The Abscopal Effect in Non-Small Cell Lung Cancer: When Treating One Tumor Shrinks Tumors Elsewhere in the Body

Table of Contents

• Key Points
• Background: What Is the Abscopal Effect?
• How Doctors Measure Tumor Response: RECIST and iRECIST
• The Goal of This Review
• How Radiotherapy Can Trigger an Immune Attack Far From the Treated Tumor
• Real Patient Cases: Abscopal Effects After Radiotherapy
• How Lung Ablation Triggers Systemic Immune Responses
• Real Patient Cases: Abscopal Effects After Ablation
• Combining Radiotherapy With Immunotherapy
• What the Prospective Clinical Trials Show
• What This Evidence Means for Patients
• The Proposed Working Definition
• Limitations of the Current Evidence
• Recommendations and What Comes Next
• Frequently Asked Questions
• Source Information

Key Points

• The abscopal effect is when untreated tumors shrink after treatment to another site; it was first described in 1953 and is still considered uncommon.
• Radiation can trigger immune activation that reaches distant tumors, but it can also suppress immunity, which may limit how often this happens.
• Ablation techniques like cryoablation and microwave ablation can release tumor antigens and stimulate immune responses, but evidence for abscopal effects remains limited to case reports.
• Standard RECIST v1.1 criteria may miss out-of-field tumor shrinkage; iRECIST helps with immunotherapy patterns but still does not systematically record abscopal responses.
• A proposed definition for NSCLC requires regression of non-irradiated lesions by iRECIST, confirmed by imaging within 4 to 8 weeks after localized therapy.

Background: What Is the Abscopal Effect?

The abscopal effect is a phenomenon in which tumors that were never directly treated begin to shrink after treatment is delivered somewhere else in the body. The term was first coined in 1953 by a researcher named Mole, who observed that distant, non-irradiated tumors regressed after localized radiotherapy (radiation treatment aimed at one specific area).

Since that first report, the abscopal effect has been documented in several cancer types, including breast cancer, melanoma, and lung cancer. For decades it was considered a medical curiosity. That changed as immunotherapy entered routine care for advanced NSCLC. Immunotherapy means treatments that help the immune system fight cancer. New local treatment strategies also entered routine care, such as lung ablation. Lung ablation uses extreme heat, cold, or electrical pulses to destroy tumors.

Despite growing interest, the abscopal effect still appears uncommon. The authors of this review point to a key unanswered question: is the effect truly rare, or are doctors simply failing to recognize it? In routine practice, a shrinking untreated tumor may be attributed to other causes, or it may not be formally recorded at all. That uncertainty is the central problem this review addresses.

How Doctors Measure Tumor Response: RECIST and iRECIST

To understand why abscopal effects may go unnoticed, you need to understand how clinical trials measure whether a cancer treatment is working. The standard tool is called RECIST version 1.1 (Response Evaluation Criteria in Solid Tumors).

Here is how RECIST v1.1 works in practice:

• Before treatment begins, doctors select "target lesions" — up to five in total, with no more than two per organ.
• These target lesions should represent the patient's overall tumor burden.
• Some lesions cannot serve as targets. For example, tumors in areas previously treated with local or regional therapy are considered "non-measurable."
• All remaining tumors are labeled "non-target lesions."
• Doctors can still declare disease progression based on non-target lesions if there is clear evidence the cancer is growing.

Here is the crux of the problem. While clear progression in non-target lesions counts, clear improvement in non-target lesions — exactly what happens in an abscopal effect — may not be captured at all within the RECIST v1.1 framework. A distant tumor shrinking on its own could simply be missed.

To address unusual response patterns, researchers developed the iRECIST criteria (immune Response Evaluation Criteria in Solid Tumors). This system was designed specifically for immunotherapy, which can cause a confusing pattern called pseudo-progression — an initial increase in tumor size or the appearance of new lesions, followed later by stabilization or shrinkage.

Pseudo-progression happens because immune cells flood into the tumor, making it look larger on a scan before it actually shrinks. Under RECIST v1.1, this would immediately be labeled progressive disease (PD). Under iRECIST, it is instead labeled unconfirmed progressive disease (iUPD). The progression must be confirmed on a follow-up scan at least 4 weeks later before doctors call it confirmed progressive disease (iCPD).

The authors note that iRECIST partially solves the problem — but not entirely. Unequivocal regression of a tumor outside the treatment field is still not systematically recorded in most trials.

