PD-L1 Testing in Cancer

by Jason Wasserman MD PhD FRCPC

March 21, 2026

PD-L1 (programmed death-ligand 1) is a protein found on the surface of cells — including cancer cells and immune cells within tumours — that acts as a brake on the immune system. Under normal circumstances, PD-L1 helps prevent the immune system from attacking healthy tissue by binding to a receptor called PD-1 on T cells, sending a signal that tells the T cell to stand down. Many cancers exploit this mechanism by producing large amounts of PD-L1, effectively disguising themselves from the immune system and suppressing the T cells that would otherwise recognise and destroy them. A class of drugs called immune checkpoint inhibitors — including pembrolizumab (Keytruda), nivolumab (Opdivo), atezolizumab (Tecentriq), durvalumab (Imfinzi), and others — work by blocking the PD-1/PD-L1 interaction, releasing the brake and allowing the immune system to attack the cancer. PD-L1 testing measures how much of this protein is present in a tumour. In many cancer types, the result determines whether checkpoint inhibitor therapy is appropriate, which drug to use, and the likelihood of a response. PD-L1 is now one of the most widely tested biomarkers in oncology. Still, it is also one of the most complex: different drugs use different antibody tests, different scoring systems, and different cut-off thresholds, and the same numerical result can mean different things depending on the cancer type and the specific drug being considered.

What the test looks for

The CD274 gene encodes the PD-L1 protein. Its normal function is to limit immune responses and prevent autoimmunity — a protective mechanism that prevents T cells from destroying healthy tissue. In cancer, PD-L1 expression on tumour cells and on immune cells that have infiltrated the tumour serves as a molecular camouflage, dampening the anti-tumour immune response.

PD-L1 testing uses immunohistochemistry (IHC) — a technique in which a specific antibody is applied to tumour tissue on a glass slide to detect the PD-L1 protein. Cells carrying PD-L1 on their surface stain brown; cells without it remain blue. A pathologist then assesses the proportion of cells that stain positive and the intensity of staining.

What makes PD-L1 testing unusually complex is that there is no single universal test. Different checkpoint inhibitor drugs were developed and approved in clinical trials using different antibody clones, different staining platforms, and different scoring algorithms — and these are not always interchangeable. A result from one assay cannot reliably be substituted for a result from another. Understanding which assay was used, which scoring system was applied, and what cut-off is relevant for the specific drug being considered is essential for correct interpretation.

The two main scoring systems

Tumour proportion score (TPS). The TPS counts only tumour cells — the cancer cells themselves — that stain positive for PD-L1, expressed as a percentage of all tumour cells assessed. A TPS of 50%, for example, means that half of the cancer cells in the sample express PD-L1. TPS is the scoring system used for most lung cancer applications and for several other tumour types.
Combined positive score (CPS). The CPS counts PD-L1-positive cells of all types — tumour cells, tumour-infiltrating lymphocytes (immune cells within the tumour), and macrophages — and divides this by the total number of tumour cells, then multiplies the result by 100. A CPS of 10 means that for every 100 tumour cells counted, there are 10 PD-L1-positive cells of any type. CPS is used for many non-lung cancer applications, including gastric, cervical, head and neck, and triple-negative breast cancer. It captures the immune microenvironment around the tumour as well as the tumour cells themselves.

A third scoring system — the immune cell (IC) score — assesses only the PD-L1-positive immune cells within and around the tumour, expressed as a percentage of the tumour area. This is used in specific applications, particularly for atezolizumab in bladder cancer.

PD-L1 testing by tumour type: diagnostic and treatment implications

PD-L1 testing plays a different role in each cancer type — different assays, different scoring systems, different cut-offs, and different consequences for treatment. The following sections explain what PD-L1 testing means in the cancers where it is most commonly applied.

