Cancer Glossary

A phenomenon where treating one tumour causes other untreated tumours elsewhere in the body to shrink. Believed to be mediated by the immune system. Being studied in relation to histotripsy and other local therapies.

A key metabolic molecule produced when cells burn fatty acids (fatty acid oxidation). In cancer, acetyl-CoA is used to chemically modify histones (DNA packaging proteins), directly linking fat metabolism to gene regulation.

A type of cancer that starts in the cells that line or cover internal organs. It is one of the most common types and can occur in the breast, lung, colon, prostate, and other organs.

A benign, precancerous tumour arising from epithelial tissue. Adenomas are non-invasive — cells pile up abnormally but remain at the primary site and do not breach the basement membrane. They can often be removed (e.g. colon polyps detected and removed during colonoscopy). However, adenomas can progress into malignant carcinomas through the accumulation of additional mutations.

Additional treatment given after the main treatment (usually surgery) to lower the risk of cancer coming back. This can include chemotherapy, radiation, or hormone therapy.

A potent liver carcinogen produced by the fungus Aspergillus flavus, found in corn, peanuts, and fermented soy products. Combined with HBV infection, it synergistically increases hepatocellular carcinoma risk up to 60-fold. Reduction in dietary aflatoxin exposure correlates with lower rates of HCC.

A class of chemotherapy drug that adds alkyl groups to DNA, forming crosslinks that block DNA replication and transcription, triggering cell death. Examples: cyclophosphamide, cisplatin, carboplatin, oxaliplatin. Platinum-based drugs are the backbone of many regimens (ovarian, lung, testicular, colorectal cancer).

A recombination-based mechanism used by ~10–15% of cancers to maintain telomere length without telomerase. Common in certain sarcomas, glioblastoma, and other cancers.

A rapid bacterial assay developed by Bruce Ames to test whether a chemical is a mutagen (and therefore likely carcinogen). Histidine-deficient bacteria are exposed to the potential mutagen; if colonies grow on histidine-free plates, the chemical caused reversion mutations. Established the critical link between mutagenesis and carcinogenesis.

Loss of differentiation in a tumour — the degree to which cancer cells have lost their resemblance to normal cells. Anaplastic cells show pleomorphism (abnormal variation in size and shape), atypical mitoses, and loss of normal tissue organisation. Anaplasia is a hallmark of malignant transformation and generally indicates a more aggressive tumour.

The standard first-line treatment for androgen-dependent prostate cancer. Approaches include surgical castration, LHRH agonists (suppressing testosterone), androgen antagonists (blocking DHT from binding the receptor), and 5α-reductase inhibitors (blocking conversion of testosterone to the more potent DHT). Most men develop resistance (castration-resistant prostate cancer, CRPC) within 2–3 years.

An abnormal number of chromosomes in a cell — too many or too few. A hallmark of cancer cells, aneuploidy results from defects in chromosome segregation during mitosis. Cancer cells often have highly abnormal karyotypes with extra chromosomes, deletions, and translocations.

The formation of new blood vessels. Tumours trigger angiogenesis by releasing VEGF (vascular endothelial growth factor) when they reach a critical size (~0.2mm) and require more oxygen and nutrients. High blood vessel density (microvessel density) in a tumour is associated with worse outcomes. Anti-angiogenic drugs (e.g. bevacizumab targeting VEGF) are used in cancer treatment.

A targeted therapy combining a monoclonal antibody with a potent cytotoxic drug (chemotherapy payload) linked by a chemical linker. The antibody delivers the drug selectively to cancer cells that express the target protein, sparing normal cells. Examples: trastuzumab emtansine (T-DM1) and trastuzumab deruxtecan (T-DXd) for HER2+ breast and gastric cancer.

Adenomatous polyposis coli — a key tumour suppressor gene mutated in >80% of colorectal cancers. APC is a negative regulator of β-catenin in the Wnt signalling pathway. Germline APC mutations cause Familial Adenomatous Polyposis (FAP), leading to thousands of colon polyps and near-certain colon cancer.

Programmed cell death — an orderly process by which the body destroys damaged or unwanted cells. Many cancer treatments work by triggering apoptosis in cancer cells. Cancer cells often develop ways to evade apoptosis.

A class of drugs that block the aromatase enzyme, which converts androgens into oestrogen in fat tissue and the adrenal glands. Used to treat hormone receptor-positive (ER+) breast cancer, particularly in postmenopausal women. Examples include letrozole, anastrozole, and exemestane.

Two master kinases of the DNA damage response. ATM is activated by DNA double-strand breaks; ATR is activated by stalled replication forks. Both phosphorylate downstream targets including p53 and BRCA1, triggering cell cycle arrest and DNA repair. ATM/ATR inhibitors are being developed for cancer therapy.

A form of targeted radionuclide therapy exploiting Auger electrons — very short-range particles that deposit intense ionising energy within nanometers of DNA when the radionuclide is internalised close to the cell nucleus, causing highly efficient DNA double-strand breaks. Terbium-161 (161Tb) is the leading Auger electron emitter in cancer theranostics, demonstrating greater therapeutic efficacy than lutetium-177 (177Lu) in preclinical and early clinical studies targeting PSMA and SSTR2.

A cellular "self-eating" process where cells degrade and recycle damaged organelles and proteins via lysosomes. Has a complex, context-dependent role in cancer: it can act as a tumour suppressor or promote cancer cell survival under stress. Autophagy inhibitors (e.g. hydroxychloroquine) are being tested in combination with chemotherapy.

Cancer affecting people typically aged 15–39, which presents unique clinical and psychosocial challenges distinct from both paediatric and older adult oncology. In Singapore, cancer cases among people under 50 increased by 90% between 1988–1992 and 2018–2022. AYA challenges include: fertility preservation, career disruption, care of dependent young children, life-milestone grief (marriage, parenthood), age-related isolation in standard support groups, and long survivorship years. AYAs often have early symptoms dismissed because cancer is incorrectly seen as an older person's disease — do not ignore persistent symptoms regardless of age. Specialised AYA support programmes exist; ask your oncologist or the Singapore Cancer Society.

Pro-apoptotic proteins of the BCL-2 family. When activated by p53-induced PUMA or NOXA after DNA damage, BAX and BAK form pores in the mitochondrial outer membrane, releasing cytochrome c — triggering the intrinsic apoptosis cascade.

A family of proteins that regulate the intrinsic apoptosis pathway by controlling mitochondrial membrane integrity. Anti-apoptotic members (BCL-2, BCL-XL, MCL-1) prevent cytochrome c release and are overexpressed in many cancers. BCL-2 is overexpressed in ~85% of follicular lymphomas. Venetoclax (ABT-199) is a BCL-2 inhibitor approved for CLL and AML.

An oncogenic fusion protein created by the Philadelphia chromosome translocation t(9;22). Found in >95% of Chronic Myeloid Leukemia (CML). BCR-ABL is a constitutively active tyrosine kinase that drives uncontrolled cell proliferation. Imatinib (Gleevec) was the first targeted therapy to directly inhibit BCR-ABL.

Not cancerous. A benign tumour does not invade nearby tissue or spread to other parts of the body, unlike a malignant (cancerous) tumour.

A monoclonal antibody that specifically blocks VEGF (vascular endothelial growth factor), preventing it from binding to its receptors and stimulating tumour angiogenesis. The first anti-angiogenic drug approved by the FDA (2004). Approved for colorectal, lung, breast, kidney cancers and others.

A biological marker found in blood, tissue, or other body fluids that signals a normal or abnormal process. In cancer, biomarkers help doctors diagnose cancer, predict how it will behave, and decide on the best treatment.

A procedure where a small sample of tissue is removed from the body and examined under a microscope to check for cancer or other disease. It is the most reliable way to confirm a cancer diagnosis.

