Oncology & Cancer Drugs
How cancer is treated: chemotherapy, targeted and immune therapy, hormone therapy, supportive care — and the drugs behind the major solid tumours.
Principles
How cancer drugs work, and the toxicity and dosing rules that govern them.
Cytotoxic Chemotherapy
The classic families — alkylators, antimetabolites, anthracyclines, microtubule agents.
Targeted Therapy
Kinase inhibitors, monoclonal antibodies, and the biomarkers that guide them.
Immunotherapy
Releasing the immune brakes — checkpoint inhibitors and engineered CAR-T cells.
Hormone Therapy
Starving hormone-driven cancers — breast and prostate endocrine therapy.
Supportive Care & Safety
Managing the fallout — nausea, neutropenia, emergencies, pain, and safe handling.
Cancers by Organ
Assembling the drugs disease by disease — lung, breast, colorectal, prostate and more.
How Cancer Drugs Work: The Cell Cycle, Log-Kill and Why We Combine Them
Cancer is one idea gone wrong: a cell that divides when it should not, and refuses to die. Almost every classical cancer drug is a counter-move to that single idea — it attacks cells while they divide. But that strategy carries three hard truths with it: each dose kills a fraction, not a number; one drug is rarely enough; and the poison cannot tell a tumour cell from your gut lining. Understand those three and the whole rhythm of chemotherapy — the cycles, the combinations, the toxicities — stops looking like a mystery and starts looking like arithmetic.
Chemotherapy Toxicity and Dosing: The Narrow Line Between Help and Harm
Cytotoxic chemotherapy has no address of its own. It kills what divides fast — and cancer is not the only thing dividing fast inside you. The same drug that shrinks a tumour also strips the bone marrow, the gut lining, the hair, the gonads. So the whole craft of oncology is a balancing act on a very narrow ledge: enough to hurt the cancer, not so much that you kill the patient. Learn the predictable toxicities, the nadir, and the maths behind mg/m² and AUC, and chemo stops being frightening and becomes something you can anticipate.
Alkylating Agents and Platinum Drugs: Cross-Linking the DNA
These are the oldest and most brutal of the cytotoxics — drugs that don't wait for a cell to divide but attack its DNA directly, gluing the two strands together so it can never copy them again. But the same reactivity that kills the tumour scars the bladder, poisons the kidney, deafens the ear, and — years later — can seed a second cancer. To use them safely you have to give the antidote alongside the poison. This chapter is the story of that bargain.
Antimetabolites: Fake Building Blocks That Jam DNA Synthesis
A dividing cell must copy its DNA, and to do that it needs a steady supply of nucleotide building blocks. Antimetabolites are counterfeit blocks — molecules so similar to the real thing that the cell either uses them and chokes, or the enzymes that make the real ones get blocked. The trick is that this hits fast-copying cells hardest — including the cancer. Master how these fakes work and you understand the S-phase, the folinic-acid rescue that saves the patient, and why one missing enzyme can turn a routine dose into a lethal one.
Anthracyclines and Topoisomerase Inhibitors: DNA-Cutting Drugs and the Heart
These drugs work by cutting DNA — jamming the enzymes that untangle the double helix and littering the genome with breaks the cancer cell cannot survive. They are among our most powerful and most-used cytotoxics. But the same knife that cures a lymphoma can, dose by dose, weaken a heart or scar a lung. This chapter is about the double edge: how anthracyclines and topoisomerase poisons kill tumours, and the signature late toxicities you must count from the very first dose.
