Cancer Metastasis and Staging Quiz

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Questions and Answers

Which pathway do cancer cells commonly utilize to travel to the liver?

Superior mesenteric veins (correct)

Pulmonary veins

Cerebral arteries

Lymphatic vessels

What is the primary role of lymph nodes in cancer metastasis?

To produce cancer cells

To enhance immune response only

To prevent blood clotting

To filter and trap cancer cells (correct)

What mechanism allows cancer to spread throughout a body cavity?

Invasion of blood vessels

Seeding along organ walls (correct)

Travel through the lymphatic system

Direct contact with healthy cells

When cancer cells move through the lymphatic system, where do they eventually travel to?

To distant sites in the body Signup and view all the answers

What is a crucial step in the mechanism of tumor metastasis?

Penetration of basement membrane Signup and view all the answers

What does Stage I of cancer staging indicate?

Cancer is confined to the organ of origin. Signup and view all the answers

In the TNM system, what does the 'N' represent?

Lymph node involvement Signup and view all the answers

Which stage indicates that cancer has not invaded local tissues?

Stage I Signup and view all the answers

What does a higher number in the TNM staging system generally indicate?

Increased extent of disease spread Signup and view all the answers

What classification is used to describe a lesion of size 2 - 5 cm?

T2 Signup and view all the answers

Which food substances are linked to an increased risk of developing cancer?

High-calcium foods over 2000 mg Signup and view all the answers

What distinguishes malignant tumors from benign tumors?

Malignant tumors consist of undifferentiated cells. Signup and view all the answers

Which of the following is a risk factor for cancer associated with infections?

Human papilloma virus infection Signup and view all the answers

What is a common characteristic of benign tumors?

They are composed of well-differentiated cells. Signup and view all the answers

What is the result of a mutation in the TP53 gene?

Decreased tumor suppressor activity Signup and view all the answers

Which mechanism is linked to the risk of cancer from obesity?

Imbalanced metabolism and endocrine regulations Signup and view all the answers

Which type of radiation exposure is a known risk factor for cancer?

X-ray radiation Signup and view all the answers

Which mutation type is associated with the formation of an oncogene through duplication?

Homologous duplication Signup and view all the answers

How do malignant tumors affect surrounding tissues?

They can block blood vessels and other structures. Signup and view all the answers

What type of mutation is characterized by the breaking of chromosomes followed by the joining of non-homologous chromosomes?

Reciprocal translocation Signup and view all the answers

In the context of carcinogenesis, which genes are primarily affected by cell mutations?

Proto-oncogenes, oncogenes, and tumor suppressor genes Signup and view all the answers

Which hereditary factors may increase the risk for breast cancer?

BRCA1 and BRCA2 genes Signup and view all the answers

What does an abnormal protein resulting from a tumor suppressor gene mutation typically lead to?

Increased cancer risk Signup and view all the answers

What is the implication of over 50% of p53 gene mutations in human cancer?

Loss of tumor suppression is common Signup and view all the answers

Which type of mutation leads to the production of a new or abnormal protein in an oncogene?

Both inversion and translocation Signup and view all the answers

What condition is exemplified by reciprocal translocation between chromosomes 9 and 22?

Chronic myelogenous leukemia (CML) Signup and view all the answers

What classification corresponds to no axillary nodes involved in the N staging system?

N0 Signup and view all the answers

Which of the following is NOT a risk factor for colorectal cancer?

Regular exercise Signup and view all the answers

What is the primary screening tool used to detect hidden blood in stool for colorectal cancer?

Faecal Occult Blood Test (FOBT) Signup and view all the answers

Which age group is targeted for colorectal cancer screening in the subsidised programme?

50 to 75 years old Signup and view all the answers

What is a common treatment option for colorectal cancer?

Radiation therapy Signup and view all the answers

Which dietary habit is associated with a higher risk of colorectal cancer?

Diets high in fats and low in fiber Signup and view all the answers

What does M0 indicate in the staging of cancer?

No metastases Signup and view all the answers

Which of the following lifestyle changes is least likely to prevent colorectal cancer?

Excessive red meat consumption Signup and view all the answers

What is the primary role of selective estrogen receptor modulators (SERMs) in breast cancer treatment?

Blocking estrogen receptors Signup and view all the answers

Which of the following drugs is classified as an aromatase inhibitor?

Anastrozole Signup and view all the answers

Which surgical procedure involves the removal of the entire breast?

Mastectomy Signup and view all the answers

What is the mechanism of action for tyrosine kinase inhibitors (TKIs) in cancer treatment?

Inhibiting signal transduction pathways Signup and view all the answers

Which drug is a monoclonal antibody used in the treatment of HER2 positive breast cancer?

