Sources and Guidelines Referenced

The clinical guidelines and landmark studies cited throughout this evidence-based text include: National Comprehensive Cancer Network (NCCN) Guidelines 2024; American Society of Clinical Oncology (ASCO) Provisional Clinical Opinions and Guidelines 2023; European Society for Medical Oncology (ESMO) Precision Oncology Working Group Recommendations 2023; World Health Organization (WHO) Classification of Tumors 2022; MOSCATO-01 Trial (Massard et al., Cancer Discovery, 2017); SHIVA Trial (Le Tourneau et al., Lancet Oncology, 2015); NCI-MATCH Trial (Flaherty et al., Journal of Clinical Oncology, 2020); IMPRESS Study (Helland et al., ESMO Open, 2022); and FDA Biomarker-Driven Tumor-Agnostic Approval Frameworks 2023.

Precision Oncology: A Comprehensive Patient Guide

1. Definition and Medical Identity

Precision oncology is a clinical framework in cancer medicine that uses molecular profiling of tumors to guide individualized treatment strategies. Also known as personalized cancer medicine or molecularly targeted therapy, this discipline belongs to precision medicine. Its primary clinical goal is identifying therapeutic options that target distinct biological mechanisms driving a specific patient's tumor growth.

Unlike traditional oncology, which selects treatments based primarily on organ site and histological appearance under light microscopy, precision oncology categorizes malignancies by their specific underlying molecular features. Modern high-throughput genomic assays, including multi-gene next-generation sequencing (NGS), analyze deoxyribonucleic acid (DNA), ribonucleic acid (RNA), and protein expression. By detecting specific driver mutations, gene amplifications, structural fusions, and genomic instability markers, oncology teams select targeted small-molecule inhibitors, monoclonal antibodies, or immunotherapies engineered to neutralize specific pathological signals (ASCO 2023).

2. The Underlying Condition or Need

Cancer develops through progressive genetic and epigenetic alterations that transform normal human cells into unconstrained malignant growths. The fundamental biological problem precision oncology addresses is the marked genomic heterogeneity found within human cancers. Tumor cells acquire driver mutations that dysregulate cell growth, inhibit programmed cell death (apoptosis), promote blood vessel formation (angiogenesis), and evade immune surveillance (WHO 2022).

In clinical practice, patients with cancer historically received standardized, broad-spectrum cytotoxic chemotherapy regimens. While effective for a subset of individuals, empirical cytotoxic therapy frequently damages rapidly dividing non-cancerous tissues, causing substantial systemic toxicity. Furthermore, two patients presenting with identical organ-site histologies (such as stage IV non-small cell lung cancer) often possess completely different driver mutations. One tumor may be driven by an epidermal growth factor receptor (EGFR) mutation, while another harbors an anaplastic lymphoma kinase (ALK) fusion or a KRAS G12C mutation. If these distinct malignancies are treated with identical cytotoxic drugs, non-responding patients experience cumulative toxicity without receiving oncological benefit. Precision oncology mitigates this therapeutic mismatch by identifying driver mutations before initiating treatment (NCCN 2024).

3. How the Treatment Works — Mechanism

Biomarker-matched targeted therapy operates by specifically inhibiting dysregulated intracellular signaling pathways essential for cancer cell survival and proliferation. Rather than indiscriminately harming all dividing cells, targeted molecules bind precisely to abnormal proteins, mutant receptors, or altered enzymatic domains present in or on malignant cells (ESMO 2023).

At the cellular level, driver mutations frequently induce constitutive activation of protein kinases—enzymes that phosphorylate amino acid residues to transmit cell survival and growth signals. Small-molecule tyrosine kinase inhibitors (TKIs) occupy the adenosine triphosphate (ATP) binding pocket of these mutant kinases, halting downstream signaling cascades such as the MAPK/ERK or PI3K/AKT/mTOR pathways. Monoclonal antibodies target extracellular domains of cell-surface receptors, interrupting ligand binding or inducing antibody-dependent cellular cytotoxicity. Other biological approaches, such as immune checkpoint inhibitors, block regulatory pathways (such as PD-1/PD-L1 or CTLA-4) that tumors use to suppress host T-cell immune responses. Furthermore, synthetic lethal interventions, such as poly(ADP-ribose) polymerase (PARP) inhibitors, exploit preexisting homologous recombination repair deficiencies (such as BRCA1 or BRCA2 mutations) to cause selective double-strand DNA breakage and apoptosis in malignant cells (ASCO 2023).