The Goal of This Review

The authors set out to do something no one had done systematically: build a consensus definition of the abscopal effect specifically for NSCLC. They drew on evidence from single-treatment and multi-treatment trials to guide future research and everyday clinical decisions.

Why does a definition matter? Without one, researchers cannot compare studies, doctors cannot reliably recognize the effect, and patients may not receive credit for a response that is actually happening. A shared vocabulary is the first step toward integrating abscopal responses into routine care.

How Radiotherapy Can Trigger an Immune Attack Far From the Treated Tumor

Radiotherapy does two opposing things to the tumor microenvironment (the mix of cells, blood vessels, and signaling molecules surrounding a tumor). It activates the immune system — and it can also suppress it.

The activating side: Ionizing radiation causes immunogenic cell death, a form of cell death that alarms the immune system rather than hiding from it. Dying tumor cells expose a protein called calreticulin on their surface and release danger-associated molecular patterns (DAMPs), including HMGB1 and heat shock proteins. These signals include cytokines (immune signaling proteins) such as TNF-α, IL-6, TGF-β, and IL-8. These signals also include reactive oxygen and nitrogen species. These signals switch on dendritic cells, macrophages, and natural killer (NK) cells inside the tumor.

DAMPs then bind to receptors such as TLR4 on dendritic cells. This drives antigen presentation through MHC-I molecules and helps dendritic cells mature. At the same time, upregulation of MHC-II helps activate CD4+ T cells. Radiation-induced DNA damage also switches on the cGAS-STING pathway, which boosts type I interferon production, cross-presentation of tumor antigens, and priming of CD8+ cytotoxic T lymphocytes (CTLs) — the immune system's killer cells.

These CTLs can then travel through the bloodstream to distant, non-irradiated tumors. There they infiltrate the tumor microenvironment and attack cancer cells carrying the same neoantigens (unique proteins found on tumor cells). The result is shrinkage of distant tumors — the hallmark of the abscopal effect.

The suppressing side: Radiotherapy can also backfire. It can cause accumulation of myeloid-derived suppressor cells (MDSCs) and increase PD-L1 on tumor cells, both of which restrain T-cell activity in the tumor microenvironment. This is likely one reason the abscopal effect is not more common. This is also one reason combining radiation with immune checkpoint inhibitors makes biological sense. Immune checkpoint inhibitors are drugs that release the brakes on T cells.

Real Patient Cases: Abscopal Effects After Radiotherapy

Several individual patient reports describe abscopal effects in NSCLC after radiotherapy alone. Together they show the phenomenon can occur even without systemic therapy.

• Rees et al. published one of the earliest cases. A patient with metastatic lung adenocarcinoma saw untreated lung metastases regress 20 months after radiotherapy was delivered to an esophageal lesion.
• Vilinovszki et al. described an 81-year-old woman with recurrent metastatic squamous NSCLC who refused systemic therapy. After palliative radiotherapy to the bulk of the mediastinal tumor, durable regression appeared both at the treated site and in bone metastases that had received no radiation. At 25 months after treatment, she remained in remission at all sites.
• Sakaguchi et al. reported abscopal regression of a vertebral metastasis after palliative irradiation of a right iliac bone lesion in a 94-year-old patient with EGFR-mutant NSCLC who was not fit for chemotherapy.
• A 2009 case described a 60-year-old man with stage IV NSCLC (KRAS and EGFR wild type — meaning no targetable mutations). He underwent removal of a cerebellar (brain) metastasis, whole-brain radiotherapy, and stereotactic radiosurgery (SRS, a highly precise form of radiation), followed by chemotherapy. He later progressed in the adrenal glands, lungs, liver, and brain. The brain metastases were treated with SRS. After radiation was completed, follow-up imaging showed complete resolution of all extracranial disease without any additional systemic therapy. He stayed disease-free for more than 5 years.
• Hamilton et al. described complete resolution of a pleural lung mass 3 months after stereotactic radiosurgery to a solitary brain metastasis.
• Takayama et al. saw regression of lung and mediastinal lesions after whole-brain radiotherapy and spinal radiotherapy in a patient with stage IV NSCLC.
• Kuroda et al. described a 76-year-old woman with EGFR-mutant NSCLC in whom thoracic irradiation of a hilar lymph node metastasis led to complete disappearance of pulmonary metastases.