Non-small cell lung cancer

Lung cancer has the most complex and extensively validated PD-L1 testing landscape of any tumour type. PD-L1 testing is mandatory for all patients with advanced or metastatic non-small cell lung cancer (NSCLC) because the result directly determines first-line treatment. The primary assay used in lung cancer is the 22C3 antibody clone (Dako/Agilent platform), which uses TPS scoring and is the FDA-approved companion diagnostic for pembrolizumab. Three TPS categories define the treatment implications:

TPS ≥ 50% (PD-L1 high). Pembrolizumab monotherapy is approved as a first-line treatment for advanced NSCLC without actionable driver mutations (EGFR, ALK, etc.) when TPS is ≥ 50%. This is one of the most important treatment thresholds in oncology. Response rates to pembrolizumab monotherapy in TPS ≥ 50% NSCLC are approximately 45%, with a meaningful proportion of patients achieving long-term disease control — something rarely seen with chemotherapy alone.
TPS 1–49% (PD-L1 low-positive). Pembrolizumab plus platinum-based chemotherapy is approved as a first-line treatment. Pembrolizumab monotherapy is not preferred in this range. The addition of chemotherapy to immunotherapy improves outcomes compared to either alone in this population.
TPS < 1% (PD-L1 negative). Pembrolizumab monotherapy is not recommended. Pembrolizumab combined with chemotherapy remains an option, as some PD-L1-negative patients still benefit from the combination. Other checkpoint inhibitor combinations — such as nivolumab plus ipilimumab — are also approved for NSCLC regardless of PD-L1 status.

Other antibody clones are also used in lung cancer — the 28-8 clone is used with nivolumab, and the SP263 clone is used with durvalumab in the locally advanced (stage III) setting. These clones produce somewhat different staining results and are not interchangeable with 22C3 for all purposes. At most major cancer centres, the 22C3 assay is run as the primary test, and the result is interpreted in the context of all available treatment options.

Critically, PD-L1 testing in lung cancer must always be interpreted alongside the full molecular profile. Patients with actionable driver mutations — EGFR, ALK, ROS1, RET, MET exon 14 skipping, BRAF V600E, and others — are treated with targeted therapy first, regardless of PD-L1 expression. Checkpoint inhibitors are generally less effective in driver-mutated NSCLC and may cause significant toxicity when combined with targeted therapies. PD-L1 testing is most relevant for treatment selection in driver-negative NSCLC.

Triple-negative breast cancer

Triple-negative breast cancer (TNBC) — defined by the absence of estrogen receptor, progesterone receptor, and HER2 expression — is the breast cancer subtype most likely to respond to immunotherapy. PD-L1 testing is recommended for all patients with locally advanced or metastatic TNBC to determine eligibility for checkpoint inhibitor therapy. Two drugs and two assays are relevant in this setting, and they are not interchangeable:

Pembrolizumab (Keytruda) with the 22C3 assay, CPS ≥ 10. Pembrolizumab combined with chemotherapy is approved as a first-line treatment for metastatic TNBC with a CPS ≥ 10 using the 22C3 assay. The KEYNOTE-522 trial also established pembrolizumab combined with neoadjuvant chemotherapy for high-risk early-stage TNBC, where PD-L1 testing is not required — pembrolizumab is used regardless of PD-L1 status in the early-stage neoadjuvant/adjuvant setting based on stage alone.
Atezolizumab (Tecentriq) with the SP142 assay, IC ≥ 1%. Atezolizumab combined with nab-paclitaxel was previously approved for PD-L1-positive (SP142 IC ≥ 1%) metastatic TNBC; however, the commercial availability of atezolizumab in this indication has been withdrawn in some markets following updated trial data. The SP142 assay and IC scoring are specific to atezolizumab and cannot be used to guide pembrolizumab prescribing.

The assay-drug pairing in TNBC is clinically critical: results from the SP142 assay cannot be used to determine pembrolizumab eligibility, and results from the 22C3 assay cannot be used to determine atezolizumab eligibility. Patients should confirm which assay was performed and which drug is being considered.

Gastric and gastroesophageal junction cancer

PD-L1 testing using CPS scoring with the 22C3 assay is standard for all patients with advanced gastric or gastroesophageal junction (GEJ) adenocarcinoma. The relevant cut-offs are:

CPS ≥ 1. Nivolumab combined with chemotherapy is approved as first-line treatment for HER2-negative gastric/GEJ cancer with CPS ≥ 1, based on the CheckMate 649 trial.
CPS ≥ 5 or CPS ≥ 10. Pembrolizumab combined with chemotherapy (with or without trastuzumab for HER2-positive disease) is approved for gastric/GEJ cancer with CPS ≥ 5 or ≥ 10, depending on the specific regimen and jurisdiction, based on the KEYNOTE-590 and KEYNOTE-811 trials.

PD-L1 testing in gastric cancer should be interpreted alongside HER2 testing, as the treatment approach differs for HER2-positive disease. MMR/MSI testing is also performed, and dMMR/MSI-H gastric cancers may have a particularly strong response to immunotherapy regardless of PD-L1 expression.

