Cancer: How Normal Cells Turn Malignant

The Rules Normal Cells Obey

By Akanksha Kumari · Science faculty, The Cavalier · B.Tech, 15 years teaching Science

Every cell in your body descends from one fertilised egg, and every one is on a leash. The sequence in which a cell duplicates its genome, makes what it needs and divides into two daughter cells is the cell cycle. A typical human cell completes it in about 24 hours, yet division itself takes only about an hour. More than 95% of the cycle is interphase, the "resting" phase of growth and preparation.

Mitosis is equational division: the daughters get the same chromosome number as the parent. Meiosis, which halves the number, is for gametes only (CDS 2026-II tested this contrast).

Checkpoints act like inspectors on an assembly line. At each one, proteins check whether the DNA is intact and whether the cell has the signals to divide. A faulty cell is repaired or told to die by apoptosis, programmed cell death. Normal cells also show contact inhibition: a dividing cell that touches its neighbours stops. Cancer is what happens when these controls fail together. The cell ignores the brakes and the order to die, and its daughters inherit the fault.

Benign, Malignant and the Spread

Cells that keep dividing form a lump called a tumour (neoplasm). Not every tumour is cancer.

A malignant tumour invades healthy tissue and starves normal cells by competing for nutrients; it also recruits its own blood vessels (angiogenesis). Most dangerous of all, shed cells reach distant sites through blood and lymph and start new tumours wherever they lodge. This is metastasis, the most feared property of cancer and the reason early detection saves lives.

Doctors name cancers by the tissue they begin in:

What Triggers It: Carcinogens and Cancer Genes

Any agent that can turn a normal cell into a cancer cell is a carcinogen. The common thread is damage to DNA: most carcinogens are also mutagens.

Peyton Rous first showed in 1911 that a virus could cause a sarcoma in chickens (Nobel Prize, 1966). Harald zur Hausen shared the 2008 Nobel Prize in Physiology or Medicine for showing that HPV causes cervical cancer, which led to the vaccine.

The real story is in the genes. Two families of genes control division:

• Proto-oncogenes are the accelerator. They are normal genes that push cells to divide when needed. A mutation or virus can switch one permanently "on", making it an oncogene; one faulty copy is enough. Examples: RAS, HER2 (breast cancer) and BCR-ABL (chronic myeloid leukaemia). Bishop and Varmus won the 1989 Nobel Prize for showing that viral oncogenes are hijacked normal genes.
• Tumour suppressor genes are the brakes. They halt the cycle or order a damaged cell to die, and cause cancer when lost (usually both copies must fail). The best known is TP53, the "guardian of the genome", damaged in about half of all human cancers. Others: RB1 (retinoblastoma, a childhood eye cancer) and BRCA1 and BRCA2 (inherited breast and ovarian cancer risk).

One mutation is rarely enough. Several hits accumulate over years, which is why risk climbs with age and why cervical cancer appears ten to twenty years after HPV infection.

Finding Cancer: Biopsy, Scans and Markers

Early detection is the biggest lever in cancer survival. The standard methods:

• Biopsy and histopathology. A piece of suspected tissue is cut into thin sections, stained and examined under a microscope: the gold standard, since only a biopsy confirms that a lump is malignant. Leukaemia is found by blood and bone-marrow tests.
• Imaging. X-ray and mammography; CT (X-rays building a three-dimensional image); MRI (strong magnetic fields, non-ionising, good for soft tissue); PET (a radioactive sugar tracer that tumours absorb greedily). The Pap smear screens the cervix.
• Tumour markers. Blood proteins such as PSA (prostate), CA-125 (ovary) and AFP (liver) help to track a cancer, but never prove it alone.

Over 1.86 lakh Ayushman Arogya Mandirs screen people above 30 for oral, breast and cervical cancer.

Treatment: From the Scalpel to CAR-T

Most patients get a combination of three classical treatments: surgery, radiation therapy and chemotherapy. Newer ones target the cancer's own biology or turn the patient's immune system against it.