Two important points stand out. First, the abscopal effect can occur after radiotherapy alone, without any immunotherapy. Second, the abscopal effect can even occur after radiation to a brain metastasis. This is remarkable, because the blood–brain barrier usually limits what passes between the brain and the rest of the body. The blood–brain barrier is a protective filter around the brain.

How Lung Ablation Triggers Systemic Immune Responses

Ablation destroys tumors locally using extreme cold, heat, or electrical pulses. Each technique triggers a somewhat different immune signature.

Cryoablation (freezing)

Cryoablation kills tumor cells by freezing them, but it also stimulates the immune system. Necrotic (dead) tumor cells release pro-inflammatory cytokines including IL-12, IFN-γ, and TNF-α, along with tumor antigens that antigen-presenting cells capture and use to activate T-cell and B-cell responses. However, in tissue that is only partially frozen, apoptosis (programmed cell death) can release immunosuppressive signals such as IL-10 and TGF-β.

Preclinical studies (lab and animal research) show that cryoablation generates tumor-specific immunity. Animals developed protection against previously ablated tumor lines, and growth of tumors on the opposite side of the body was suppressed — consistent with an abscopal effect. Mechanistically, cryoablation activates the IFN-γ, IL-2/STAT5, IL-6/JAK/STAT3, and type I interferon pathways. Single-cell transcriptomics (detailed gene-activity profiling) reveal enhanced antigen presentation and a transitional IFN-stimulated T-cell state that prolongs CD8+ effector activity. STING-TBK1 signaling contributes to the systemic response, and blocking type I interferons reduces it.

In patients, cryoablation increases circulating CD8+ T cells. Cryoablation also raises the ratio of CD8+ cells to regulatory T cells (Tregs, which normally suppress immune responses). Cryoablation reduces FoxP3+ Tregs. Cryoablation remodels the tumor microenvironment to favor immune infiltration.

Microwave ablation (MWA)

Microwave ablation of lung tumors produces measurable immune changes: an increase in cytotoxic CD8+ T cells and a decrease in Treg cells. The shift in helper T-cell subtypes is less clear. One study found significantly elevated Th1-associated cytokines — IL-2, IFN-γ, TNF-α, and IL-12p70 — while Th2-associated cytokines (IL-4 and IL-10) stayed unchanged. Another study found that IL-2 decreased in 59.1% of patients one month after percutaneous MWA, which the authors propose as a mechanism for Treg downregulation. More research on IL-2 is needed for a definitive answer.

Pulsed electric field (PEF) therapy

PEF therapy uses short electrical pulses to kill tumor cells. It releases DAMPs such as HMGB1, which stimulate dendritic cells and tumor-specific CD8+ T cells. PEF also increases antigen-presenting cell activity, reduces Tregs and M2 macrophages, and modulates immune signaling pathways including IL-6, JAK–STAT, and Th17/IL-17, with early activation followed by later downregulation. Importantly, PEF preserves the extracellular matrix and local blood vessels. That keeps tumor antigens intact and makes it easier for immune cells to get in — an advantage over heat-based ablation.

Real Patient Cases: Abscopal Effects After Ablation

Evidence for abscopal effects after tumor ablation in metastatic NSCLC is scarce. So far, the literature consists mainly of isolated case reports.

Shao et al. reported a 69-year-old man with advanced squamous NSCLC who had already received four different lines of systemic therapy. He then developed oligo-progression (growth in just a few spots) with enlargement of the primary lung tumor and mediastinal 4R and 7 lymph nodes. Because of severe COPD (chronic obstructive pulmonary disease), he could not tolerate radiotherapy to both sites. CT-guided microwave ablation was performed on the primary tumor only. Follow-up imaging showed gradual absorption of the ablated lung lesion and — simultaneously — shrinkage of the untreated mediastinal lymph nodes, consistent with an abscopal effect.

Abscopal effects from microwave ablation have also been reported in lung metastases from other cancer types, including endometrial and colorectal carcinoma, though some of this evidence comes from preclinical models.

The authors are clear about the limits here. These observations suggest ablation may trigger systemic immune activation through antigen release and inflammatory signaling. However, the current level of evidence remains limited. Unlike radiation-based strategies, which have been studied in multiple clinical trials, the immune-modulating effects of ablation techniques have not been well defined.