Cervical cancer

PD-L1 testing with the 22C3 assay using CPS scoring is recommended for patients with recurrent or metastatic cervical cancer. Pembrolizumab combined with chemotherapy (with or without bevacizumab) is approved for cervical cancer with CPS ≥ 1, based on the KEYNOTE-826 trial — a landmark study that established immunotherapy as part of the first-line standard of care for advanced cervical cancer. The CPS ≥ 1 threshold is relatively low, and the majority of cervical cancers meet this criterion, reflecting the generally immunogenic nature of HPV-driven cancers.

Head and neck squamous cell carcinoma

PD-L1 testing is standard for all patients with recurrent or metastatic head and neck squamous cell carcinoma (HNSCC). The 22C3 assay with CPS scoring is used, and two cut-offs are clinically meaningful:

CPS ≥ 1. Pembrolizumab combined with platinum-based chemotherapy is approved for first-line treatment of recurrent/metastatic HNSCC with CPS ≥ 1, based on the KEYNOTE-048 trial.
CPS ≥ 20. Pembrolizumab monotherapy (without chemotherapy) is approved as first-line treatment for CPS ≥ 20, based on demonstrated non-inferiority to chemotherapy with a more favourable tolerability profile. This higher threshold identifies patients most likely to achieve durable responses from immunotherapy alone.

HPV-positive oropharyngeal cancers tend to have higher PD-L1 expression than HPV-negative cancers, though both subtypes benefit from pembrolizumab in the CPS-eligible populations.

Esophageal cancer

PD-L1 testing is recommended for patients with advanced esophageal squamous cell carcinoma and oesophageal adenocarcinoma. For esophageal squamous cell carcinoma, pembrolizumab combined with chemotherapy is approved for CPS ≥ 10 based on the KEYNOTE-590 trial. Nivolumab combined with chemotherapy or with ipilimumab is also approved regardless of PD-L1 status in esophageal squamous cell carcinoma. For esophageal adenocarcinoma, the same considerations as for GEJ adenocarcinoma apply.

Bladder and urothelial cancer

PD-L1 testing in urothelial carcinoma has a complex history, with several approvals and subsequent label revisions. The currently most clinically relevant application is in cisplatin-ineligible patients with advanced urothelial cancer, where PD-L1 status has been used to guide whether to use atezolizumab or pembrolizumab as first-line monotherapy in patients who cannot receive platinum-based chemotherapy. The SP142 assay (IC scoring≥ 5%) has been used to select atezolizumab in this setting. For pembrolizumab, the 22C3 CPS ≥ 10 threshold has been relevant. Your oncologist will advise on the current approved indications in your jurisdiction, as this landscape has evolved with updated trial data. In the second-line setting after platinum chemotherapy, pembrolizumab and nivolumab are approved regardless of PD-L1 status.

Endometrial cancer

PD-L1 expression in endometrial cancer is closely intertwined with MMR/MSI status and must be interpreted in that context. Pembrolizumab combined with lenvatinib is approved for advanced endometrial cancer that is not dMMR/MSI-H and has progressed after prior platinum-based chemotherapy. This combination does not require PD-L1 testing and is approved regardless of PD-L1 expression. For MMR-deficient endometrial cancers, pembrolizumab monotherapy or dostarlimab monotherapy is approved based on MMR status rather than PD-L1 expression. The practical implication is that MMR/MSI testing is the primary biomarker in endometrial cancer; PD-L1 testing plays a secondary role and is generally not the key determinant of immunotherapy eligibility in this tumour type.

Melanoma

PD-L1 testing in melanoma occupies a unique position: it is routinely performed and reported, but it is a relatively weak predictor of response compared to other tumour types, and treatment decisions are generally not gated on PD-L1 status. Checkpoint inhibitors — pembrolizumab, nivolumab, and the combination of nivolumab plus ipilimumab — are approved for advanced melanoma regardless of PD-L1 expression. High PD-L1 expression may slightly increase the likelihood of response to PD-1 monotherapy. It may favour monotherapy over the more toxic nivolumab/ipilimumab combination, but the evidence is not strong enough to withhold treatment from PD-L1-negative patients. PD-L1 testing in melanoma is therefore informative rather than gatekeeping, and your oncologist will not typically use the result alone to determine whether immunotherapy is appropriate.