4. Types and Variations

Precision oncology comprises several therapeutic modalities and testing frameworks. Clinicians determine the appropriate testing protocol and treatment platform based on tumor histology, stage, disease acuity, tissue availability, and recognized targetable alterations defined in standard practice guidelines (NCCN 2024).

Selection among these variants depends on molecular tumor board consensus, clinical trial availability, performance status, prior treatment history, and specific diagnostic findings obtained from somatic and germline genomic profiling.

5. Who the Treatment Is For — Indications

Biomarker testing and targeted therapy are indicated for patients diagnosed with advanced, recurrent, metastatic, or high-risk solid tumors and hematologic malignancies where approved targeted options exist. Indications are guided by established practice guidelines (NCCN 2024; ASCO 2023).

• Advanced or Metastatic Solid Tumors: Non-small cell lung cancer, colorectal cancer, breast cancer, cutaneous melanoma, prostate cancer, ovarian cancer, gastrointestinal stromal tumors (GIST), thyroid carcinoma, and pancreatic ductal adenocarcinoma.
• Tumor-Agnostic Indications: Malignancies harboring specific rare genomic alterations, including neurotrophic tyrosine receptor kinase (NTRK) fusions, RET fusions, high microsatellite instability (MSI-H), deficient mismatch repair (dMMR), or high tumor mutational burden (TMB-High ≥10 mutations/megabase).
• Relapsed or Refractory Hematologic Malignancies: Acute myeloid leukemia (AML) with FLT3 or IDH1/2 mutations, chronic lymphocytic leukemia (CLL) with TP53 or deletion 17p alterations, and specific subtypes of diffuse large B-cell lymphoma.
• High-Risk Early-Stage Disease: Selected early-stage cancers with specific risk-conferring markers, such as HER2-positive early breast cancer receiving adjuvant anti-HER2 targeted therapy or resected EGFR-mutant lung cancer receiving adjuvant osimertinib.

Diagnostic workup requires formal tissue acquisition via core needle biopsy, surgical excision, or validated cell-free circulating tumor DNA (ctDNA) liquid biopsy assays. Pharmacogenomic and biomarker testing should occur prior to initiating first-line systemic therapy whenever feasible, allowing clinicians to administer targeted agents in the optimal sequence (NCCN 2024).

6. Who the Treatment Is NOT For — Contraindications

Precision oncology therapies are contraindicated when specific targetable biomarkers are absent, or when a patient possesses medical conditions that render targeted agents unsafe. Administering targeted agents in the absence of an actionable alteration is medically ineffective and exposes patients to unnecessary toxicity (ASCO 2023).

Absolute Contraindications:

• Absence of the corresponding target biomarker or presence of a known primary resistance mutation (e.g., administering anti-EGFR monoclonal antibodies to patients with KRAS-mutant metastatic colorectal cancer).
• Severe allergic hypersensitivity or anaphylactic reaction to the targeted therapeutic agent or its excipients.
• Severe, uncontrolled organ dysfunction specific to agent toxicities (e.g., active, non-infectious pneumonitis prior to initiating mTOR inhibitors or anti-PD-1 immunotherapies).

Relative Contraindications and Cautionary Factors:

• Severe renal or hepatic impairment requiring significant dose adjustments or absolute drug avoidance.
• Baseline prolonged QTc interval or severe cardiac dysfunction for agents known to cause cardiotoxicity or fatal ventricular dysrhythmias (e.g., HER2-targeted agents or specific multikinase inhibitors).
• Active, unmanaged autoimmune disease when considering immune checkpoint inhibitor therapy.
• Inadequate tissue sample quality or quantity yielding uninterpretable genomic results without available liquid biopsy alternative.

7. Alternatives and Clinical Comparison

Standard cytotoxic chemotherapy and unselected systemic interventions represent the primary historical alternatives to biomarker-driven precision therapies. Clinicians evaluate alternative regimens based on disease aggressiveness, clinical urgency, availability of targetable alterations, and patient organ reserve (ESMO 2023).

When multi-gene NGS testing fails to identify actionable driver alterations, or when a patient develops acquired resistance to targeted therapies, clinicians pivot to standard systemic chemotherapy, combination chemo-immunotherapy regimens, or phase I/II clinical trials (NCCN 2024).

