Thomas's Case
Apoptosis
Metastasis
Disorders of Growth
Oncogenes and Tumour Suppressors
100

Why does a child with ALL often develop nosebleeds and bruises?

Because bone marrow infiltration leads to thrombocytopenia, reducing the ability to form clots.

100

What microscopic features help you identify a cell undergoing apoptosis? Name 2. 

Cell shrinkage, chromatin condensation, and formation of apoptotic bodies.

100

What does the term “secondary tumour” refer to in oncology?

A tumour that forms at a distant site due to metastatic spread from the primary tumour.

100

What is the term for an increase in the number of normal cells in a tissue?

Hyperplasia.

100

What is the role of the c-Myc gene in cancer biology?

It promotes cell proliferation and is often overexpressed in cancers.

200

What type of abnormal cell is found in the bone marrow and blood in ALL?

Lymphoblasts—immature lymphoid cells that crowd out normal hematopoietic cells.

200

What enzymes are responsible for executing apoptosis by cleaving cellular proteins?

Caspases

200

Through what pathway do most carcinomas spread first?

Through lymphatic vessels to regional lymph nodes.

200

What condition causes non-malignant enlargement of the prostate gland in older men?

Benign prostatic hyperplasia (BPH).

200

What are tumour suppressor genes, and what do they do?

They regulate cell growth, DNA repair, and apoptosis, preventing uncontrolled division.

300

What does a reduced red blood cell count in a child with ALL typically cause? Name 3. 

Anaemia, leading to pallor, fatigue, and reduced oxygen-carrying capacity.

300

What is the role of p53 in apoptosis?

It senses DNA damage and activates pro-apoptotic pathways or cell cycle arrest.

300

What is the preferred route of metastatic spread for sarcomas?

Hematogenous spread via blood vessels.


300

What is it called when one differentiated cell type is replaced by another?

Metaplasia.

300

Why is p53 called the “guardian of the genome”?

Because it halts the cell cycle and induces apoptosis in response to DNA damage.

400

Why is it necessary to perform a lumbar puncture in cases of ALL?

To assess for CNS involvement by checking for lymphoblasts in the cerebrospinal fluid.

400

How are apoptotic cells cleared without causing inflammation?

They form apoptotic bodies that are phagocytosed by macrophages.

400

Why is the liver a common site of metastasis for gastrointestinal cancers?

Because it receives blood from the intestines via the portal vein.

400

What term describes abnormal but non-invasive growth that may precede cancer?

Dysplasia.

400

What does the two-hit hypothesis explain about tumour suppressor genes?

That both alleles must be inactivated or mutated for loss of function and cancer to occur.

500

How does PEG-asparaginase treat ALL in children?

It depletes asparagine, an amino acid that lymphoblasts rely on but cannot synthesise themselves.

500

What role does Bcl-2 play in regulating apoptosis?

It inhibits apoptosis by preventing mitochondrial cytochrome c release.

500

What molecular changes allow cancer cells to detach from the primary tumour and invade surrounding tissues?

Downregulation of E-cadherin, secretion of matrix metalloproteinases (MMPs), and changes in integrin expression enable invasion and migration.

500

What is a hamartoma?

A benign, disorganised overgrowth of tissue native to its site.

500

How do cyclin-CDK complexes regulate cell cycle progression, and how can their dysregulation contribute to oncogenesis?

Cyclin-CDK complexes phosphorylate target proteins to drive the cell through different phases of the cell cycle (e.g., Cyclin D/CDK4 pushes the cell past G1 checkpoint). Overexpression of cyclins or loss of CDK inhibitors (like p21 or p16) leads to uncontrolled cell cycle progression and promotes tumour development.