Hepatocellular carcinoma

Atezolizumab combined with bevacizumab is approved as a first-line treatment for unresectable hepatocellular carcinoma (HCC) based on the IMbrave150 trial, which did not use PD-L1 as a selection criterion. Durvalumab combined with tremelimumab (a CTLA-4 inhibitor) is also approved regardless of PD-L1 status. PD-L1 testing is not currently required to determine eligibility for first-line immunotherapy in HCC, though it may be performed as part of a broader molecular assessment.

Renal cell carcinoma

Checkpoint inhibitor combinations are now standard first-line treatment for advanced clear cell renal cell carcinoma (RCC), including pembrolizumab plus axitinib, nivolumab plus ipilimumab, and nivolumab plus cabozantinib. PD-L1 testing is performed but is generally not used as the primary criterion for treatment eligibility in RCC. These combinations are approved across PD-L1 expression levels, though PD-L1 expression may influence the relative benefit of immunotherapy monotherapy versus combination regimens in some subgroups. Treatment selection in RCC is more strongly guided by risk score (e.g., IMDC risk criteria) than by PD-L1 expression alone.

Colorectal cancer

PD-L1 expression in colorectal cancer, as measured by standard IHC, is generally not the primary biomarker used to guide immunotherapy eligibility. Instead, MMR/MSI status is the key determinant: dMMR/MSI-H colorectal cancers respond strongly to checkpoint inhibitors — pembrolizumab is approved as first-line therapy for dMMR/MSI-H metastatic colorectal cancer — while pMMR/MSS colorectal cancers (the majority) respond poorly to immunotherapy regardless of PD-L1 expression. The reason is that dMMR/MSI-H cancers accumulate very large numbers of mutations, generating many abnormal proteins that the immune system can recognise, making them inherently immunogenic. In this context, PD-L1 testing adds little to MMR testing in colorectal cancer and is not routinely used to guide immunotherapy decisions in this tumour type.

Why is the test done

To determine eligibility for checkpoint inhibitor therapy. In many tumour types, PD-L1 expression above a specific threshold is required for approval of pembrolizumab or other checkpoint inhibitors. Testing identifies which patients qualify.
To select the most appropriate checkpoint inhibitor regimen. In some cancers, the PD-L1 result determines not just whether to use immunotherapy but also which combination — monotherapy versus chemotherapy — is most appropriate.
To predict the likelihood of response. Higher PD-L1 expression generally (though not always) correlates with higher response rates to checkpoint inhibitors. This information helps oncologists and patients weigh the expected benefits against side effects when making treatment decisions.
To comply with regulatory approval criteria. Some checkpoint inhibitor approvals require PD-L1 testing with a specific assay and a specific cut-off as a condition of use. Testing is not optional in these settings — it is a regulatory requirement.
To complement other biomarkers. PD-L1 testing is most informative when interpreted alongside other biomarkers — tumour mutational burden (TMB), MMR/MSI status, and molecular driver mutations — that together provide a fuller picture of the tumour’s immune microenvironment and likely responsiveness to immunotherapy.

Who should be tested

PD-L1 testing is recommended for all patients with the following advanced or metastatic cancers, as part of the standard diagnostic workup:

Non-small cell lung cancer — mandatory at diagnosis for all patients with advanced disease
Triple-negative breast cancer — mandatory for locally advanced or metastatic disease
Gastric and gastroesophageal junction adenocarcinoma — mandatory for advanced disease
Cervical cancer — recommended for recurrent or metastatic disease
Head and neck squamous cell carcinoma — mandatory for recurrent or metastatic disease
Esophageal squamous cell carcinoma and adenocarcinoma — recommended for advanced disease
Urothelial carcinoma — recommended for advanced or metastatic disease, particularly in cisplatin-ineligible patients

PD-L1 testing is also routinely performed in melanoma, renal cell carcinoma, hepatocellular carcinoma, endometrial cancer, and other tumour types, though in some of these cancers, it is informative rather than gatekeeping.

How the test is performed

PD-L1 testing is performed using immunohistochemistry (IHC) on tumour tissue obtained from a biopsy or surgical specimen. A thin slice of tumour tissue is mounted on a glass slide, treated with a PD-L1-specific antibody, and examined under the microscope by a pathologist, who scores the result using the appropriate scoring system for the clinical context.