8. Pre-Treatment Phase

Pre-treatment clinical workup in precision oncology centers on tissue acquisition, molecular profiling, multidisciplinary case evaluation, and patient risk stratification. This pre-treatment preparation ensures accurate target identification and baseline safety verification (ASCO 2023).

The initial evaluation begins with detailed clinical history, performance status scoring (ECOG or Karnofsky scale), and anatomical disease staging using high-resolution cross-sectional imaging (CT, MRI, or PET-CT). Diagnostic tissue is reviewed by an experienced academic anatomical pathologist to confirm tumor histology and judge adequacy for molecular testing. If archived tissue is insufficient, a fresh image-guided core needle biopsy is scheduled, or a liquid biopsy using peripheral blood plasma is drawn to obtain circulating tumor DNA (ctDNA).

Tissue or plasma samples undergo comprehensive genomic profiling using multi-gene next-generation sequencing panels. Testing results are evaluated by a multidisciplinary molecular tumor board (MTB) comprising medical oncologists, clinical geneticists, molecular pathologists, bioinformaticians, and translational researchers. The MTB analyzes the clinical pathogenicity of detected variants, cross-references variant databases (such as OncoKB or CIViC), and formulates an evidence-based recommendation. Pre-treatment baseline organ function testing (complete blood count, renal and liver function panels, baseline electrocardiogram, and echocardiogram when indicated) is performed alongside formal informed consent discussing financial coverage, off-label considerations, potential incidental germline findings, and anticipated toxicity (ESMO 2023).

9. The Procedure — Step-by-Step Clinical Detail

Precision oncology workflow follows a structured, multi-step diagnostic and therapeutic sequence from initial tissue acquisition to drug administration and longitudinal monitoring (NCCN 2024).

Step 1: Tissue or Biomarker Sample Acquisition

The clinical path begins with obtaining malignant cells. An interventional radiologist performs an image-guided (CT or ultrasound) core needle biopsy, acquiring 3 to 5 tissue cores using an 18-gauge or 16-gauge biopsy needle under local anesthesia. Alternatively, a peripheral blood sample (two 10 mL specialized blood collection tubes) is drawn for cell-free ctDNA liquid biopsy if tissue biopsy is contraindicated or insufficient.

Step 2: Pathological Verification and Nucleic Acid Extraction

The tissue sample is formalin-fixed and paraffin-embedded (FFPE). A pathologist reviews hematoxylin and eosin (H&E) stained slides to verify cancer cell content, requiring at least 20% tumor nucleated content for optimal NGS yield. Nucleic acids (DNA and RNA) are extracted, quantified, and assessed for structural integrity using automated microfluidic assays.

Step 3: High-Throughput Next-Generation Sequencing (NGS)

Extracted DNA/RNA undergoes library preparation, target enrichment, and high-throughput sequencing on modern sequencing platforms. Sequence reads are aligned against the human reference genome using bioinformatic pipelines to detect single nucleotide variants (SNVs), copy number variations (CNVs), insertions/deletions (indels), and structural gene fusions.

Step 4: Molecular Tumor Board Review and Variant Classification

A specialized team reviews detected genomic alterations. Mutations are classified according to joint consensus recommendations from the Association for Molecular Pathology (AMP), ASCO, and College of American Pathologists (CAP) into Tier I (strong clinical significance), Tier II (potential clinical significance), Tier III (unknown clinical significance), or Tier IV (benign/likely benign). Actionable Tier I and II targets receive therapeutic recommendations.

Step 5: Medication Selection and Therapeutic Initiation

The patient's medical oncologist prescribes the recommended targeted agent, which may be an oral small-molecule TKI (administered daily at home) or an intravenous monoclonal antibody/ADC (administered in an outpatient infusion suite). Dosing is individualized based on body surface area, renal function, and hepatic reserve according to regulatory approved package inserts.

Step 6: Longitudinal Therapeutic Monitoring

Patients undergo continuous clinical, laboratory, and radiological surveillance. Physical examinations and toxicological lab panels occur every 2 to 4 weeks during early therapy. Re-imaging via CT or PET-CT is performed every 8 to 12 weeks to assess objective tumor response using Response Evaluation Criteria in Solid Tumors (RECIST v1.1) guidelines.