An engineered antibody that binds two different antigens simultaneously — typically one antigen on a cancer cell and one on an immune cell (usually CD3 on T cells). Bispecific antibodies form the basis of T cell engager (TCE) therapy. Different formats include 1+1 (one tumour binder + one CD3 binder), 2+1 (two tumour binders for higher avidity + one CD3), and trispecific 1+1+1 constructs targeting two tumour antigens plus CD3 to prevent antigen escape.

A broad population of cells originating from the bone marrow, including haematopoietic stem cells, endothelial progenitor cells (EPCs), mesenchymal stem cells, and myeloid progenitors. Tumours actively recruit BMDCs via signals like VEGF, PlGF, and SDF-1 to support tumour angiogenesis and immunosuppression.

A recognised side effect of cancer treatment — particularly chemotherapy — characterised by cognitive slowing, memory difficulties, poor concentration, and difficulty multitasking. Also called "chemo brain" or cognitive impairment. It is a real, documented medical condition that can persist months or years after treatment ends. Patients experiencing these symptoms should inform their oncologist; occupational therapy and cognitive rehabilitation strategies are available.

Genes that normally help suppress tumour growth. Inherited mutations in these genes significantly increase the risk of breast and ovarian cancers. Testing positive does not mean you will definitely get cancer.

A cycle of chromosomal instability that occurs when telomeres are critically shortened and chromosome ends fuse. During cell division, fused chromosomes are pulled apart, causing DNA breaks that generate new fusions in the next cycle. This generates massive genomic rearrangements, accelerating the accumulation of cancer-driving mutations.

A tumour marker found in blood, particularly elevated in pancreatic cancer. High CA 19-9 levels before and after surgery are associated with poorer prognosis. Used to monitor treatment response and detect recurrence.

Singapore's Ministry of Health list of cancer drugs covered under MediShield Life and MediSave. Each drug has specific claim limits. The CDL is updated three times a year. Non-CDL drugs are not covered for outpatient treatment.

A broad set of therapies aimed at improving quality of life, restoring function, and reducing disability caused by cancer or its treatment. Includes: prehabilitation (physical conditioning and psychological preparation before treatment begins), active treatment-phase rehabilitation, functional recovery therapy after treatment, and palliative rehabilitation to manage symptoms in advanced disease. Encompasses physiotherapy, occupational therapy, speech therapy, lymphedema management, psychological counselling, and nutritional support.

A small subpopulation of cancer cells with stem cell-like properties — they can self-renew, generate the bulk of the tumour, and are often more resistant to chemotherapy. Also called tumour-initiating cells (TICs). Targeting CSCs is a major research focus.

A cancer immunotherapy in which a patient's own T-cells are extracted, genetically re-engineered to express chimeric antigen receptors (CARs) that recognise specific cancer proteins, then infused back. Highly effective in certain blood cancers (leukemia, lymphoma, myeloma). Key side effect: cytokine release syndrome (CRS), a potentially severe inflammatory reaction.

Any agent that can cause cancer by damaging DNA or disrupting cellular regulation. Categories: (1) Chemical carcinogens (tobacco smoke, asbestos, aflatoxin); (2) Physical carcinogens (UV radiation → skin cancer; ionising radiation → leukemia); (3) Biological carcinogens (oncogenic viruses: HPV, HBV/HCV, EBV).

The most common type of cancer, which starts in the cells that line the skin or the internal organs (epithelial cells). Examples include breast carcinoma, lung carcinoma, and colorectal carcinoma.

A state of physical, emotional, and mental exhaustion experienced by people caring for a cancer patient. Caregivers frequently absorb the patient's emotional needs, coordinate appointments, manage finances, and protect children from distress — often suppressing their own needs. Caregiver burnout is common and recognised. Seeking psychological support, respite care, or joining a caregiver support group is strongly recommended and is not a sign of weakness.

A class of cancer-related genes whose normal function is to maintain genome integrity — through DNA repair and ensuring correct chromosome segregation. Loss of caretaker genes indirectly drives cancer by allowing cells to accumulate further mutations. Example: BRCA1 is a caretaker gene.

Cysteine-aspartate proteases — the executioner enzymes of apoptosis. Initiator caspases (caspase-8 in the extrinsic pathway; caspase-9 in the intrinsic pathway) activate executioner caspases (caspase-3, -6, -7), which cleave hundreds of cellular proteins, producing the characteristic features of apoptosis.

Prostate cancer that continues to grow despite medical or surgical testosterone suppression. Occurs in nearly all men with advanced prostate cancer within 2–3 years of starting androgen deprivation therapy. The androgen receptor (AR) remains active through amplification, mutation, or growth factor signalling crosstalk. Newer drugs (enzalutamide, abiraterone) target this resistance.

The rapid formation and collapse of microscopic bubbles in tissue. This is the mechanism by which histotripsy destroys tumours — focused ultrasound waves create cavitation that mechanically obliterates cancer cells without heat or radiation.

Enzymes that drive progression through the cell cycle. CDKs are only active when bound to specific cyclin partner proteins. Different cyclin-CDK complexes are active at different cell cycle phases: Cyclin D/CDK4/6 in G1; Cyclin E/CDK2 at the R point; Cyclin A/CDK2 in S phase; Cyclin B/CDK1 in mitosis. Almost all cancers have mutations in CDK regulation.

A type of targeted therapy drug that blocks proteins (CDK4 and CDK6) that help cancer cells divide and grow. Commonly used for hormone receptor-positive, HER2-negative breast cancer.

The ordered series of events by which a cell replicates and divides. Consists of G1 (growth/preparation), S (DNA synthesis), G2 (preparation for division), and M (mitosis). Cell cycle checkpoints detect damage and pause progression for repair. Cancer cells often have defective checkpoints, allowing them to accumulate mutations and divide uncontrollably.

A class of immunotherapy drugs that block immune checkpoint proteins (PD-1, PD-L1, CTLA-4) that cancer cells exploit to hide from the immune system. Removing these "brakes" allows the immune system to attack cancer. Examples: pembrolizumab, nivolumab (PD-1 blockers); atezolizumab (PD-L1 blocker); ipilimumab (CTLA-4 blocker). Used in melanoma, lung cancer, liver cancer, and many others.

The induction of cancer by chemical agents. First observed by Sir Percival Pott (1775, scrotal cancer in chimney sweeps from coal tar exposure). Most carcinogens require metabolic activation to reactive electrophilic intermediates that covalently bind to DNA. Carcinogen-induced cancer follows three stages: initiation, promotion, and progression.

Treatment using drugs that kill rapidly dividing cells. It targets cancer cells but can also affect some healthy cells, which causes side effects. It can be given as tablets, injections, or infusions.

The complex of DNA and proteins (mainly histones) that makes up chromosomes. The 3D organisation of chromatin — how genes are folded and positioned in the nucleus — plays a critical role in determining which genes are active or silenced in cancer cells.

A catastrophic one-step genomic event in which chromosomes shatter into many fragments and are randomly reassembled. This can generate dozens to hundreds of mutations simultaneously, accelerating cancer evolution. It is strongly linked to TP53 mutations.

A research study that tests new treatments, drugs, or procedures in people. Participating may give access to cutting-edge therapies before they are widely available. Ask your oncologist if you qualify.

The process by which a tumour develops from a single transformed cell that proliferates and acquires additional mutations over time, generating increasingly malignant subclones.

A field combining evolutionary biology, ecology, veterinary medicine, and clinical oncology to study cancer across the animal kingdom — from fruit flies and naked mole rats to elephants, whales, and bats. The goal is to understand why some species are highly cancer-resistant (e.g., elephants have 20 copies of TP53; naked mole rats secrete ultra-high-molecular-weight hyaluronan preventing hyperplasia; bowhead whales have unusually efficient DNA repair) and translate these natural mechanisms into human cancer therapies.

