trial for patients with EGFR-mutant non-small cell lung cancer. In that study, patients who received ivonescimab plus chemotherapy were 48 percent less likely to experience cancer progression or death compared to those receiving chemotherapy alone. The median time without disease worsening was 6.8 months for the combination group, versus 4.4 months for chemotherapy alone. These results, published in The Lancet Oncology, show that adding immunotherapy to standard treatment can extend control of the disease while maintaining a manageable safety profile. The trial’s co-lead, Dr. Xiuning Le, noted that despite advances in EGFR-targeted therapies, resistance remains common, and options after progression are limited. The addition of ivonescimab offers a new way to delay that resistance.
Another area of progress involves overcoming how tumors resist treatment. Research from MD Anderson, led by Dr. Di Zhao and Dr. Nicholas Navin, found that in castration-resistant prostate cancer, the immune checkpoint molecule B7-H3 does more than suppress immune activity—it also reshapes the tumor microenvironment. This reprogramming of surrounding cells helps cancer grow and resist therapy. The study, published in Cancer Discovery, showed that combining a B7-H3-targeted therapy with MEK inhibition improved antitumor responses and prolonged survival in preclinical models. This suggests that blocking B7-H3 alone may not be enough because the molecule acts as a physical barrier that protects the tumor. Effective treatment may require targeting both the immune checkpoint and the support structures it creates.
Scientists are also exploring ways to make cancer cells more visible to the immune system. A preclinical study from Penn State College of Medicine, published in the journal Autophagy, found that blocking the protein VPS34 increases levels of GD2 on the surface of neuroblastoma cells. GD2 is a target molecule for certain immunotherapies, such as the monoclonal antibodies dinutuximab and naxitamab. When GD2 levels rise, tumor cells become easier for these antibodies to detect and bind to, marking them for destruction by immune cells. The study showed that VPS34 inhibition not only enhances the effectiveness of anti-GD2 immunotherapy but also makes the tumor microenvironment less supportive of cancer growth. According to corresponding author Dr. Hong-Gang Wang, this approach could help patients who currently relapse or develop resistance due to cancer’s ability to hide from immune detection.
Immunotherapy’s effectiveness is also being improved when combined with cell-based strategies. The Wikipedia entry notes that in various cancers, efficacy is enhanced by 20 to 30 percent when immunotherapy is used alongside approaches like adoptive cell transfer or cancer vaccines. This combination helps the immune system mount a stronger and more lasting response. Additionally, the 2018 Nobel Prize in Physiology or Medicine was awarded to James P. Allison and Tasuku Honjo for their discovery of cancer therapy through inhibition of negative immune regulation—a foundational breakthrough that led to the development of checkpoint inhibitors, which are now a key part of immunotherapy.
Looking ahead, researchers are developing blood tests to identify patients who might safely avoid chemotherapy altogether. These tests aim to determine who is likely to benefit from immunotherapy alone, sparing others from unnecessary toxicity. While these tools are still under study, they represent a move toward more personalized oncology, where treatment is matched to the individual’s cancer biology and immune profile.
Patients should understand that while immunotherapy offers promising advances, it is not without risks. Side effects can include immune-related adverse events, such as inflammation in healthy organs, which require monitoring and management. The encouraging part is that these effects are often predictable and treatable when caught early. As with any medical decision, individuals should talk to their doctor about the potential benefits and risks of immunotherapy based on their specific condition, overall health, and treatment goals. Early findings suggest that for many, this approach provides a way to control disease with greater precision and fewer systemic toxicities than traditional chemotherapy. Consult your doctor.
Understanding The Role Of B7-H3 In Tumor Microenvironment Reprogramming
Research from MD Anderson Cancer Center has revealed that the immune checkpoint molecule B7-H3 does more than suppress immune activity in castration-resistant prostate cancer—it also actively reshapes the tumor microenvironment. Led by Dr. Di Zhao and Dr. Nicholas Navin, the study found that B7-H3 reprograms surrounding cells to create conditions that support tumor growth and resistance to therapy. This dual function means B7-H3 acts not only as an immune brake but also as a structural facilitator of cancer progression.
The findings, published in Cancer Discovery, show that targeting B7-H3 alone has limited effectiveness because the molecule establishes a physical barrier that shields tumors from immune attack. In preclinical models, combining B7-H3-directed therapy with MEK inhibition led to improved antitumor responses and prolonged survival. This suggests that overcoming tumor resistance may require disrupting both the immunosuppressive and microenvironment-altering roles of B7-H3 simultaneously.
Sources
- MD Anderson Unveils Wave of Cancer Breakthroughs From Lung Immunotherapy to
- Immunotherapy
- Making pediatric cancer more ‘visible’ boosts immunotherapy response
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