10. Immediate Post-Procedure Period

Immediate care following the diagnostic phase or commencement of targeted therapy focuses on monitoring minor biopsy recovery, managing initial drug toxicities, and establishing home administration safety protocols (ASCO 2023).

For patients undergoing image-guided biopsy, recovery involves 2 to 4 hours of post-procedure observation in a day-surgery recovery unit to monitor for immediate complications such as localized hematoma formation, internal hemorrhage, or pneumothorax (following lung biopsies). Vital signs are checked every 15 to 30 minutes, and pain at the biopsy site is managed with mild oral analgesics such as acetaminophen.

When initiating daily oral targeted agents or first-dose intravenous targeted therapies, patients are observed for immediate hypersensitivity reactions, infusion-related chills, fever, or acute gastrointestinal distress. Patients receive comprehensive education regarding specific administration requirements (such as taking oral TKIs with or without food, managing drug-drug interactions with cytochrome P450 inhibitors, and avoiding grapefruit products). Emergency contact procedures and symptom logs are provided to track early adverse effects during the first 14 days of home therapy.

11. Recovery — Short and Long Term

Recovery timeline in precision oncology differs fundamentally from surgical or standard cytotoxic treatment recovery. Because many targeted agents are taken continuously as long-term daily oral medications, recovery refers to maintaining functional quality of life and managing chronic low-grade toxicities (ESMO 2023).

Most patients receiving oral targeted therapies or modern immunotherapies maintain normal daily activities, return to regular workplace duties, and engage in moderate aerobic physical activity. Intimacy and travel are generally permissible provided patient blood counts remain stable and acute toxicities are well-managed under medical guidance (NCCN 2024).

12. Risks, Side Effects, and Complications

Adverse events associated with precision oncology differ markedly from standard cytotoxic chemotherapy. While targeted therapies generally spare non-cancer tissues, target expression in healthy organs or off-target cross-reactivity causes distinct toxicological profiles (ASCO 2023).

A major long-term challenge in precision oncology is acquired therapeutic resistance. Tumor cells under selective pressure from targeted inhibitors frequently acquire secondary mutations (such as the EGFR T790M or C797S mutations, or ALK resistance mutations) or activate bypass signaling pathways (such as MET amplification). Patients and clinicians must monitor for warning signs of progressive disease or severe toxicity, including worsening shortness of breath, severe intractable diarrhea, chest pain, jaundice, or rapid neurological decline, which warrant emergency clinical evaluation (NCCN 2024).

13. Lifestyle and Behavioural Considerations

Lifestyle factors can influence drug metabolism, overall treatment tolerance, and therapeutic efficacy during precision oncology regimens. Patients should adopt evidence-based supportive habits while avoiding interactions that impair targeted drug activity (ASCO 2023).

Nutritional and supplement management is vital during targeted oral therapy. Many small-molecule TKIs are heavily metabolized by hepatic cytochrome P450 3A4 (CYP3A4) enzymes. Patients must avoid consuming grapefruit, Seville oranges, and over-the-counter herbal supplements such as St. John’s Wort, which significantly alter drug plasma concentrations, causing severe toxicity or subtherapeutic therapeutic levels. Alcohol consumption should be minimized or eliminated to prevent additive hepatotoxicity during oral TKI therapy.

Regular moderate physical activity, including light walking or resistance exercises, is encouraged by clinical guidelines to mitigate therapy-related fatigue and maintain functional muscle mass. Thorough skin care—including daily application of alcohol-free moisturizers, broad-spectrum UVA/UVB sunscreen (SPF 30+), and avoiding scalding hot bath water—is recommended to mitigate targeted epidermal growth factor pathway skin toxicities (ESMO 2023).

14. How Outcomes Are Measured

Treatment success in precision oncology is evaluated using standardized clinical endpoints, molecular biomarkers, and patient-reported outcomes rather than visual inspection alone (NCCN 2024).

Clinical efficacy is primarily assessed using Response Evaluation Criteria in Solid Tumors (RECIST v1.1) on cross-sectional CT or MRI imaging. Outcomes are categorized into four standardized states: Complete Response (CR, disappearance of all target lesions), Partial Response (PR, at least a 30% decrease in the sum of target lesion diameters), Stable Disease (SD, insufficient shrinkage to qualify for PR nor sufficient growth to qualify for progressive disease), and Progressive Disease (PD, at least a 20% increase in the sum of target lesion diameters or appearance of new lesions).

