Clear, evidence-based explanations of cutting-edge cancer treatment strategies — so you can have more informed conversations with your care team.
How genomic profiling is transforming cancer treatment — and why understanding your tumour's molecular fingerprint matters.
Cancer treatment has historically been guided primarily by the location and histology of the tumour. Patients diagnosed with the same type of cancer often received similar treatment strategies, typically involving combinations of surgery, chemotherapy, and radiation therapy. Over the past decade, however, a new approach has emerged: precision oncology.
Precision oncology focuses on understanding the molecular characteristics of an individual tumour. Instead of treating cancers solely based on where they arise in the body, clinicians can now examine the genetic alterations and molecular pathways driving tumour growth.
Advances in next-generation sequencing (NGS) have made it possible to analyse hundreds of cancer-related genes simultaneously. Comprehensive genomic profiling can identify mutations, gene amplifications, gene fusions, and other alterations that may help guide treatment decisions.
Tumours harbouring specific alterations in genes involved in signalling pathways, DNA repair, or immune regulation may respond to targeted therapies or immunotherapy designed to exploit these vulnerabilities. Molecular profiling can also help determine whether a patient may be eligible for clinical trials investigating novel targeted treatments.
Genomic reports often contain numerous genetic alterations. Distinguishing clinically actionable findings from passenger mutations requires careful interpretation of scientific evidence, clinical guidelines, and the patient's clinical context.
Integrating molecular data with pathology findings, imaging results, and clinical history has become increasingly important — and is at the core of what precision oncology consultants do.
Precision oncology represents a shift toward more individualised cancer care, where treatment decisions are informed not only by tumour type but also by the unique molecular features of each patient's disease. While genomic profiling does not replace traditional cancer therapies, it provides an additional layer of insight that can help clinicians and patients explore more personalised treatment strategies and potential therapeutic opportunities.
Two of oncology's most powerful tools — Antibody-Drug Conjugates (ADCs) and immune checkpoint inhibitors (ICIs) — are now being studied together. The science behind this combination is compelling: each therapy enhances the other in a self-reinforcing cycle that attacks cancer from multiple angles simultaneously.
ADCs kill cancer cells in a way that teaches the immune system to recognize and attack them — a process called immunogenic cell death. Adding an ICI then removes the "brakes" that cancer uses to suppress that immune response.
This combination is particularly relevant in cancers like HER2-positive and triple-negative breast cancer, where clinical trials are showing early promise for patients who have not responded to standard therapies.
A landmark 2025 study in Cancer Discovery found that consuming sucralose — a common artificial sweetener found in diet sodas, protein powders, and sugar-free foods — was significantly associated with poorer immunotherapy response in patients with melanoma and lung cancer.
Researchers at the University of Pittsburgh studied 132 patients receiving anti-PD-1 checkpoint inhibitor therapy and found a striking pattern: patients with higher sucralose intake responded significantly worse to treatment — and had shorter survival — than those who consumed little or none.
In melanoma patients, median progression-free survival was 13 months in low sucralose consumers vs. only 8 months in high consumers. In lung cancer (NSCLC), the gap was even wider: 18 months vs. 7 months.
The mechanism isn't that sucralose directly attacks immune cells — it's more subtle and more systemic. Sucralose disrupts the gut microbiome, causing an overgrowth of bacteria that break down arginine, an amino acid that T-cells critically depend on to function. Without enough arginine, T-cells become exhausted — unable to find and destroy cancer cells even when immunotherapy removes the brakes.
A landmark 2026 study in Nature Cancer used advanced imaging technology to map the tumour's immune landscape — and found that what happens during treatment predicts response far better than anything measurable before it begins.
Triple-negative breast cancer (TNBC) is one of the most aggressive breast cancer subtypes, and immune checkpoint inhibitors (ICI) — drugs that release the immune system's brakes — have transformed its treatment. Yet only a fraction of patients truly respond. The critical question has always been: who will benefit?
Scientists from Stanford and The Netherlands Cancer Institute analyzed tumour biopsies from 103 patients with metastatic TNBC across four time points — including the primary tumour, before treatment, and during immunotherapy. Using highly multiplexed imaging (MIBI), they simultaneously measured 37 proteins in each tumour sample to map the full immune landscape.
They built an open-source tool called SpaceCat to extract over 800 features from these images — not just which immune cells are present, but where they are, how they're organized, and how they interact with cancer cells. The result was the most detailed spatial picture of the metastatic TNBC tumour microenvironment to date.
The primary tumour — the cancer at diagnosis — was almost useless for predicting who would respond to immunotherapy later, in the metastatic setting. On-treatment biopsies, taken after three cycles of nivolumab, were dramatically more informative, achieving a prediction accuracy (AUC) of 0.90.
This challenges the common assumption that pre-treatment biopsies are sufficient. The tumour microenvironment evolves — and the immune response that unfolds during early treatment is the most reliable window into whether therapy will work.
Immunotherapy has transformed cancer treatment — but it has also introduced new complexities in how response is assessed. An apparent increase in tumour size shortly after therapy begins may not represent treatment failure. Understanding the difference could mean the difference between staying on life-prolonging therapy or stopping it prematurely.
Unlike conventional chemotherapy, immune checkpoint inhibitors activate the body's own immune system to fight cancer. This fundamentally different mechanism produces imaging patterns that can be alarming — and deeply misleading — if not properly understood.
Pseudoprogression refers to a transient increase in tumour size or the appearance of new lesions on imaging, followed by subsequent tumour regression — without any change in therapy. It is most commonly seen with PD-1, PD-L1, and CTLA-4 inhibitors and reflects immune-mediated effects rather than true disease worsening: infiltration of activated T cells, inflammation, oedema, and tumour necrosis all alter how lesions appear on a scan.
The mechanism is rooted in immune activation within the tumour microenvironment. After immunotherapy begins, activated immune cells infiltrate the tumour. The resulting inflammatory response increases lesion volume. Necrotic changes further alter how the tumour appears on imaging.
As a result, radiographic findings may temporarily suggest tumour growth — even when the overall tumour burden is biologically decreasing.
Pseudoprogression typically occurs within the first 6–12 weeks of therapy. Genuine tumour shrinkage, however, may only become evident months later — making early imaging particularly prone to misinterpretation. Delayed responses are not uncommon.
Standard response criteria — RECIST — were developed for cytotoxic chemotherapy. Under these criteria, an increase in tumour size is classified as progressive disease, which typically triggers a switch to a different regimen.
Applied to immunotherapy, this creates a serious risk of misclassification. A patient on the path to a genuine, durable response may be told their treatment is failing — and switched to something less effective.
Recognising the limitations of RECIST, immune-specific response criteria (iRECIST) have been developed. Under iRECIST, initial radiographic worsening is classified as "unconfirmed progression" — treatment may continue if the patient is clinically stable, with a confirmatory scan 4–8 weeks later. This framework allows clinicians to treat beyond initial apparent progression when appropriate, preventing early cessation of potentially life-prolonging therapy.
No single parameter is definitive. Accurate interpretation requires a multidimensional clinical approach, integrating converging evidence from multiple sources.