When all signs of cancer have disappeared after treatment. It does not always mean cancer is cured — follow-up is still needed to watch for recurrence.

A region of DNA rich in cytosine-guanine base pairs, often found near gene promoters (the "on/off switch" of a gene). In cancer, CpG islands near tumour suppressor genes are often hypermethylated (chemically blocked), silencing the protective genes.

Cytotoxic T-lymphocyte antigen-4 — an immune checkpoint receptor on T-cells that suppresses T-cell activation. Tumours exploit CTLA-4 to dampen anti-tumour immunity. Ipilimumab (Yervoy), an anti-CTLA-4 antibody, was the first immune checkpoint inhibitor approved (for melanoma, 2011).

Proteins whose levels rise and fall during the cell cycle, activating CDKs at specific phases. Key cyclins include: Cyclin D (G1, responds to growth factor signals), Cyclin E (late G1, drives the Restriction Point), Cyclin A (S phase), Cyclin B (M phase). Cyclin D1 is overexpressed in many breast cancers. CDK4/6 inhibitors (e.g. palbociclib) block Cyclin D-CDK4/6 activity and are approved for ER+ breast cancer.

A protein normally residing in the mitochondrial intermembrane space that acts as a critical trigger for apoptosis. When pro-apoptotic proteins (BAX, BAK) form pores in the mitochondrial membrane, cytochrome c is released and binds APAF-1 to form the "apoptosome" — a caspase-activating complex that triggers programmed cell death.

A potentially severe immune reaction that can occur after CAR T-cell therapy or other immunotherapies. Caused by massive release of inflammatory molecules (cytokines) from activated immune cells. Symptoms range from flu-like illness to life-threatening organ failure. Managed with anti-inflammatory drugs including tocilizumab (an IL-6 receptor blocker).

The study of individual cells under a microscope. Used to check if cells are normal or cancerous, often from samples like a Pap smear or fluid drawn from a tumour.

A radiation therapy technique used for left-sided breast cancer. The patient takes a deep breath and holds it during treatment to move the heart away from the radiation field, reducing the dose to the heart.

A subset of machine learning using artificial neural networks with multiple hidden layers (deep neural networks) to learn complex patterns from large datasets. In cancer pathology, deep learning — particularly convolutional neural networks (CNNs) and transformer-based architectures — is used to automatically detect tumours, classify cancer subtypes, predict molecular biomarkers (MSI, KRAS, BRAF mutations), and predict patient survival from whole-slide histopathology images.

The most dangerous form of DNA damage, in which both strands of the DNA double helix are broken. Cells repair DSBs via two main pathways: homologous recombination (HR — high fidelity, requires BRCA1/2) and non-homologous end joining (NHEJ — error-prone but faster). Unrepaired DSBs trigger apoptosis or genomic instability.

A chemical modification of DNA where a methyl group is added to cytosine bases, typically silencing nearby genes. In cancer, excessive methylation at tumour suppressor gene promoters shuts off protective genes — this is a key epigenetic mechanism exploited in cancer development.

Enzymes (DNMT1, DNMT3A, DNMT3B) that add methyl groups to DNA. DNMT1 maintains existing methylation patterns during cell division. Drugs that inhibit DNMTs (such as azacytidine and decitabine) are used to treat myelodysplastic syndrome and some leukaemias.

A mutation in a cancer cell that directly contributes to the development of cancer — typically in an oncogene or tumour suppressor gene. Of the hundreds to thousands of mutations found in a typical cancer genome, only about 5–20 are true driver mutations. Identifying driver mutations is a central goal of cancer genomics and precision oncology.

"Disordered growth" — in epithelial tissues, a state between hyperplasia (increased cell number) and carcinoma in situ (preinvasive neoplasia). Features include abnormal cell architecture, loss of polarity, and atypical mitoses. Dysplasia is considered a premalignant lesion in many tissues.

A transmembrane cell adhesion protein expressed on epithelial cells that acts as "cellular Velcro," linking adjacent cells together to maintain tissue integrity. In cancer, E-cadherin expression is suppressed during EMT by transcription factors (Twist, Snail, Slug), causing cells to become less adhesive and more migratory. Loss of E-cadherin is a hallmark of invasive cancer.

Transcription factors that activate genes needed for S phase entry (DNA replication). In early G1, E2F is held inactive by the tumour suppressor RB (Retinoblastoma protein). When RB is hyperphosphorylated by Cyclin E-CDK2 at the Restriction Point, it releases E2F, which then activates cyclin E and DNA replication genes — committing the cell to division.

Epidermal Growth Factor Receptor — a protein found on cell surfaces that, when mutated, can cause cells to grow uncontrollably. Mutations in EGFR are common in non-small cell lung cancer and can be targeted with specific drugs.

The fundamental inability of DNA polymerase to fully copy the very ends (telomeres) of linear chromosomes during cell division. With each replication, telomeres shorten by ~50–200 base pairs. After a finite number of divisions, critically short telomeres trigger replicative senescence — explaining why cancer cells must reactivate telomerase to become immortal.

Also called hormone therapy. It uses drugs to reduce or block the effect of hormones (like oestrogen or testosterone) that fuel certain cancers, such as hormone receptor-positive breast cancer or prostate cancer.

Changes in gene activity that do not involve changes to the underlying DNA sequence. Epigenetic mechanisms include DNA methylation and histone modification, and they control which genes are switched on or off. Cancer cells have widespread epigenetic abnormalities.

A process where cancer cells lose their epithelial (organised, less aggressive) characteristics and gain mesenchymal (invasive, stem cell-like, drug-resistant) properties. EMT is a key driver of cancer metastasis. The reverse process (MET) may reduce aggressiveness.

A reversible process in which cancer cells switch from an epithelial state (high adhesion, organised, low motility) to a mesenchymal state (low adhesion, invasive, highly migratory). EMT allows cancer cells to break away from the primary tumour, invade surrounding tissue, enter blood vessels, and metastasise to distant organs.

A common human virus (also called human herpesvirus 4) that causes infectious mononucleosis (glandular fever). EBV is also closely associated with nasopharyngeal cancer in Southeast Asia and contributes to tumour growth by altering gene regulation in infected cells.

An enzyme that deposits repressive histone marks (H3K27me3) on chromatin, silencing nearby genes. It acts as a "super-silencer" in cancer cells, turning off tumour suppressor genes. EZH2 inhibitor drugs (e.g., tazemetostat) are approved for certain lymphomas and sarcomas.

A hereditary cancer syndrome caused by germline mutations in the APC tumour suppressor gene. Affected individuals develop hundreds to thousands of polyps (adenomas) lining the colon, with near-certain progression to colon cancer without prophylactic surgery.

A condition in which an inherited germline mutation in a tumour suppressor or caretaker gene creates a strong predisposition to developing specific cancers. About 10% of cancers have a clear familial pattern. Examples: familial retinoblastoma (RB mutation), familial adenomatous polyposis (APC mutation), hereditary breast/ovarian cancer (BRCA1/2 mutations), Li-Fraumeni syndrome (p53 mutation).

A molecular imaging technique using PET tracers targeting fibroblast activation protein (FAP), which is highly expressed on cancer-associated fibroblasts in the tumour microenvironment. 68Ga-FAPI PET demonstrates superior lesion detection and higher tumour uptake compared to FDG-PET in many solid cancers including pancreatic, colorectal, and lung cancers.

The metabolic process of breaking down fatty acids to generate energy. Aggressive (mesenchymal) breast cancer cells rely heavily on FAO to maintain their invasive state. FAO inhibitors (like etomoxir) can block metastasis in laboratory models.

