In the previous article, we outlined the relationship between genes and cancer. Here, we review the mainstream cancer treatments to date and explain how genomic data is now being applied to deliver precision medicine.
Bryant Chen, Medical Affairs Manager, BE Capital

Current Treatment Modalities
Cancer treatment plans depend on disease status—cancer type, stage, recurrence, and tumor biology. Broadly, therapies are either systemic (affecting the whole body) or local/region-specific (targeting a lesion or body part). Below are seven commonly used modalities:
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Surgery:
Excision of tumor tissue. Most patients undergo surgery first, followed by adjuvant therapies to complete a treatment course. -
Chemotherapy:
Cytotoxic drugs that inhibit proliferation or induce apoptosis of cancer cells. Because most agents are non-selective, they circulate systemically and also affect normal cells—hence common adverse effects such as alopecia and nausea. -
Radiotherapy:
High-dose ionizing radiation damages tumor DNA to halt division and trigger death. Typically delivered locally over days to weeks to minimize injury to surrounding normal tissues. -
Hormone Therapy:
For hormone-dependent tumors (e.g., breast, ovarian, prostate), drugs block hormone–receptor signaling to suppress growth. Use depends on tumor receptor status. -
Hematopoietic Stem Cell Transplantation (HSCT):
High-dose chemo/irradiation eradicates malignant cells and suppresses immunity, followed by infusion of healthy stem cells to reconstitute hematopoiesis and immune function—primarily for hematologic malignancies (leukemia, lymphoma, multiple myeloma).
The above five are indirect approaches (not genetically selective). The next two leverage genomic data to directly target tumor-specific alterations, aiming to raise efficacy and reduce toxicity.
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Targeted Therapy:
Drugs designed to act on cancers harboring specific genetic alterations, blocking or modulating oncogenic signaling while sparing normal cells—hence typically fewer side effects than chemotherapy. -
Immunotherapy:
Although malignant cells display abnormal molecules, tumors may evade immune attack by exploiting immune checkpoints and microenvironmental mechanisms. Checkpoint inhibitors release these brakes so the immune system can recognize and destroy cancer.
Targeted Therapy Makes Care “Precise”
Decades of research show carcinogenesis is driven by accumulated genetic alterations. Targeting the driver mutation can markedly improve outcomes. In lung adenocarcinoma, a high-incidence cancer in Taiwan, common drivers and Taiwan-approved therapies include:
| Gene | Variant Frequency | Approved Targeted Agents (Taiwan) |
|---|---|---|
| EGFR (epidermal growth factor receptor) | 55% | Gefitinib (Iressa), Erlotinib (Tarceva), Afatinib (Gilotrif), Osimertinib (Tagrisso) |
| ALK (anaplastic lymphoma kinase) | 5% | Crizotinib (Xalkori), Ceritinib (Zykadia), Alectinib (Alecensa) |
| KRAS (Kirsten rat sarcoma viral oncogene homolog) | 5% | — |
| MET (MET tyrosine kinase receptor) | 2–3% | Tepotinib (Tepmetko) |
| ROS1 (ROS tyrosine kinase receptor) | 1–2% | Crizotinib (Xalkori) |
| BRAF (B-Raf serine/threonine kinase) | <1% | Dabrafenib (Tafinlar), Trametinib (Mekinist) |
| NTRK (neurotrophic tyrosine kinase receptor) | <1% | Entrectinib (Rozlytrek) |
Note: Table lists selected, commonly tested genes in lung adenocarcinoma and agents approved in Taiwan.
Genomic landscapes differ between cancer types, among patients with the same cancer, and even across ethnicities (e.g., EGFR mutations are more prevalent in East Asian lung adenocarcinoma, whereas KRAS predominates in Western cohorts). Hence, high-level treatment strategies must be personalized.
A New Milestone: Immunotherapy
When pathogens or cancer cells arise, immunity should eliminate them. Tumors, however, up-regulate immune checkpoints to masquerade as “self,” dampening immune activation. Checkpoint blockade either inhibits tumor immune-escape signals or augments antitumor immunity.
In Taiwan, four checkpoint inhibitors are widely used across indications (e.g., melanoma, lung, urothelial, gastric, colorectal, head & neck), improving 5-year overall survival and progression-free survival:
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Ipilimumab (Yervoy, anti-CTLA-4)
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Nivolumab (Opdivo, anti-PD-1)
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Pembrolizumab (Keytruda, anti-PD-1)
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Atezolizumab (Tecentriq, anti-PD-L1)
Not all patients benefit. Biomarkers such as high checkpoint expression, microsatellite instability (MSI-H), and high tumor mutational burden (TMB-H) enrich for response. Practical care requires composite assessment and rational combinations to maximize benefit.
Closing
We have seen how genomics enables precision in cancer therapy—via targeted agents and immuno-oncology. In the next article, we will discuss how genomic data integrates with Artificial Intelligence to further transform oncology.
For more information, please contact:Bryant.chen@be.tworg.app









