Cancer Therapies
Traditional cancer treatments target cancer cells through different mechanisms, and understanding how each one works at the cellular level connects directly to what you've learned about cell cycle regulation. These therapies can be used alone or in combination, depending on the type and stage of cancer.
Types of cancer therapies
Surgery physically removes cancerous tissue or tumors from the body. If the cancer is localized and the surgeon can remove it entirely, surgery alone can be curative. It's often combined with radiation or chemotherapy to catch any remaining cancer cells that weren't visible during the procedure.
Radiation therapy uses high-energy radiation to damage the DNA of cancer cells, preventing them from dividing. It can be delivered externally (a beam aimed at the tumor from outside the body) or internally through brachytherapy, where a radioactive source is placed directly inside or next to the tumor. Because radiation can't perfectly distinguish cancer cells from normal cells, side effects like skin irritation and fatigue occur when nearby healthy tissues absorb radiation too.
Chemotherapy uses cytotoxic drugs that kill rapidly dividing cells. This connects to a key principle from cell cycle biology: cancer cells divide more frequently than most normal cells, making them more vulnerable to drugs that disrupt division. However, healthy cells that also divide quickly (hair follicles, gut lining, bone marrow) get caught in the crossfire, which explains common side effects like hair loss, nausea, and immune suppression.
Chemo drugs work through different mechanisms:
- Alkylating agents (e.g., cisplatin) crosslink DNA strands, preventing replication
- Antimetabolites (e.g., methotrexate) mimic normal metabolites and block DNA synthesis
- Plant alkaloids (e.g., vincristine) disrupt the mitotic spindle, arresting cells in mitosis
- Antitumor antibiotics (e.g., doxorubicin) intercalate into DNA or inhibit topoisomerase, blocking replication
Targeted Cancer Treatments and Personalized Medicine
Principles of targeted treatments
Unlike chemotherapy, which broadly attacks dividing cells, targeted therapies zero in on specific molecules that cancer cells depend on for growth and survival. This makes them more selective and generally causes fewer side effects.
Small molecule inhibitors are drugs small enough to enter cells and block the activity of specific proteins driving cancer growth:
- Tyrosine kinase inhibitors like imatinib block the BCR-ABL fusion protein in chronic myelogenous leukemia (CML). BCR-ABL is a constitutively active kinase that drives uncontrolled proliferation, so blocking it shuts down the growth signal.
- PARP inhibitors like olaparib prevent cancer cells from repairing DNA damage. This is especially effective in ovarian and breast cancers with BRCA1/2 mutations, because those cells already have defective homologous recombination repair. Blocking PARP removes their backup repair pathway, a strategy called synthetic lethality.
Monoclonal antibodies are engineered antibodies that bind specific antigens on cancer cell surfaces:
- Trastuzumab targets the HER2 receptor, which is overexpressed in some breast cancers. By binding HER2, it blocks growth signaling and flags the cell for immune destruction.
- Bevacizumab targets VEGF (vascular endothelial growth factor), cutting off the blood supply tumors need to grow. This is used in colorectal cancer and other solid tumors.
Personalized medicine for cancer
Personalized medicine tailors treatment to an individual patient's genetic profile and tumor characteristics rather than using a one-size-fits-all approach.
The process starts with molecular profiling of the tumor to identify specific mutations or biomarkers. For example, testing for EGFR mutations in lung cancer or KRAS mutations in colorectal cancer determines whether certain targeted therapies will work. A patient whose tumor has an EGFR-activating mutation may respond well to EGFR inhibitors, while a patient with a KRAS mutation typically won't respond to anti-EGFR antibodies.
The potential benefits are significant: patients receive therapies more likely to work for their specific cancer, side effects decrease because ineffective treatments are avoided, and healthcare resources are used more efficiently.
Challenges in cancer treatment
Even with these advances, several major obstacles remain:
- Drug resistance is one of the biggest problems. Cancer cells can acquire new mutations or activate alternative signaling pathways that bypass the drug's target. For example, a tumor initially sensitive to imatinib may develop a secondary mutation in BCR-ABL that prevents the drug from binding.
- Tumor heterogeneity means that different cells within the same tumor carry different mutations. A drug might kill 99% of cells but leave a resistant subpopulation that repopulates the tumor.
- Side effects still occur because targeted therapies aren't perfectly specific. Normal cells that express the same target molecule can be affected, limiting how much drug a patient can tolerate.
- Metastatic disease remains difficult to treat because cancer that has spread to multiple organs is harder to reach and often more genetically diverse.
To address these challenges, several novel approaches are being developed:
- Immunotherapies like checkpoint inhibitors (e.g., pembrolizumab, which blocks PD-1) release the brakes on the immune system so T cells can recognize and attack cancer cells. CAR T-cell therapy engineers a patient's own T cells to target specific tumor antigens.
- Combination therapies target multiple pathways at once to reduce the chance of resistance. For example, combining BRAF and MEK inhibitors in melanoma blocks two steps in the same signaling cascade.
- Nanoparticle-based drug delivery systems encapsulate drugs in nanoparticles that accumulate preferentially in tumors, improving specificity and reducing toxicity to healthy tissues.
- Epigenetic therapies target chromatin modifications rather than DNA mutations. Histone deacetylase (HDAC) inhibitors, for instance, can reactivate silenced tumor suppressor genes by restoring open chromatin structure.