The financial burden, stress, and hardship caused by the costs of cancer treatment — including direct medical costs, lost income, and non-medical out-of-pocket expenses such as transport, dietary supplements, special food, domestic helpers, and rehabilitation. Singapore-specific context: hidden costs (taxis, lymphedema therapy, dietary requirements) are common and often emerge only after initial treatment decisions are made. Financial toxicity is associated with treatment non-adherence, reduced quality of life, and higher mortality. Patients facing financial difficulty should contact a Medical Social Worker (MSW) at their hospital or the Singapore Cancer Society. Do not assume private insurance covers all costs — always verify outpatient scan and therapy coverage explicitly.

The first treatment given for a cancer. If it does not work or stops working, second-line or third-line treatments may be tried.

A large artificial intelligence model trained on massive, diverse datasets (typically >100,000 whole-slide images in pathology) that develops general-purpose representations adaptable to many downstream clinical tasks with minimal additional labelled data. Examples in computational pathology include CONCH, UNI, Virchow, and Prov-GigaPath.

A type of mutation, particularly in TP53, where the mutant protein does not simply lose its normal function but actively acquires new cancer-promoting properties. Gain-of-function p53 mutations upregulate the mevalonate pathway and promote tumour growth.

A mechanism of oncogene activation in which the number of copies of a gene increases dramatically from the normal two copies to tens or hundreds of copies, resulting in greatly elevated protein levels. Classic example: HER2 gene amplification occurs in ~30% of breast cancers.

A gene change that is inherited from a parent and is present in every cell of the body from birth. It can be passed on to children.

A metabolic enzyme that breaks down glycine and produces a molecule (CH2-THF) needed for DNA synthesis. GLDC is highly expressed in lung cancer tumour-initiating cells and acts as an oncogene — overexpression alone can transform normal cells into cancerous ones.

Glucose transporter 1 — a protein on cell surfaces that imports glucose. In cancer cells, GLUT1 is massively upregulated (driven by Myc, HIF1α, and Ras signalling), allowing them to take up far more glucose than normal cells. This is the basis of the Warburg Effect and the reason PET scans can detect tumours using radioactively labelled glucose.

A chemical mark on histone proteins that represses gene activity. Regions rich in H3K27me3 can act as "super-silencers" that switch off tumour suppressor genes across long genomic distances via chromatin looping. EZH2 is the enzyme that deposits this mark.

The branch of medicine concerned with blood and blood-forming tissues. Blood cancers such as leukaemia, lymphoma, and myeloma are treated by haematologists.

The fundamental biological capabilities that a normal cell must acquire to become cancerous, as defined by Hanahan & Weinberg: (1) self-sufficiency in growth signals, (2) insensitivity to anti-growth signals, (3) evasion of apoptosis, (4) limitless replicative potential, (5) sustained angiogenesis, (6) tissue invasion and metastasis. Enabling features include genomic instability and tumour-promoting inflammation.

The most common primary liver cancer, arising from liver cells. It is particularly prevalent in Asia due to high rates of hepatitis B and C infection. HCC is 3–5 times more common in men. Early diagnosis is key as treatment options are better at early stages.

Human Epidermal Growth Factor Receptor 2 — a protein that promotes cell growth. HER2-positive cancers have too much of this protein and tend to grow faster. They can be treated with targeted therapies like trastuzumab (Herceptin).

Non-medical out-of-pocket expenses incurred during and after cancer treatment that are often not anticipated at diagnosis. Common hidden costs in Singapore include: taxi fares (many patients cannot tolerate public transport due to nausea or fatigue), special dietary requirements, lymphedema therapy, rehabilitation, hiring a domestic helper, nutritional supplements, and childcare. These costs can accumulate significantly, especially during prolonged treatment or survivorship. Discuss anticipated hidden costs early with your Medical Social Worker to plan ahead.

A transcription factor activated when oxygen is low (hypoxia) inside tumours. HIF-1α upregulates VEGF (promoting tumour angiogenesis), glucose transporters, and glycolytic enzymes — driving the Warburg Effect. It also promotes EMT and metastasis. HIF-1α is activated by multiple oncogenic pathways (Ras, PI3K/Akt) even when oxygen is available.

A non-invasive, non-thermal ultrasound-based treatment that destroys tumours using focused sound waves to generate microbubbles (cavitation) that mechanically break down cancer cells. FDA-approved for liver tumours since 2023. Clinical trials are launching in Singapore from 2025 at NCCS and NCIS.

A high-fidelity DNA repair pathway that fixes double-strand breaks using a homologous DNA sequence (usually the sister chromatid) as a template. Requires BRCA1, BRCA2, RAD51, and other proteins. When HR is defective (BRCA1/2 mutations), cells rely on error-prone repair, causing genomic instability. BRCA1/2 deficiency creates "synthetic lethality" with PARP inhibitors.

A cancer that has receptors for hormones like oestrogen (ER+) or progesterone (PR+). These cancers may respond well to hormone (endocrine) therapy.

Specific DNA sequences in gene promoters where nuclear receptors (hormone receptors) bind. When a hormone binds its nuclear receptor, the receptor-hormone complex binds to HREs and recruits co-activators or co-repressors to switch target genes on or off. Mutations in HREs or co-regulators can dysregulate hormone-driven gene expression in cancer.

Two viral proteins encoded by high-risk HPV strains that directly cause cervical cancer by inactivating key tumour suppressors: E6 inhibits p53, and E7 inhibits RB. This explains why the HPV vaccine (Gardasil) prevents cervical cancer — by blocking HPV infection before E6 and E7 can inactivate p53 and RB.

An increased number of cells in a tissue where the overall architecture remains otherwise normal. Hyperplasia is the earliest recognisable stage of abnormal cell growth and may be the first step toward a benign tumour. Unlike dysplasia or cancer, hyperplasia is not inherently dangerous and does not necessarily progress.

A family of proteins that block apoptosis by directly inhibiting caspases. Key members include survivin (overexpressed in many cancers) and XIAP. Cancer cells frequently overexpress IAPs to resist chemotherapy-induced apoptosis.

Mutations in the isocitrate dehydrogenase genes (IDH1/IDH2) found in ~80% of low-grade gliomas, ~20% of AML, and cholangiocarcinoma. These mutations produce an oncometabolite (2-hydroxyglutarate) that disrupts normal epigenetic regulation. Targeted inhibitors (enasidenib, ivosidenib) are now approved.

The first successful tyrosine kinase inhibitor (TKI) in cancer. Selectively inhibits BCR-ABL (the driver of CML). Transformed CML from a disease with ~20% 5-year survival to >90% with imatinib. A landmark proof-of-concept for targeted therapy.

Treatment that helps your immune system find and destroy cancer cells. Types include checkpoint inhibitors, CAR T-cell therapy, and cancer vaccines.

Intensity Modulated Radiation Therapy — a high-precision form of radiation therapy that shapes the radiation beam to match the tumour, sparing surrounding healthy tissue.

Giving fluids, medicines, or nutrients directly into a vein (intravenously) through a drip. Many cancer drugs including chemotherapy and immunotherapy are given by infusion.

The classic model of multistage carcinogenesis. Initiation is an irreversible genotoxic event creating a mutated "initiated" cell. Promotion is the clonal expansion of initiated cells by sustained exposure to a tumour promoter. Key rule: initiation must precede promotion.

The pressure within the fluid-filled spaces between cells in a tumour. In human tumours, IFP is typically 10–40 mmHg vs. 0 in normal tissue, caused by lack of functional lymphatics and high vascular permeability. High IFP impairs convective drug delivery into tumours.

The presence of genetically and molecularly distinct cancer cell populations within a single tumour. ITH makes treatment challenging because different subpopulations may respond differently to therapy. In liver cancer, the presence of aggressive cell subtypes ("bad apple" effect) is more prognostically important than overall heterogeneity.