In addition to anatomical restaging, outcome evaluation tracks key statistical endpoints: Progression-Free Survival (PFS), Overall Survival (OS), Duration of Response (DoR), and Objective Response Rate (ORR). Longitudinal monitoring of cell-free circulating tumor DNA (ctDNA) dynamics—known as molecular residual disease (MRD) assessment—is increasingly utilized to detect therapeutic response or clearance of tumor DNA weeks to months before radiological changes become visible on cross-sectional scans (ASCO 2023).

15. Recent Advances and Current Standard of Care

The standard of care in precision oncology has advanced rapidly over the past decade, shifting from single-gene testing (such as individual PCR assays for EGFR or KRAS) to comprehensive multi-gene NGS panels, liquid biopsies, and novel targeted drug platforms (ASCO 2023; ESMO 2023).

Major evolutionary advances include:

• Tumor-Agnostic Drug Approvals: Regulatory approvals based entirely on molecular biomarkers regardless of tissue origin, such as tissue-agnostic approvals for NTRK fusions (larotrectinib, entrectinib), RET fusions (selpercatinib), and MSI-H/dMMR solid tumors (pembrolizumab).
• Antibody-Drug Conjugates (ADCs): Development of sophisticated payload-delivering molecules, such as trastuzumab deruxtecan (T-DXd), which target specific surface receptors (HER2) and release potent cytotoxic payloads directly inside tumor cells, demonstrating efficacy even in HER2-low malignancies.
• Circulating Tumor DNA (ctDNA) Liquid Biopsies: Non-invasive real-time profiling of single or multi-gene resistance mutations and molecular residual disease (MRD) detection without requiring invasive tissue re-biopsies.
• KRAS Inhibition: Overcoming previously untargetable oncogenic drivers with direct KRAS G12C covalent inhibitors (sotorasib, adagrasib) in non-small cell lung cancer and colorectal cancer.

Active research focuses on developing bispecific antibodies, neoantigen-targeted cancer vaccines, tertiary resistance bypass inhibitors, and artificial intelligence models designed to predict structural protein mutations and therapy response trajectories (NCCN 2024).

16. Common Myths and Misconceptions

Myth: Precision oncology guarantees a cure for all advanced cancer patients.
Reality: While precision oncology significantly improves response rates and extends progression-free survival, most targeted therapies in advanced stage disease control cancer rather than eradicate it permanently, as tumors eventually develop resistance mutations (ASCO 2023).

Myth: Targeted therapy and personalized medicine are identical to gentle, non-toxic holistic natural treatments.
Reality: Precision oncology uses potent synthetic pharmaceutical agents, biological immunotherapies, and engineered antibodies that carry distinct organ toxicities, including severe rash, pneumonitis, hypertension, and colitis (ESMO 2023).

Myth: A standard liquid biopsy blood test eliminates the need for tissue biopsies in all patients.
Reality: Although liquid biopsy is highly specific and convenient, it suffers from false-negative rates when tumors shed low levels of DNA; diagnostic tissue biopsy remains the gold standard for initial histological classification (NCCN 2024).

Myth: Every single cancer patient has an actionable genetic mutation that can be matched to an FDA-approved drug.
Reality: Broad clinical trials, such as NCI-MATCH, show that actionable target mutations are currently identified in approximately 20% to 40% of tested solid tumor patients, depending on cancer subtype and disease stage (Flaherty et al., JCO, 2020).

Myth: Precision oncology therapies are only available for rare or exotic cancers.
Reality: Biomarker-driven precision therapy is now standard first-line care for widespread common malignancies, including non-small cell lung cancer, breast cancer, colorectal cancer, melanoma, and prostate cancer (NCCN 2024).

Myth: If a targeted drug works for a patient's genetic mutation, it will keep working indefinitely.
Reality: Malignant cells undergo clonal evolution under therapeutic pressure, eventually developing secondary resistance alterations that require treatment adjustment or drug rotation (ASCO 2023).

17. Frequently Asked Questions

What is the primary difference between chemotherapy and precision oncology?

Traditional cytotoxic chemotherapy acts broadly by damaging all rapidly dividing cells throughout the human body, causing widespread off-target side effects like hair loss and severe blood count drops. Precision oncology specifically identifies and targets unique genetic alterations or abnormal proteins exclusive to cancer cells, aiming to block cancer growth with reduced non-specific systemic toxicity (ASCO 2023).

