HMM103: Cell Technology – Cancer

Vocabulary flashcards covering key terms and concepts from the HMM103 Cell Technology lecture on cancer.

Cell Cycle

Ordered series of events through which a cell grows, replicates its DNA, and divides into two daughter cells.

Interphase

Stage of the cell cycle (G1, S, G2) in which the cell grows and duplicates DNA and organelles before mitosis.

Mitosis

Phase of the cell cycle in which duplicated chromosomes are separated into two nuclei; followed by cytokinesis.

Cytokinesis

Physical division of the cytoplasm to form two distinct daughter cells after mitosis.

G1 Phase (Gap 1)

Interphase stage of cell growth and normal function; prepares for DNA synthesis.

S Phase (Synthesis)

Interphase stage in which the cell replicates its DNA.

G2 Phase (Gap 2)

Interphase stage for final growth and preparation for mitosis.

Checkpoint

Go/no-go control point ensuring proper completion of key events before progression in the cell cycle.

Cyclins

Regulatory proteins whose concentrations fluctuate to activate CDKs and drive cell-cycle transitions.

Cyclin-Dependent Kinases (CDKs)

Serine/threonine kinases that, when bound to cyclins, phosphorylate target proteins to advance the cell cycle.

G1/S-Cyclins

Cyclins that activate CDKs late in G1 to trigger S-phase entry; levels fall during S phase.

S-Cyclins

Cyclins that bind CDKs after G1/S transition to stimulate chromosome duplication; remain high until mitosis.

M-Cyclins

Cyclins that activate CDKs at the G2/M checkpoint to initiate mitosis; destroyed mid-mitosis.

Positive Regulators

Molecules (e.g., cyclin–CDK complexes) that promote progression through the cell cycle.

Negative Regulators

Molecules (e.g., CDK inhibitors, tumour suppressors) that halt or slow cell-cycle progression.

CDK Inhibitors (CKIs)

Proteins that bind specific CDKs to block their activity and pause the cell cycle.

Tumour Suppressor Genes (TSGs)

Normal genes that restrain cell growth or trigger apoptosis; loss-of-function mutations promote cancer.

Oncogenes

Mutated or over-expressed proto-oncogenes that drive uncontrolled cell proliferation; dominant gain-of-function.

Proto-Oncogene

Normal gene involved in growth signalling that can become an oncogene when mutated or over-expressed.

Genome Stability Genes

Caretaker genes that repair DNA or maintain chromosomal integrity; their loss increases mutation rates.

Apoptosis

Programmed cell death that removes damaged or unwanted cells.

Neoplasm

Abnormal mass of tissue resulting from uncontrolled cell proliferation; may be benign or malignant.

Benign Tumour

Non-cancerous growth that does not invade nearby tissue or metastasise and rarely recurs once removed.

Pre-Malignant

Lesion with abnormal cells that are not yet cancerous but have a high chance of becoming malignant.

Malignant Tumour

Cancerous growth capable of invading surrounding tissues and metastasising to distant sites.

Carcinoma

Cancer arising from epithelial cells lining organs or skin (e.g., breast, lung, colon).

Sarcoma

Cancer that originates in connective tissues such as bone, cartilage, fat, or muscle.

Leukemia

Cancer of blood-forming tissues causing large numbers of abnormal blood cells in circulation.

Lymphoma

Cancer that begins in lymphocytes and affects lymph nodes or other lymphoid tissues.

Hallmarks of Cancer

Shared biological capabilities that enable tumour growth and metastasis (e.g., sustaining proliferation, evading suppressors).

Sustained Proliferative Signalling

Cancer ability to grow independently of external growth factors.

Evading Growth Suppressors

Cancer cells bypass inhibitory signals such as those mediated by p53 or Rb proteins.

Enabling Replicative Immortality

Cancer cells divide indefinitely, often through telomerase activation.

Deregulating Cellular Energetics

Metabolic re-programming that allows cancer cells to survive under hypoxic conditions (e.g., Warburg effect).

Genome Instability & Mutation

High mutation rate in tumours due to defective DNA repair mechanisms.

Unlocking Phenotypic Plasticity

Cancer cells maintain partial differentiation states to adapt and survive.

Senescent Cells

Viable but non-dividing cells that can escape therapies targeting proliferating cells.

Avoiding Immune Destruction

Tumour evasion of T-cell and NK-cell recognition via immunosurveillance escape mechanisms.

Tumour-Promoting Inflammation

Use of inflammatory responses to supply growth factors, blood flow, and survival signals to cancer.

Inducing Angiogenesis

Stimulation of new blood-vessel formation to supply oxygen and nutrients to the tumour.

Activating Invasion & Metastasis

Cancer cell dissemination from the primary site to establish secondary tumours.