Pancreatic intraepithelial neoplasia — a pre-cancerous change in the cells lining the pancreatic ducts. Research shows that cells from even low-grade PanIN lesions can circulate in the bloodstream before full cancer forms, suggesting metastasis begins very early.

The process by which cancer cells enter blood or lymphatic vessels during metastasis. Requires cancer cells to undergo EMT, degrade the basement membrane using MMPs, and penetrate the vessel wall. Intravasation is one of the rate-limiting (inefficient) steps of metastasis — its efficiency correlates with a tumour's metastatic potential.

Symptoms that are not outwardly visible but significantly impact a cancer survivor's ability to work, socialise, and function. In the cancer context, common invisible disabilities include: severe post-treatment fatigue, peripheral neuropathy (numbness and tingling in hands and feet), lymphedema, cognitive fog ("chemo brain"), and chronic pain. Because these conditions are not visible, employers, colleagues, or family members may not understand their impact. A medical memo from your oncologist can help document functional limitations when requesting workplace accommodations.

The most commonly mutated oncogene in human cancer (~30% of all cancers). KRAS is a GTPase in the RAS/MAPK growth signalling pathway. Mutations lock KRAS in a constitutively active state, driving uncontrolled cell proliferation. KRAS G12C can now be targeted with sotorasib or adagrasib — the first direct KRAS inhibitors.

Cancer of the blood and bone marrow, where the body produces abnormal white blood cells. There are several types, including acute lymphoblastic leukaemia (ALL) and chronic myeloid leukaemia (CML).

A rare inherited condition caused by germline TP53 mutations that greatly increases lifetime cancer risk. People with LFS can develop multiple types of cancer at young ages. Associated with a very high rate of chromothripsis (36%) in resulting cancers. DNA-damaging therapies (radiotherapy) should be used with caution.

The process by which a cell loses the remaining wild-type copy of a tumour suppressor gene, leaving only the mutant copy — resulting in complete loss of tumour suppressor function. This is the "second hit" in Knudson's two-hit hypothesis.

The primary beta-emitting radioisotope used in radioligand therapy (RLT). Half-life: 6.7 days. When attached to tumour-targeting molecules (such as DOTATATE for neuroendocrine tumours or PSMA-617 for prostate cancer), 177Lu delivers targeted beta radiation directly to cancer cells. FDA-approved [177Lu]DOTATATE (Lutathera) and [177Lu]PSMA-617 (Pluvicto) have demonstrated significant survival benefits in clinical trials.

Small bean-shaped structures that are part of the immune system. Cancer can spread to nearby lymph nodes, which is an important factor in staging and treatment planning.

Chronic swelling (usually in an arm or leg) caused by damage to or removal of lymph nodes during cancer surgery or radiation therapy. It occurs when the lymphatic system cannot properly drain lymph fluid. Lymphedema is common after breast cancer surgery, gynaecological cancer treatment, and other procedures involving lymph node dissection. It is a lifelong condition requiring management through specialised compression garments, manual lymphatic drainage therapy, exercise, and skin care. Early referral to a certified lymphedema therapist is important.

Cancer of the lymphatic system — the network of tissues and organs that help rid the body of toxins. The two main types are Hodgkin lymphoma and Non-Hodgkin lymphoma.

An inherited condition caused by mutations in DNA mismatch repair genes (MLH1, MSH2, MSH6, PMS2). It significantly increases the risk of colorectal, endometrial, and ovarian cancers, often at a younger age. Identified by genetic testing; affected individuals should undergo regular screening.

Cancerous. Malignant cells can invade and destroy nearby tissue and spread (metastasise) to other parts of the body, unlike benign (non-cancerous) cells.

A family of enzymes that degrade components of the extracellular matrix (ECM). MMPs play key roles in: cancer cell invasion (degrading basement membrane); metastasis; and angiogenesis.

A healthcare professional at Singapore public hospitals who helps patients and families navigate financial, social, and emotional challenges related to illness. MSWs can assist with applications to the Ministry of Health Assistance Fund (MAF) and other financial support schemes.

Singapore's national medical savings scheme. Patients can use MediSave to pay for cancer drug treatments listed on the Cancer Drug List (CDL), within specified withdrawal limits per month per drug.

Singapore's mandatory health insurance scheme. From September 2022, MediShield Life only covers cancer drugs listed on the Cancer Drug List (CDL) for outpatient treatment, with specific claim limits per drug per month.

The spread of cancer from where it first started to another part of the body. For example, breast cancer that spreads to the lungs is called metastatic breast cancer, not lung cancer.

A metabolic pathway responsible for cholesterol synthesis and the chemical modification of key signalling proteins (like Ras and RhoA). Gain-of-function TP53 mutations drive upregulation of this pathway in breast cancer. Statins, which inhibit this pathway, may have anti-cancer effects in TP53-mutated tumours.

Proteins on the surface of all cells that "display" samples of intracellular proteins to cytotoxic T-cells. If a cell is infected or cancerous, its abnormal proteins are displayed and trigger immune attack. Many cancer cells downregulate MHC-I to hide from immune surveillance — a key mechanism of immune evasion.

A form of genomic instability caused by defective mismatch repair (MMR). Cancers with high MSI (MSI-H) have an extremely high mutation burden, producing many neoantigens. MSI-H cancers respond exceptionally well to PD-1 checkpoint immunotherapy (pembrolizumab) — the first tumour-agnostic FDA approval regardless of cancer type.

A DNA repair pathway that corrects errors introduced during DNA replication. Key proteins: MLH1, MSH2, MSH6, PMS2. Defective MMR leads to microsatellite instability (MSI) and a high mutation burden. Germline MMR mutations cause Lynch Syndrome. MSI-H tumours are strongly predicted to respond to checkpoint immunotherapy.

A protein that acts as a key mediator of necroptosis (programmed necrotic cell death) downstream of the kinase RIP3. RIP3 phosphorylates MLKL at specific sites (T357/S358), activating the cell death program. Understanding this pathway may help develop therapies for tissue damage conditions.

The study of cancer risk factors using biological markers (biomarkers) at the molecular level, including carcinogen-macromolecular adducts, somatic mutations in target genes, and normal DNA sequence variants (SNPs).

A scan that uses magnetic fields and radio waves — not X-rays — to create detailed images of the inside of the body. Commonly used to detect and monitor cancer.

A personalised or off-the-shelf cancer vaccine using messenger RNA encoding tumour antigens, delivered via lipid nanoparticles (LNPs) to antigen-presenting cells. mRNA-4157 (V940) in combination with pembrolizumab became the first personalised neoantigen vaccine to improve recurrence-free survival in melanoma (Phase IIb KEYNOTE-942 trial, 2024) and is now in Phase III trials.

A team of different health professionals — such as oncologists, surgeons, radiologists, and nurses — who work together to plan and deliver the best care for a cancer patient.

A cancer of plasma cells in the bone marrow. It can weaken bones, cause fatigue, and affect kidney function. Treatment includes targeted therapy, immunotherapy, and stem cell transplant.

A change in the DNA sequence of a gene. Some mutations can cause normal cells to become cancerous. Mutations can be inherited (germline) or acquired during a person's lifetime (somatic).

A transcription factor oncogene that drives cell proliferation, metabolism, and growth. Overexpressed or amplified in many cancers: Burkitt lymphoma (MYC-IgH translocation), lung cancer, colorectal cancer, neuroblastoma. MYC also upregulates the glycolytic machinery (Warburg effect).

A cancer of the nasopharynx (back of the nasal cavity). Singapore has one of the highest rates globally (~300 new cases/year). Nearly all cases in Southeast Asia are associated with Epstein-Barr virus (EBV). Primarily treated with radiotherapy and chemotherapy.