How is genetic testing for precision oncology performed?

Genetic testing requires analyzing nucleic acids extracted from tissue obtained during a standard biopsy or surgical resection. Alternatively, liquid biopsy assays utilize a peripheral blood draw to isolate cell-free circulating tumor DNA (ctDNA). These samples undergo high-throughput next-generation sequencing in an accredited molecular diagnostic laboratory to detect somatic driver alterations (NCCN 2024).

How long does it take to get genomic testing results back?

Turnaround time for comprehensive next-generation sequencing assays typically ranges from 10 to 21 business days after the pathology laboratory receives acceptable tissue or blood samples. In urgent clinical scenarios, liquid biopsy or rapid single-gene assays (such as rapid PCR) can provide actionable driver gene results within 3 to 7 days (ESMO 2023).

What is a molecular tumor board?

A molecular tumor board is an expert multidisciplinary clinical committee consisting of medical oncologists, clinical geneticists, molecular pathologists, bioinformaticians, and oncology pharmacists. The team reviews a patient's complex genomic sequencing results alongside clinical history to recommend individualized, evidence-based targeted therapies or novel clinical trial options (ASCO 2023).

Is genomic testing done on my healthy cells or my cancer cells?

Precision oncology primarily performs somatic profiling, which analyzes the mutated DNA of the cancer cells themselves. However, germline testing on healthy host cells (such as white blood cells or saliva) is also conducted when evaluating hereditary cancer syndromes, such as inherited BRCA1/2 or Lynch syndrome mutations (NCCN 2024).

What happens if genomic testing finds no actionable mutations?

If genomic sequencing does not detect a targetable driver alteration, your medical oncologist will recommend established standard-of-care treatments, such as combination cytotoxic chemotherapy, broad-spectrum immunotherapies, radiotherapy, or enrollment in clinical trials investigating novel non-biomarker therapeutic strategies (ESMO 2023).

Are targeted therapies taken as pills or intravenous infusions?

Targeted oncology therapies encompass both administration forms. Many small-molecule kinase inhibitors are oral daily pills taken conveniently at home. Monoclonal antibodies, immune checkpoint inhibitors, and antibody-drug conjugates are delivered as periodic intravenous infusions in an outpatient infusion clinic (ASCO 2023).

What is liquid biopsy and when is it used?

Liquid biopsy is a non-invasive blood test that analyzes fragments of circulating tumor DNA (ctDNA) shed by malignant cells into the bloodstream. It is used when tissue biopsies are unsafe, when archived tissue is insufficient, or to monitor emerging drug resistance mutations in real time during ongoing therapy (NCCN 2024).

Can target therapies stop working over time?

Yes. Malignant cells often acquire secondary resistance mutations or activate alternative survival pathways after months or years of targeted therapy pressure. When disease progression occurs, repeat tissue or liquid biopsies are performed to identify new resistance mechanisms and select next-generation targeted drugs (ASCO 2023).

What are tumor-agnostic therapies?

Tumor-agnostic therapies are molecular treatments approved to treat any solid cancer, regardless of the anatomical organ site where it originated, as long as the tumor harbors a specific genetic alteration, such as an NTRK gene fusion or microsatellite instability (dMMR/MSI-H) (ESMO 2023).

Do targeted therapies cause hair loss?

Complete hair loss (alopecia) is far less common with targeted therapies than with conventional cytotoxic chemotherapy. However, specific targeted drugs may cause mild hair thinning, changes in hair texture or color, or dermatologic side effects such as skin rashes and nail changes (ASCO 2023).

How do doctors monitor whether a targeted treatment is working?

Oncologists monitor treatment response using periodic CT, PET-CT, or MRI scans scored according to standardized criteria (RECIST 1.1), alongside routine clinical examinations, routine organ function blood panels, serum tumor markers, and serial liquid biopsy measurements of ctDNA levels (NCCN 2024).

Can I participate in clinical trials through precision oncology?

Yes. Comprehensive genomic profiling frequently identifies rare genetic alterations that qualify patients for targeted clinical trials, including umbrella trials testing multiple targeted drugs in one cancer type, or basket trials testing one targeted drug across many different cancer types (ESMO 2023).