Combining Radiotherapy With Immunotherapy

Adding an immune checkpoint inhibitor (a drug that releases the brakes on immune cells) to radiotherapy appears to amplify the abscopal effect. Multiple preclinical models support this combination.

Wei et al. studied antitumor activity at both the treated and distant tumor sites. They found that the strength of the abscopal response depended on when the anti-PD-1 antibody was given relative to radiation. When PD-1 blockade followed local irradiation, it expanded polyfunctional CD8+ T cells inside the tumor, reduced dysfunctional CD8+ T cells, and triggered strong abscopal effects.

Huang et al. studied stereotactic body radiation therapy (SBRT, very precise high-dose radiation) followed by pembrolizumab (an anti-PD-1 immunotherapy) in patients with metastatic NSCLC. Patients with immunologically "cold" tumors (tumors that immune cells largely ignore) had improved progression-free survival when SBRT came before immunotherapy. Levels of IFN-γ, IFN-α, and antigen processing and presentation gene sets were significantly higher in non-irradiated tumor sites after SBRT. Researchers also saw significant expansion of both new and pre-existing T-cell clones in the non-irradiated tumor (the abscopal site) and in the blood (the systemic response).

What the Prospective Clinical Trials Show

Many prospective clinical trials (studies that follow patients forward in time) have tested radiotherapy plus immunotherapy in NSCLC patients. They vary widely in treatment combinations, size, and what they measure — a reflection of their different objectives.

Endpoints across these trials have included progression-free survival (time without the cancer getting worse), overall survival, time to metastatic disease, local and regional recurrence, and safety. Endpoints have also included measures of systemic immune response such as the abscopal effect. Response assessment methods also differ. Some trials used RECIST v1.1; others used iRECIST to catch atypical patterns like pseudo-progression. Only two studies included out-of-field regression as an endpoint.

Here is what the major trials looked like:

• I-SABR — randomized phase II trial, 156 patients, nivolumab plus SABR (stereotactic ablative radiotherapy). Primary outcome was event-free survival.
• NCT03223155 — randomized phase I trial, 37 patients, nivolumab plus ipilimumab plus SBRT. Primary outcomes were progression-free and overall survival. A modified version of RECIST v1.1 allowed both irradiated and nonirradiated metastases as target and nontarget lesions.
• ASTEROID — randomized phase II trial (ongoing), 47 patients, durvalumab plus SBRT. Primary outcome was time to progression.
• PACIFIC — randomized phase III trial, 713 patients, durvalumab plus chemoradiotherapy (CRT). Primary outcomes were progression-free and overall survival, assessed by RECIST v1.1.
• LUN14-179 — single-arm phase II trial, 93 patients, pembrolizumab plus chemoradiotherapy. Primary outcome was time to metastatic disease.
• DETERRED — phase II trial, 40 patients, atezolizumab plus chemoradiotherapy. Primary outcomes were safety and tolerability.
• DOLPHIN — single-arm phase trial, 74 patients, durvalumab plus radiotherapy. Primary outcome was progression-free survival. Used RECIST v1.1 with no adjustments for abscopal effect.
• PACIFIC-6 — single-arm phase II trial, 117 patients, durvalumab plus chemoradiotherapy. Primary outcome was toxicity. Used RECIST v1.1 with no adjustments for abscopal effect.
• KEYNOTE-001 — phase I trial, 98 patients, pembrolizumab plus radiotherapy. Primary outcomes were progression-free and overall survival. Used iRECIST 4.0.
• SICI — phase I trial, 15 patients, durvalumab plus tremelimumab plus SBRT. Primary outcome was safety. Used RECIST v1.1 with no adjustments.
• SWORD trial — phase II trial, 55 patients, sintilimab (an anti-PD1 antibody) plus SBRT plus granulocyte-macrophage colony-stimulating factor (GM-CSF). Primary outcomes included objective response rate and out-of-field response rate (ASR). The abscopal effect was a secondary endpoint.
• Pembro-RT — prospective randomized phase I/II trial, 148 patients, pembrolizumab plus radiotherapy. Primary outcomes included abscopal response rate, abscopal control rate, progression-free survival, and overall survival. RECIST v1.1 was applied by an independent reviewer, and the irradiated lesion was excluded from measurements. Pseudo-progression was not counted as progressive disease for the primary endpoint.
• Schoenfeld et al. — randomized phase II trial, 78 patients, durvalumab plus tremelimumab, alone or combined with low-dose or hypofractionated radiotherapy. Primary outcome was objective response rate. RECIST v1.1 was used with the irradiated lesion excluded. Local control within irradiated fields and abscopal response rates were not uniformly collected and therefore not reported.
• Welsh et al. — prospective randomized phase I/II trial, 100 patients, SBRT plus pembrolizumab. Primary outcomes were toxicity and best out-of-field lesion response, assessed with immune-related response criteria.