A form of programmed (non-apoptotic) cell death that results in cell rupture and inflammation. Mediated by the RIP3-MLKL signalling pathway. Unlike apoptosis, necroptosis releases cell contents that can trigger immune responses — relevant to both cancer therapy and tissue damage.

Treatment given before the main treatment (usually surgery) to shrink a tumour and make it easier to remove, or to test how the cancer responds to therapy.

A tumour-specific antigen arising from somatic mutations unique to a patient's cancer cells — not present in normal cells. Because neoantigens are not subject to central tolerance, they can generate stronger and more specific T cell responses than tumour-associated antigens shared with normal tissue. Neoantigens are the basis for personalised cancer vaccines.

An error-prone DNA repair pathway that joins the broken ends of double-strand breaks without requiring a template. Active throughout the cell cycle, NHEJ can introduce small insertions or deletions at the break site. CRISPR-Cas9 gene editing exploits NHEJ to create targeted gene knockouts.

The largest family of eukaryotic transcription regulators. Nuclear receptors (including steroid hormone receptors for estrogen, testosterone, and progesterone) reside in or translocate to the nucleus when bound by their hormone ligand, directly regulating gene transcription at hormone response elements. Estrogen receptor (ER) and androgen receptor (AR) are critical drivers of breast and prostate cancer respectively.

A DNA repair pathway that removes bulky DNA lesions, particularly UV-induced thymine dimers and chemical adducts. Germline defects in NER cause Xeroderma Pigmentosum (XP) — an extreme sun-sensitivity disorder with >1,000-fold increased risk of skin cancer.

A mutated or overexpressed proto-oncogene that drives uncontrolled cell growth. Oncogenes act dominantly — only one mutated copy is required. Examples: RAS (point mutation locking it in active state); MYC (amplification or translocation); HER2 (amplification); BCR-ABL (chromosomal translocation).

A doctor who specialises in treating cancer. Medical oncologists use drugs (like chemo and immunotherapy); radiation oncologists use radiation; surgical oncologists perform cancer surgery.

A metabolite produced by mutated cancer cells that drives tumour progression. Examples include 2-hydroxyglutarate (from IDH1/2 mutations) and sarcosine (elevated in prostate cancer and GLDC-overexpressing lung cancers). Oncometabolites can disrupt normal epigenetic regulation.

A CDK inhibitor and tumour suppressor protein that inhibits Cyclin D-CDK4/6, preventing RB phosphorylation and cell cycle progression. p16 is one of the most commonly inactivated tumour suppressors in human cancer — frequently silenced by epigenetic DNA methylation of its promoter in melanoma, lung, colorectal, and many other cancers. p16 loss allows uncontrolled cycling past the Restriction Point.

A CDK inhibitor that acts as a key brake on the cell cycle. p21 is strongly induced by DNA damage (via the p53 tumour suppressor), causing cell cycle arrest to allow time for DNA repair. p21 also inhibits Cyclin E-CDK2 and other CDK complexes. Loss of p21 (or loss of the p53 that induces it) allows damaged cells to continue dividing and accumulate mutations.

Specialised care that focuses on relieving symptoms, pain, and stress caused by cancer. It can be provided alongside curative treatment at any stage — not just at end of life.

A class of targeted therapy that blocks PARP (poly-ADP-ribose polymerase) enzymes involved in base excision repair. In BRCA1/2-deficient cells, blocking PARP creates lethal DNA damage — this "synthetic lethality" is the basis of PARP inhibitor therapy. Approved drugs: olaparib, niraparib, rucaparib, talazoparib — for BRCA-mutated breast, ovarian, prostate, and pancreatic cancers.

A newly identified tumour suppressor gene in Asian lung adenocarcinoma. PARP4 interacts with the RNA splicing factor hnRNPM. Loss of PARP4 (by gene deletion or mutation) promotes tumour formation, particularly in EGFR/KRAS-driven cancers. Associated with worse survival when expression is low.

A mutation found in a cancer cell that does not contribute to the cancer phenotype. Of the hundreds or thousands of mutations in a cancer genome, only ~5–20 are driver mutations; the rest are passengers that accumulated coincidentally. Distinguishing passengers from drivers is a major challenge in cancer genomics.

The study of disease by examining tissues and cells. A pathologist analyses biopsy samples and writes a report that describes the type, grade, and features of a cancer.

A trained healthcare professional — typically a nurse, social worker, or community health worker — who guides cancer patients through the complex healthcare system. Patient navigators help with: understanding treatment options, coordinating appointments across departments, identifying financial assistance schemes, connecting patients to community support services, and bridging the gap between acute hospital care and home recovery. Not all Singapore hospitals have dedicated navigators, but Medical Social Workers (MSWs) fulfil a similar role. Ask your care team whether a navigator or MSW is available.

Programmed Death-Ligand 1 — a protein on some cancer cells that helps them hide from the immune system. Testing for PD-L1 levels helps doctors decide if checkpoint inhibitor immunotherapy is likely to work.

PD-1 (Programmed Death-1) is an immune checkpoint receptor on T-cells. PD-L1 is its ligand, expressed on cancer cells to suppress T-cell activity and evade immune destruction. PD-L1 testing helps predict whether checkpoint immunotherapy (e.g. pembrolizumab) is likely to work. Note: single-biopsy PD-L1 testing may miss heterogeneous expression in different tumour regions.

Nerve damage causing numbness, tingling, burning, or pain — typically in the hands and feet — as a side effect of certain chemotherapy drugs (especially platinum agents like oxaliplatin and cisplatin, and taxanes like paclitaxel). Can also cause loss of fine motor skills, balance problems, and sensitivity to cold. Peripheral neuropathy may be temporary or, in some patients, persistent. It is one of the most common "invisible disabilities" in cancer survivors and should always be reported to your oncologist.

Positron Emission Tomography — an imaging scan that uses a mildly radioactive tracer to show how tissues and organs are functioning. Used in cancer to detect spread or monitor treatment response.

The observation that cancer rates do not scale with body size or lifespan across species as expected. Named after Richard Peto (1977), Peto's paradox implies that large and long-lived animals must have evolved enhanced cancer suppression mechanisms — including extra TP53 gene copies (elephants), early contact inhibition (naked mole rats), and efficient DNA repair (bowhead whales).

A characteristic chromosomal abnormality found in >95% of Chronic Myeloid Leukemia (CML): a reciprocal translocation t(9;22) that fuses BCR with ABL kinase, creating BCR-ABL. The Philadelphia chromosome was the first recurrent chromosomal translocation identified in cancer (1960) and led directly to the development of imatinib.

A psychological phenomenon experienced by many cancer patients immediately after active treatment ends. When chemotherapy, radiation, or surgery concludes, the intense medical monitoring and structured hospital visits stop. Many patients feel suddenly isolated, anxious, and vulnerable — at a time when society may expect them to "bounce back." The post-treatment period often requires the most psychological support, even though it can be the least monitored phase. Seeking proactive psychological or counselling support after treatment ends is strongly encouraged.

A treatment approach that uses information about a person's genes, proteins, and environment to tailor the best treatment for their specific cancer. Also called personalised medicine.

Matching cancer treatment to the specific molecular features (gene mutations, protein expression) of a patient's tumour. Goes beyond traditional cancer type/stage classification. Requires genetic testing of the tumour. Examples include targeting EGFR mutations in lung cancer or BRCA mutations in breast/ovarian cancer.

A proactive programme of physical exercise, nutritional optimisation, and psychological preparation undertaken before cancer treatment begins (surgery, chemotherapy, or radiation). The goal is to build the patient's physical and mental resilience so they can better tolerate treatment, recover faster, and experience fewer complications. Evidence shows prehabilitation improves surgical outcomes, reduces hospital length of stay, and supports faster functional recovery. Ask your oncologist whether a prehabilitation programme is available at your treating centre.