Radiotherapy works because ionising radiation breaks DNA; our radioactivity and nuclear energy page covers the isotopes.

Checkpoint inhibitors earned James Allison and Tasuku Honjo the 2018 Nobel Prize in Physiology or Medicine. T cells carry "off switches" such as PD-1, which some tumours press to hide. These antibody drugs release the brake. Nivolumab and pembrolizumab are on the list of 137 medicines under the margin cap.

CAR-T therapy goes further. Doctors collect the patient's T cells, engineer them in the laboratory to carry a chimeric antigen receptor that recognises a protein on the cancer cell (CD19, in B-cell leukaemias and lymphomas), multiply them and return them as a "living drug". In October 2023 the CDSCO approved NexCAR19, India's first indigenous CAR-T therapy, developed by ImmunoACT, a company incubated at IIT Bombay, with clinical work at Tata Memorial, for relapsed or resistant B-cell leukaemia and lymphoma.

Prevention and Cost: HPV Vaccine and the Margin Cap

The best cancer is the one that never starts, and two cancers have a vaccine against their cause: the hepatitis B vaccine (liver cancer) and the HPV vaccine (cervical cancer). HPV types 16 and 18 cause about 70% of cervical cancers. India's National HPV Vaccination Campaign, launched on 28 February 2026, gives free single-dose vaccination to about 1.15 crore girls aged 14, and over 80 lakh doses had been given by 11 September. The vaccine is preventive and does nothing for an existing cancer. See our campaign explainer and the immunity and vaccination page.

The third lever is cost. The gap between a manufacturer's price to the distributor and the MRP a patient pays is the trade margin. From the PIB backgrounder:

Know the difference between the two kinds of drug. A scheduled drug, on the National List of Essential Medicines (NLEM 2022: 384 medicines), has a government-fixed ceiling price. A non-scheduled drug is only monitored, and its MRP may rise by no more than 10% in twelve months. The margin cap is a third tool that trims the margin without fixing the price. Our earlier explainer covers the legal route. Ayushman Bharat PM-JAY adds cashless cover of ₹5 lakh per family per year, including oncology.

How UPSC Has Asked It: Past Papers Solved

Cancer questions are seldom stand-alone: UPSC tests the idea inside questions on mitosis, radiation and X-rays, and the latest paper combined a gene, a virus and spread.

Practice MCQs (with answers)

1. In which phase of the cell cycle is DNA replicated?
   1. G1 phase
   2. S phase
   3. G2 phase
   4. M phase
2. Normal cells stop dividing when they touch their neighbours. This property, which cancer cells lose, is called
   1. metastasis
   2. angiogenesis
   3. contact inhibition
   4. apoptosis
3. A cancer that begins in bone or muscle is called a
   1. sarcoma
   2. carcinoma
   3. lymphoma
   4. leukaemia
4. Which of the following is a bacterium linked to stomach cancer?
   1. Vibrio cholerae
   2. Salmonella typhi
   3. Mycobacterium tuberculosis
   4. Helicobacter pylori
5. A gene that normally halts the cell cycle or orders a damaged cell to die, and whose loss promotes cancer, is a
   1. tumour suppressor gene
   2. proto-oncogene
   3. viral oncogene
   4. mitochondrial gene
6. Which of these is NOT a feature of a malignant tumour?
   1. Rapid growth
   2. Invasion of neighbouring tissue
   3. Staying confined to the original site
   4. Spread to distant organs
7. In CAR-T therapy, the cells taken from the patient and genetically modified are
   1. red blood cells
   2. platelets
   3. bone cells
   4. T cells
8. Chemotherapy causes hair loss mainly because
   1. it destroys all the cells of the body equally
   2. it damages rapidly dividing cells, including those of hair follicles
   3. it releases radiation
   4. it changes the colour of hair pigment

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