This variability in how responses are measured underscores how hard it is to standardize outcomes in trials combining radiotherapy with immunotherapy. It also highlights how important it is to choose the right criteria — ones that capture both local treatment response and abscopal effects.

What This Evidence Means for Patients

The big picture: the abscopal effect, once thought to be a rare curiosity, has become far more relevant in the era of combined treatments and immune checkpoint inhibition.

Several trials in this review suggest that local irradiation may strengthen the body's systemic antitumor immune response when paired with immune checkpoint blockade. Radiotherapy induces immunogenic cell death and helps release tumor-associated antigens, which supports antigen presentation and activation of cytotoxic T cells. Combined with checkpoint inhibitors, this process may amplify systemic immune responses and make regression of distant, non-irradiated lesions more likely.

Some trials tried to capture these systemic effects directly. The Pembro-RT trial excluded irradiated lesions from RECIST measurements to better evaluate systemic tumor responses. The SWORD trial included out-of-field response rate as a secondary endpoint. In contrast, larger trials such as PACIFIC focused mainly on survival outcomes and applied conventional RECIST criteria, which may underestimate how often abscopal responses occur.

The authors emphasize a critical point: the ability to detect and count abscopal responses depends entirely on the method used to assess tumor regression. Conventional RECIST v1.1 often fails to capture all out-of-field tumor regression, leading to under-recognition of systemic effects. iRECIST partially addresses these limitations, but not all immunotherapy trials use it. And unequivocal out-of-field regression is still not included as a standard criterion.

The Proposed Working Definition

Based on the evidence, the authors put forward a working definition of the abscopal effect in NSCLC. This is their core contribution.

The abscopal effect is defined as:

1. Regression — either complete or partial response by iRECIST criteria — of one or more non-irradiated lesions.
2. The lesions must be distant from the primary treatment site.
3. The regression must occur after localized therapy, with or without systemic treatment.
4. It must be confirmed by follow-up imaging within 4 to 8 weeks.

Establishing standardized terminology and assessment criteria will be essential for accurately identifying and integrating potential abscopal responses in future NSCLC research and clinical practice.

Limitations of the Current Evidence

The authors are candid about the weaknesses in this field. Several limitations shape how confidently any conclusion can be drawn.

• Most evidence comes from preclinical models and early-phase studies, not large randomized trials designed specifically to test the abscopal effect.
• Study designs vary widely, including treatment combinations, endpoints, and methods of measuring response. This makes direct comparison across studies difficult.
• Very few trials were designed to evaluate out-of-field tumor regression. Most were built to measure survival or safety, not abscopal responses.
• Abscopal response data were often not uniformly collected — as in the Schoenfeld et al. trial, where abscopal response rates were not reported because the data were incomplete.
• Evidence for ablation-triggered abscopal effects is especially thin, resting largely on isolated case reports. The immune-modulating effects of ablation techniques remain poorly defined compared with radiotherapy.
• The incidence of the abscopal effect in NSCLC is likely underestimated because standard response criteria do not capture it.

Recommendations and What Comes Next

The authors offer a clear path forward. The central recommendation is adoption of a standardized definition and objective assessment criteria for the abscopal effect in NSCLC. Without them, real responses will keep slipping through the cracks.

Standardization would allow researchers to:

1. Recognize abscopal responses reliably instead of missing them.
2. Evaluate them systematically across studies.
3. Compare results between different trials and treatment combinations.
4. Integrate abscopal effects into real clinical decision-making.

For patients, the practical takeaway is this. If you receive radiation or ablation to one tumor and other tumors appear to shrink, that is a meaningful signal. That signal is worth discussing with your oncology team. Ask whether your imaging is being assessed with criteria that can capture out-of-field responses, such as iRECIST, and whether an abscopal response could explain what your scans show.

The authors also call for more research into the immune effects of ablation techniques, which lag behind radiotherapy in evidence. Their hope is that a shared vocabulary will let the field finally measure how often the abscopal effect happens — and use it to help more patients.