The likely outcome or course of a disease — the chance of recovery or recurrence. It is based on factors like cancer type, stage, and how it responds to treatment.

An epigenetic mechanism by which the second functional copy of a tumour suppressor gene is silenced in cancer cells — without a DNA sequence mutation. Methylation of cytosine residues at the gene's promoter blocks transcription, effectively eliminating expression of the gene.

A normal cellular gene that promotes cell growth and division in a regulated, controlled manner. Proto-oncogenes become oncogenes when mutated or overexpressed, causing constitutive (unregulated) growth signalling. They include growth factor receptors (HER2, EGFR), intracellular signal transducers (RAS, RAF), and transcription factors (MYC).

An advanced form of radiation therapy that uses protons instead of X-rays. Protons can be directed more precisely at the tumour, causing less damage to surrounding healthy tissue.

A glycoprotein produced by prostate cells, measurable in blood. Elevated PSA can indicate prostate cancer but is also raised in benign prostate enlargement and prostatitis. The PSA test is used for prostate cancer screening and monitoring, but is controversial due to over-diagnosis and over-treatment concerns. PSA level accurately tracks cancer cell activity once diagnosis is established.

A protein highly expressed on prostate cancer cell surfaces, used as both a diagnostic and therapeutic target. [177Lu]PSMA-617 (Pluvicto) is FDA-approved for metastatic castration-resistant prostate cancer (mCRPC). PSMA expression is detected in 95% of mCRPC patients, making it an excellent theranostic target.

The use of high-energy radiation to destroy cancer cells or slow their growth. It is painless and carefully targeted to minimise damage to healthy tissue.

A targeted cancer treatment in which a radioactive isotope is attached to a ligand (antibody, peptide, or small molecule) that selectively binds to a cancer-specific target. The radioligand delivers radiation directly to cancer cells while minimising damage to surrounding healthy tissue. FDA-approved examples: [177Lu]DOTATATE (Lutathera) and [177Lu]PSMA-617 (Pluvicto).

A key growth signalling cascade activated by growth factors. Growth factor → receptor tyrosine kinase → RAS → RAF → MEK → ERK → gene transcription. Constitutive activation of any step drives cancer. KRAS mutations (~30% of cancers) are the most common activating mutation.

A critical tumour suppressor protein that governs the Restriction Point of the cell cycle. When hypophosphorylated (active), RB binds and inactivates E2F transcription factors, blocking cell division. When Cyclin D-CDK4/6 and Cyclin E-CDK2 hyperphosphorylate RB, E2F is released and the cell commits to dividing. Nearly all cancers have defects in the RB pathway.

When cancer comes back after treatment. A local recurrence is in the same location; a regional recurrence is in nearby lymph nodes; a distant recurrence (metastasis) is in another part of the body.

A decrease in or disappearance of signs and symptoms of cancer. In a partial remission, some cancer signs remain. In a complete remission, all signs of cancer have gone away.

A permanent state of cell cycle arrest triggered when telomeres shorten to a critical length. Senescence acts as a tumour suppressor mechanism, but cells with p53 or RB mutations can bypass it, leading to genomic crisis. Cancer cells escape by reactivating telomerase and achieving immortality.

A critical checkpoint in late G1 phase of the cell cycle. Before the R point, the cell integrates signals from growth factors and tumour suppressors. Once a cell crosses the R point (driven by RB hyperphosphorylation and E2F release), it is irreversibly committed to completing cell division — regardless of external signals. Many cancer mutations force cells across the R point inappropriately.

A class of compounds derived from vitamin A. In cancer research, retinoids (such as bexarotene) have been found to reverse the mesenchymal (aggressive) state of triple-negative breast cancer cells, making them more sensitive to standard chemotherapy. Currently under clinical trial for TNBC (NCT04664829).

The process of resuming employment after cancer treatment, which often requires careful planning and phased reintegration. Many cancer survivors experience fatigue, neuropathy, cognitive changes, or emotional adjustment challenges that affect their ability to return to full-time work immediately. Key steps: (1) Consult your medical team or MSW about your readiness; (2) Request a medical memo documenting your functional limitations; (3) Discuss reasonable workplace accommodations with your employer (part-time hours, flexible scheduling, modified duties). Do not resign immediately — explore accommodations first.

Receptor-Interacting Serine-Threonine Kinase 3 — a key regulator of programmed necrosis (necroptosis). When activated, RIP3 phosphorylates MLKL to execute cell death. RIP3 is elevated in tissue damage conditions (pancreatitis, retinal detachment). Inhibiting RIP3 may reduce inflammation-driven tissue injury.

The process by which non-coding segments (introns) are removed from RNA and the remaining segments (exons) are joined together to produce the final messenger RNA for a protein. Errors in splicing — for example, caused by loss of PARP4 or hnRNPM in lung cancer — can contribute to tumour development.

A cancer that starts in connective tissues such as bone, muscle, fat, cartilage, or blood vessels. Sarcomas are less common than carcinomas.

A person's knowledge and understanding of cancer screening recommendations — including which tests to have, at what age to start, and how often to repeat them. A 2026 Singapore Cancer Society survey found that fewer than 60% of women surveyed correctly identified the recommended screening age bands for breast, cervical, and colorectal cancers. Low screening literacy is a major barrier to early detection, which is when cancers are most treatable. Key Singapore screening recommendations: Colorectal cancer (FIT annually or colonoscopy every 10 years from age 45); Breast cancer (annual mammogram from age 40); Cervical cancer (HPV test every 5 years, ages 25–69).

Drugs that act as estrogen antagonists in some tissues and agonists in others, allowing tissue-specific effects. Tamoxifen blocks estrogen in breast tissue (treating breast cancer) but acts as an agonist in the uterus (increasing endometrial cancer risk). Raloxifene was developed to block both breast and uterine cancer risk while protecting bones. Used for breast cancer treatment and prevention.

A gene change that occurs during a person's lifetime — not inherited from a parent. These mutations are found only in tumour cells, not in all body cells, and cannot be passed on to children.

The process of determining how far a cancer has spread. Stages are typically numbered 1–4. Stage 1 is localised; Stage 4 means the cancer has spread to distant parts of the body (metastasised).

A class of cholesterol-lowering drugs (e.g., simvastatin) that inhibit the enzyme HMG-CoA reductase in the mevalonate pathway. Research suggests statins may have anti-cancer effects specifically in tumours with TP53 gain-of-function mutations, where the mevalonate pathway is overactive.

A highly focused form of radiation therapy that delivers a precise, high dose of radiation to a small tumour in the brain, spine, or lung, while minimising damage to surrounding tissue.

A branch of surgery focused on removing cancerous tumours and surrounding tissue. Surgical oncologists work closely with medical and radiation oncologists to deliver comprehensive cancer care.

Specialised healthcare and support for people who have completed active cancer treatment. Survivorship care addresses: monitoring for cancer recurrence, managing long-term side effects (fatigue, neuropathy, lymphedema, cognitive changes), screening for second cancers, managing increased cardiovascular and metabolic risks, psychological wellbeing, and returning to work and social roles. Cancer survivors have a higher lifetime risk of heart disease, hypertension, and other conditions depending on their treatment. Ask your oncologist about a survivorship care plan at the conclusion of active treatment.

A situation where simultaneous defects in two genes or pathways are lethal to a cell, while loss of either alone is tolerable. The most clinically important example: BRCA1/2 deficiency + PARP inhibition. This principle guides the development of many new targeted therapies.

An engineered immunotherapeutic molecule — typically a bispecific or multispecific antibody — that simultaneously binds a tumour-associated antigen on cancer cells and the CD3 receptor on T cells, forming a physical bridge that triggers T cell activation and directed tumour cell killing.