The specific antibody clone used matters — the four most widely used clones in clinical practice are 22C3 (Dako/Agilent), 28-8 (Dako/Agilent), SP263 (Ventana/Roche), and SP142 (Ventana/Roche). Each was developed as a companion diagnostic for a specific drug and validated in a corresponding clinical trial. Studies comparing their performance have shown meaningful differences in staining intensity and in which cell types stain positive, particularly between SP142, which tends to yield lower staining scores, and the other three clones, which show better concordance among themselves. The practical consequence is that the assay used must match the drug being considered, particularly in tumour types where the cut-off is clinically critical.

Most major cancer centres run one or two validated PD-L1 assays and report results that cover the most clinically relevant thresholds. If you are being treated at a centre that uses a different assay than the one used in the pivotal trial for the drug your oncologist is considering, this is worth discussing.

How results are reported

PD-L1 results are reported as a numerical score using the scoring system appropriate for the tumour type and assay used. A typical report might read:

“PD-L1 TPS: 65% (22C3 clone)” — for a lung cancer specimen
“PD-L1 CPS: 12 (22C3 clone)” — for a gastric cancer specimen
“PD-L1 IC score: 2% (SP142 clone)” — for a urothelial cancer specimen

The report will typically note whether the result exceeds the relevant clinical threshold — for example, “TPS ≥ 50%: positive” or “CPS ≥ 1: positive.” In some cases, multiple thresholds are reported simultaneously — for example, a lung cancer report may note whether TPS is <1%, 1–49%, or ≥50%, because all three ranges have treatment implications.

It is important to note the antibody clone and scoring system used when discussing your result with your oncologist, because the same numerical score can mean different things across different assays.

What the result means

PD-L1 high (above the relevant high threshold for your cancer type). The tumour expresses substantial amounts of PD-L1. In most cancer types with established PD-L1 thresholds — particularly NSCLC with TPS ≥ 50%, HNSCC with CPS ≥ 20%, and cervical cancer with CPS ≥ 1 — a high result supports the use of checkpoint inhibitor monotherapy or combination therapy. High PD-L1 expression is generally associated with a higher probability of response to checkpoint inhibitor drugs. However, it does not guarantee a response, and some patients with high PD-L1 do not respond, while some with low PD-L1 do.
PD-L1 intermediate (between relevant thresholds, varies by cancer type). An intermediate result — for example, TPS 1–49% in NSCLC, or CPS 1–9 in some gastric cancer contexts — typically supports the use of checkpoint inhibitors in combination with chemotherapy rather than as monotherapy. The added chemotherapy provides a treatment backbone that improves outcomes in patients whose tumours are not strongly immunogenic enough to respond to immunotherapy alone.
PD-L1 negative or low (below the relevant threshold). A low or negative result means the tumour expresses little or no PD-L1 by the assay used. In tumour types where PD-L1 is a strict eligibility criterion — such as pembrolizumab monotherapy in NSCLC — a result below the threshold means that the specific regimen is not approved. However, a negative PD-L1 result does not mean immunotherapy is never appropriate: in many tumour types, checkpoint inhibitor combinations are approved regardless of PD-L1 expression, and some PD-L1-negative patients still achieve meaningful responses. Your oncologist will explain whether immunotherapy is still an option despite a low or negative PD-L1 result in your specific situation.
The result obtained on a biopsy may not represent the whole tumour. PD-L1 expression can vary between different parts of the same tumour and between the primary tumour and metastatic sites. A result from a single biopsy is a snapshot — it may not capture the full range of PD-L1 expression across all tumour deposits. This is particularly relevant when a result falls near a clinically important threshold. If your result is close to a cut-off, discussing whether re-biopsy or testing of a different site is appropriate may be worthwhile.

Limitations of PD-L1 testing

PD-L1 testing is an imperfect biomarker, and understanding its limitations is important for setting realistic expectations:

PD-L1 expression is dynamic. PD-L1 levels on tumour cells can change over time, in response to treatment, and between the primary tumour and metastatic sites. A result obtained at diagnosis may not reflect PD-L1 status at a later point in the disease course. For this reason, retesting on new biopsy material is sometimes recommended when a patient progresses, and further immunotherapy lines are being considered.
Assay heterogeneity. The four major PD-L1 antibody clones do not produce identical results. SP142 in particular tends to score lower than the other three clones on the same tissue section, meaning that a patient who tests negative with SP142 might test positive with 22C3. Laboratories that run only one assay may produce results that cannot directly guide decisions about drugs approved using a different assay.
Tumour heterogeneity. PD-L1 expression can vary considerably within a single tumour — some areas may stain strongly positive while others are negative. A biopsy from one part of the tumour may not represent the whole.
Predictive but not deterministic. PD-L1 expression predicts — imperfectly — the likelihood of response to checkpoint inhibitors. Many patients with high PD-L1 expression do not respond to immunotherapy, whereas many with low or absent PD-L1 expression do respond. PD-L1 is a probabilistic guide, not a binary predictor of success or failure.
Interaction with other biomarkers. PD-L1 expression must be interpreted alongside MMR/MSI status, TMB, and molecular driver mutation status to give the most complete picture. In some settings — such as dMMR/MSI-H tumours, which are typically highly immunogenic regardless of PD-L1 score — MMR status is more informative than PD-L1 alone.

PD-L1 testing and other biomarkers

PD-L1 testing rarely stands alone. In clinical practice, it is almost always interpreted alongside:

MMR/MSI status — in colorectal, endometrial, gastric, and other cancers, dMMR/MSI-H status is a stronger predictor of immunotherapy benefit than PD-L1 expression and takes precedence in treatment decisions.
Tumour mutational burden (TMB) — a high TMB reflects a large number of tumour mutations and is associated with increased immunotherapy benefit, independently of PD-L1. Pembrolizumab is approved for TMB-high tumours (≥ 10 mutations per megabase) on a tumour-agnostic basis, regardless of PD-L1 expression.
Driver mutations (in lung cancer) — as discussed above, patients with targetable driver mutations in NSCLC receive targeted therapy first,t and immunotherapy is generally deferred, regardless of PD-L1 expression.
HER2 status (in gastric cancer) — HER2-positive gastric cancers are treated with trastuzumab-based regimens; pembrolizumab can be added to first-line chemotherapy plus trastuzumab in CPS ≥ 1 disease, making the combination of HER2 and PD-L1 testing both important.

PD-L1 testing: germline vs. somatic

PD-L1 expression as measured by IHC reflects the behaviour of the cancer cells and their immune microenvironment — it is not a germline finding and has no hereditary implications. A high or low PD-L1 result does not indicate a genetic predisposition to cancer, cannot be passed to family members, and does not require cascade testing of relatives. This is entirely distinct from biomarkers such as BRCA1/2 or MMR genes, where the tumour finding can reflect an underlying inherited mutation.

What happens next

If PD-L1 is high (above the relevant threshold for your cancer type and drug): Your oncologist will discuss checkpoint inhibitor therapy — potentially as monotherapy if the threshold supports it, or in combination with chemotherapy. The specific drug, regimen, and schedule will depend on your cancer type, PD-L1 score, other biomarker results, and overall clinical status.
If PD-L1 is intermediate: Checkpoint inhibitor therapy combined with chemotherapy is typically the appropriate approach in cancer types with established intermediate-range approvals. Your oncologist will explain the rationale for the combination and what to expect.
If PD-L1 is low or negative, your oncologist will explain whether immunotherapy remains an option through combination regimens or tumour-agnostic approvals (e.g., TMB-high or dMMR status). In some tumour types, immunotherapy combinations are approved regardless of PD-L1. A negative result does not necessarily mean immunotherapy is off the table.
If your result is near a threshold, discuss with your oncologist whether it should be interpreted conservatively or whether retesting on additional tissue would change the treatment approach.
If you have a driver mutation (in lung cancer): PD-L1 results will be noted but targeted therapy will be prioritised. Your oncologist will explain when and whether immunotherapy might be considered later in your treatment course.

Questions to ask your doctor

What is my PD-L1 score, and which antibody clone and scoring system was used?
What threshold is relevant for the specific drug being considered for my cancer type?
Does my PD-L1 result qualify me for checkpoint inhibitor monotherapy, combination therapy, or neither?
If my PD-L1 is low or negative, is immunotherapy still an option for me through a combination regimen or another pathway?
Has my tumour been tested for MMR/MSI status and tumour mutational burden alongside PD-L1?
If I have a driver mutation, when — if ever — would immunotherapy be considered in my treatment course?
What side effects should I expect from checkpoint inhibitor therapy, and how are immune-related side effects recognised and managed?
If my cancer progresses on immunotherapy, will PD-L1 be retested?
Are there clinical trials studying new immunotherapy approaches that I might be eligible for?