Frequently Asked Questions

What is the abscopal effect?

The abscopal effect is when tumors that were never directly treated begin to shrink after treatment is delivered somewhere else in the body. It was first described in 1953 and has been seen in several cancers, including lung cancer. It is still considered uncommon, though experts think it may be underrecognized.

How might radiation to one tumor shrink another?

Radiation can cause immunogenic cell death, releasing signals that activate dendritic cells and killer T cells. These T cells can travel through the bloodstream to distant, untreated tumors and attack cancer cells carrying the same proteins. Radiation can also suppress immune activity, which is one reason the effect is not more common.

Can ablation of a lung tumor trigger an abscopal effect?

Ablation techniques such as cryoablation, microwave ablation, and pulsed electric field therapy can release tumor antigens and stimulate immune responses. In one case report, a 69-year-old man with advanced squamous NSCLC had microwave ablation to his primary lung tumor, and untreated mediastinal lymph nodes later shrank. However, evidence for ablation-triggered abscopal effects remains limited to isolated case reports.

Why might my scans not show an abscopal response?

Standard response criteria called RECIST v1.1 focus on selected target lesions and may not capture shrinkage in non-target or non-irradiated tumors. iRECIST was designed for immunotherapy and can account for pseudo-progression, but it still does not systematically record out-of-field regression. This means abscopal responses may be missed on routine assessments.

What is the proposed definition of the abscopal effect in NSCLC?

The authors propose defining it as regression—complete or partial response by iRECIST—of one or more non-irradiated lesions distant from the treated site. It must occur after localized therapy, with or without systemic treatment, and be confirmed by follow-up imaging within 4 to 8 weeks. This definition aims to standardize how the effect is identified.

Does combining radiation with immunotherapy increase the chance of an abscopal effect?

Preclinical and early clinical studies suggest that adding an immune checkpoint inhibitor to radiation may amplify the abscopal effect. For example, in a study by Huang et al., patients with metastatic NSCLC who received stereotactic body radiation therapy before pembrolizumab showed immune changes in non-irradiated tumors. However, prospective trials vary widely in design and how they measure responses.

If I receive radiation or ablation and other tumors shrink, what should I do?

That is a meaningful signal worth discussing with your oncology team. Ask whether your imaging is being assessed with criteria that can capture out-of-field responses, such as iRECIST, and whether an abscopal response could explain what your scans show. The authors recommend standardized assessment to ensure such responses are recognized.

If radiation or ablation to one lung tumor shrinks other untreated tumors, when should I seek a second opinion on my scans?

If you receive radiation or ablation to one tumor and other, untreated tumors appear to shrink, that is a meaningful signal worth discussing with your oncology team. Standard RECIST v1.1 criteria often fail to capture regression in non-irradiated lesions, so an abscopal response may go unrecognized. Ask whether your imaging is assessed with criteria such as iRECIST that can capture out-of-field responses, and whether an abscopal response could explain your scans. A second opinion can review whether your imaging was measured with criteria able to detect these responses. Diagnostic Detectives Network provides independent expert second opinions.

Source Information

Original article title: Defining the abscopal effect in non-small cell lung cancer in the era of immunotherapy and lung ablation treatment: a narrative review.

Authors: Illaa Smesseim, Phillip N. Perez, Abraham Chachoua, Benjamin T. Cooper, and Daniel H. Sterman

Author affiliations: Department of Thoracic Oncology, Netherlands Cancer Institute, Amsterdam, Netherlands; Department of Pulmonary Diseases, Leiden University Medical Center, Leiden, Netherlands; NYU Pulmonary Oncology Research Team (NYU PORT), Division of Pulmonary, Critical Care & Sleep Medicine, Department of Medicine, NYU Langone Health, New York, NY, United States; Department of Medicine, NYU Grossman School of Medicine, New York, NY, United States; Department of Radiation Oncology, NYU Langone Health, New York, NY, United States

Journal: Frontiers in Medicine, volume 13, article 1804711

Article type: Review

Publication date: Published 23 April 2026 (received 05 February 2026; revised 25 March 2026; accepted 30 March 2026)

DOI: 10.3389/fmed.2026.1804711

Note: This patient-friendly article is based on peer-reviewed research. It is intended for educational purposes and should not replace personalized medical advice from your own oncology team. If you have questions about your treatment or imaging results, speak with your treating physician.