Drugs or other substances that attack specific proteins or genes in cancer cells that help them grow. Unlike chemotherapy, targeted therapy causes less harm to normal cells.

A class of chemotherapy drugs (paclitaxel, docetaxel, nab-paclitaxel) that stabilise microtubules, preventing their normal breakdown during cell division, arresting cells in mitosis and triggering apoptosis. Used in breast, ovarian, lung, and prostate cancers. Key side effects: peripheral neuropathy, hair loss, bone marrow suppression.

A ribonucleoprotein enzyme (TERT protein + TERC RNA template) that extends telomeres by adding TTAGGG repeats. Normally silenced in adult somatic cells. Reactivated in ~85–90% of cancers, allowing tumour cells to divide indefinitely (achieving immortality). Telomerase inhibitors (imetelstat) are in clinical trials.

Repetitive DNA sequences (TTAGGG) and associated proteins at chromosome ends, protecting chromosomes from being recognised as DNA breaks and preventing end-to-end fusions. In normal cells, telomeres shorten with each cell division. Critically short telomeres trigger replicative senescence or genomic crisis. Cancer cells maintain telomeres through telomerase reactivation or ALT.

A next-generation radionuclide for targeted radionuclide therapy with a similar half-life to lutetium-177 (6.9 days) but additional emission of Auger electrons and internal conversion electrons, causing more efficient DNA double-strand breaks. [161Tb]PSMA-617 has shown greater therapeutic efficacy than [177Lu]PSMA-617 in preclinical studies.

Hotspot mutations (C228T and C250T) in the promoter of the TERT gene that create new binding sites for ETS transcription factors, driving TERT overexpression and telomerase reactivation. Extremely common in melanoma (~70%), glioblastoma (~80%), bladder cancer (~60%), liver cancer, and thyroid cancer.

A portmanteau of "therapeutics" and "diagnostics" — an integrated approach combining cancer diagnosis and therapy using the same targeting molecule labelled with different radionuclides. Examples: PSMA-theranostics for prostate cancer; DOTATATE-theranostics for neuroendocrine tumours. Theranostics exemplifies precision medicine — treating only patients confirmed to express the target.

A protein that binds to specific DNA sequences to switch genes on or off. Transcription factors such as FOXA1, FOXA2 act as gatekeepers of sex hormone signalling in liver cancer, helping explain why men are 3–5 times more likely to develop hepatocellular carcinoma than women.

A rare form of cancer that can spread between individual animals as living cancer cells. Three known transmissible cancers in mammals: devil facial tumour disease in Tasmanian devils, and canine transmissible venereal tumour. Studying transmissible cancers provides unique insights into immune evasion strategies relevant to metastasis and immunotherapy resistance in human cancers.

A type of breast cancer that tests negative for oestrogen receptors, progesterone receptors, and HER2. It tends to grow faster and has fewer targeted treatment options, though immunotherapy may be used.

An abnormal mass of tissue formed when cells grow and divide more than they should. Tumours can be benign (non-cancerous) or malignant (cancerous).

A substance produced by cancer cells or the body in response to cancer, measurable in blood or tissue. Examples include PSA (prostate), CA-125 (ovarian), and CEA (colorectal). Used to help diagnose or monitor cancer.

The cellular and molecular environment surrounding a tumour, including stromal cells (fibroblasts, immune cells), blood vessels, and extracellular matrix. Cancer cells actively recruit stromal cells by secreting signalling molecules. Targeting the tumour microenvironment is an active area of cancer therapy development.

The complex ecosystem surrounding a tumour, including cancer-associated fibroblasts, blood vessels, immune cells (macrophages, lymphocytes, NK cells), and extracellular matrix. Tumours actively remodel their microenvironment to promote growth, suppress immune attack, and facilitate metastasis. The TME is increasingly recognised as a key therapeutic target.

An agent that accelerates tumour development in previously initiated cells by stimulating clonal expansion, without being a mutagen itself. Examples: TPA/phorbol esters (skin); phenobarbital, DDT (liver); asbestos (lung).

A gene that normally controls cell growth and prevents tumour formation. When both copies are inactivated — by mutation, deletion, or epigenetic silencing — cells can grow uncontrollably. Key examples include TP53, BRCA1/2, RB1, and CDKN2A (p16). PARP4 has recently been identified as a new tumour suppressor in Asian lung cancer.

Knudson's hypothesis (1971) explaining how tumour suppressor genes are inactivated. Both copies of a tumour suppressor gene must be lost for cancer to develop. In hereditary cancer syndromes, the first "hit" is an inherited germline mutation present in every cell; the second "hit" occurs somatically in one cell.

Small-molecule drugs that block the activity of tyrosine kinase enzymes in signalling pathways. TKIs are among the most successful targeted therapies: imatinib (BCR-ABL in CML), gefitinib/erlotinib/osimertinib (EGFR in NSCLC), vemurafenib/dabrafenib (BRAF in melanoma). Resistance commonly develops through target gene mutations.

A protein that recruits the DNA methyltransferase DNMT1 to sites of existing DNA methylation, maintaining the epigenetic silencing of tumour suppressor genes. Reducing UHRF1 can enhance the effectiveness of epigenetic drugs (DNMT inhibitors) used in cancer treatment.

A concept describing how anti-angiogenic therapy at the right dose and timing can improve the structural and functional abnormalities of tumour vessels — normalised vessels have better pericyte coverage, reduced permeability, and lower interstitial fluid pressure, improving drug penetration.

The formation of new blood vessels from endothelial progenitor cells (angioblasts) that differentiate in situ — distinct from angiogenesis (sprouting from pre-existing vessels). Tumours can harness both vasculogenesis and angiogenesis to build their blood supply.

A key signalling protein that stimulates angiogenesis (new blood vessel growth). Tumours secrete VEGF when they outgrow their blood supply, triggering new vessels to supply oxygen and nutrients — and providing routes for metastatic spread. Bevacizumab (Avastin), an anti-VEGF antibody, is used in colorectal, lung, and other cancers to cut off the tumour's blood supply.

A BCL-2 inhibitor (a BH3-mimetic drug) that specifically blocks the anti-apoptotic BCL-2 protein, triggering cancer cell death. Approved for Chronic Lymphocytic Leukemia (CLL) and Acute Myeloid Leukemia (AML). Represents the successful clinical translation of understanding apoptosis regulation in cancer.

A tumour suppressor gene whose protein targets HIF-1α for degradation under normal oxygen levels. When VHL is mutated (as in ~70% of sporadic clear cell renal cell carcinoma), HIF-1α cannot be degraded, leading to constitutive upregulation of VEGF, GLUT1, and other hypoxia-response genes.

The observation that cancer cells preferentially use glycolysis (breaking down glucose) for energy even when oxygen is present — unlike normal cells which would use more efficient oxidative phosphorylation. Named after Otto Warburg. This metabolic reprogramming supports rapid cell division and is a hallmark of cancer.

A genomic technique that reads all protein-coding regions of the genome. Used to identify cancer-causing mutations. A Singapore study of 302 Asian lung adenocarcinoma patients using this technique identified PARP4 as a new tumour suppressor gene specific to Asian populations.

Digital pathology technology that scans entire glass histopathology slides at high resolution, enabling computational analysis by artificial intelligence. AI algorithms applied to WSIs can automatically detect tumours, grade cancer, quantify biomarkers, predict molecular features, and assess patient prognosis.

A rare inherited condition caused by defects in nucleotide excision repair (NER) — the pathway that repairs UV-induced DNA damage. Patients are extremely sensitive to sunlight and have a >1,000-fold increased risk of skin cancers. Demonstrates directly that impaired DNA repair causes cancer when the repair system is defective.