Non-Mutational Epigenetic Reprogramming

Epigenetic changes (DNA methylation, histone modification) that alter oncogene or TSG expression without DNA mutation.

Proliferating Cell Nuclear Antigen (PCNA)

DNA clamp protein that increases DNA polymerase processivity during replication; marker of cell proliferation.

Cell Growth Checkpoint

Late-G1 control point that verifies cell size and protein reserves before S phase entry.

DNA Synthesis Checkpoint

Control point that ensures DNA has been accurately replicated before mitosis.

Mitosis Checkpoint

Control point during M phase that verifies proper chromosome attachment and segregation.

BRCA1

Genome stability gene encoding a DNA repair protein; loss increases risk of breast and ovarian cancers.

Epidermal Growth Factor Receptor (EGFR)

Growth-factor receptor oncogene frequently amplified or mutated in cancers.

p53

TSG encoding a transcription factor that triggers DNA repair, cell-cycle arrest, or apoptosis after damage.

Retinoblastoma Protein (Rb)

TSG that inhibits cell-cycle progression from G1 to S phase by regulating E2F transcription factors.

Ras

Small GTPase oncogene involved in transmitting growth-factor signals to proliferation pathways.

Bcl-2

Oncoprotein that inhibits mitochondrial apoptosis, contributing to cell-death resistance.

Adenomatous Polyposis Coli (APC)

TSG involved in regulating Wnt signalling and tissue architecture; mutated in colorectal cancer.

SOCS Proteins

Family of TSGs that negatively regulate cytokine signalling pathways.

Wee1 Kinase

Negative regulator that inhibits CDK1 to prevent premature entry into mitosis.

Chemotherapy

Use of cytotoxic drugs systemically to kill rapidly dividing cancer cells.

Radiotherapy

Targeted ionising radiation used to destroy cancer cells by DNA damage.

Multimodal Treatment

Combination of surgery, radiotherapy, and chemotherapy at lower doses to enhance efficacy.

Targeted Therapy

Treatment using agents that specifically inhibit molecular drivers of a patient’s cancer.

Gene Therapy

Therapeutic delivery or editing of genetic material to correct or counteract cancer-related genes.

Radiomics

Computational extraction of quantitative features from medical images for cancer characterisation and stratification.

Pathomics

High-throughput quantitative analysis of digital pathology images to inform diagnosis and prognosis.

Telomerase Inhibitors

Drugs that block telomerase activity to limit replicative immortality of cancer cells.

PARP Inhibitors

Agents that block poly(ADP-ribose) polymerase to exploit DNA repair defects in tumours.

BH3 Mimetics

Pro-apoptotic drugs that mimic BH3-only proteins to neutralise Bcl-2 family anti-apoptotic proteins.

VEGF Signalling Inhibitors

Therapies that block vascular endothelial growth factor pathways to prevent tumour angiogenesis.

Anti-CTLA4 Monoclonal Antibody

Immune-activating antibody that enhances T-cell responses against tumours.

Aerobic Glycolysis Inhibitors

Agents that target the Warburg effect to disrupt cancer cell metabolism.

HGF/c-Met Inhibitors

Drugs that block hepatocyte growth factor signalling, limiting invasion and metastasis.

Nanomedicine

Use of nanoscale materials for targeted drug delivery, imaging, or therapy in cancer.

Thermal Ablation

Local destruction of tumour tissue using extreme heat (e.g., radiofrequency, microwave).

Magnetic Hyperthermia

Cancer treatment in which magnetic nanoparticles are heated in an alternating magnetic field to kill tumour cells.

Tumour Markers

Substances in blood, urine, or tissue that may indicate the presence or progression of cancer.

Biopsy

Removal of a tissue sample for microscopic examination to diagnose cancer.

Computed Tomography (CT)

Imaging technique that uses X-rays to create detailed cross-sectional images of the body.

Magnetic Resonance Imaging (MRI)

Imaging method that uses magnetic fields and radio waves to produce high-resolution body images.

Cytogenetics

Laboratory analysis of chromosomes to detect genetic abnormalities in cancer cells.

Smoking (Cancer Risk Factor)

Major environmental cause of multiple cancers, notably lung, due to carcinogenic compounds in tobacco.

Obesity

Excess body fat (BMI ≥ 30) linked to increased risk of several cancers through hormonal and inflammatory changes.

Differentiation Signals

Cellular cues (e.g., p15, p16 induction) that direct cells to exit the cell cycle and specialise.

Growth Factors

Extracellular proteins that bind receptors to stimulate cell proliferation and survival.

Cellular Senescence

Permanent cell-cycle arrest that acts as a tumour-suppressive mechanism but may contribute to inflammation.

Immune Surveillance

Process by which the immune system detects and eliminates nascent tumour cells.

Angiogenesis

Formation of new blood vessels; exploited by tumours for oxygen and nutrient supply.