Trastuzumab Signup and view all the answers

Which of the following best describes the purpose of vascular endothelial growth factor (VEGF) signaling in cancer?

To promote angiogenesis Signup and view all the answers

What is the primary target of Imatinib (Gleevec) in cancer treatment?

Fusion proteins BCR-ABL Signup and view all the answers

What mechanism do aromatase inhibitors utilize to combat breast cancer?

Inhibiting estrogen synthesis Signup and view all the answers

Study Notes

Lecture 12: Neoplasm and Cancer Therapy

Learning Outcomes: Students should be able to identify, describe, and differentiate concepts of cell differentiation and growth, cancer and cell cycle checkpoints, oncogenes and tumor suppressor genes, benign and malignant tumor differences, classification of neoplasia, etiology of malignant neoplasia, clinical manifestation, and diagnosis and treatment.

Cancer Terminology

Dysplasia: Abnormal development of tissues.
Mutant Cells: Disruption of RNA and DNA within normal cells resulting in cells differing in form and function from normal cells.
Neoplasm/Tumor: Abnormal new growth of cells (not necessarily cancer).
Benign Tumors: Cells are encapsulated, well-differentiated, with normal tissue structure, do not invade other tissues. May or may not transform to malignancy.
Malignant Tumors: Arise from abnormal and uncontrolled cell proliferation, invading and destroying surrounding tissues.
Primary Tumor: The original site where the tumor arises.
Invasion: The process where cancer cells invade surrounding tissues.
Metastasis: The process where cancer cells spread to distant sites via the bloodstream or lymph or across body cavities to form secondary tumors.
Anaplasia: A typical malignant tumor where cells are poorly differentiated.
Angiogenesis: The formation of new blood vessels to supply nutrients for tumor growth.
Tumorigenesis: The process of tumor formation.
Carcinogenesis: The process where normal cells transform into cancer cells.

Proliferation and Differentiation

Proliferation: The process of increasing cell numbers by mitotic cell division (mitosis).
Differentiation: The process whereby proliferating cells become more specialized.
Apoptosis: A form of programmed cell death that eliminates injured or unwanted cells.

The Normal Cell Cycle

The duration of the cell cycle varies between cell types (10-30 hours in mammalian cells).
The phases must follow in a specific order, with errors in coordination leading to chromosomal alterations.
Coordination is determined by cyclins and cyclin-dependent kinases (CDKs).

Cellular Adaptation

Atrophy: Decrease in cell size.
Hypertrophy: Increase in cell size.
Hyperplasia: Increase in cell number.
Metaplasia: Change in cell type.
Dysplasia: Abnormal cell size, shape, appearance, and differentiation.

What is Cancer?

Cancer is characterized by uncontrolled differentiation and growth, spread of abnormal cells.
New cells are only formed for growth or to replace dead ones.
Cancerous cells do not self-destruct; they divide rapidly.
No apoptosis function.
Mutated genes have altered DNA sequences from normal genes.
Mutations may result in cancer development.
Factors that bring about DNA mutation are called mutagens.
Cancer-causing agents are called carcinogens.
Mutagens are often carcinogenic.

How do Normal Cells Become Cancerous?

Several mutations are required for normal cells to become cancerous.
Cells proliferate too much and may look abnormal.
Structural changes occur.
Selection occurs within the tumor for the "most cancerous" cells.

Oncogenes, Tumor Suppressor Genes, and Cancer

Proto-oncogenes: Normal genes involved in regulating cell proliferation.
Mutated proto-oncogenes transform into oncogenes that promote uncontrolled cell proliferation and cancer development. Example: RAS oncogene.
Tumor Suppressor Genes: Encode proteins that inhibit tumor formation when DNA is damaged, stop cell division, and induce apoptosis.
Mutated tumor suppressor genes lose their ability to prevent DNA damage and uncontrolled cell proliferation. Example: TP53 gene.

Possible Types of Mutations Leading to Oncogene Activation

Deletion
Duplication
Inversion
Reciprocal translocation

Oncogene Activation by Chromosomal Translocation

Chronic Myelogenous Leukemia (CML): Reciprocal translocation between chromosomes 9 and 22 creates the Philadelphia chromosome (Ph1), leading to a hybrid oncogenic protein (bcr-abl).

The Mutation of Tumor Suppressor Genes

Tumor suppressor genes produce normal proteins that control cell growth.
When mutated, these genes cannot produce normal proteins, lose control of cell growth, cell division becomes uncontrolled, resulting in a limited number of cells and size.

Examples of Tumor Suppressor Genes

Retinoblastoma gene (Rb gene): Loss or mutation accelerates the cell cycle, increasing proliferation in retinoblastoma.
Adenomatous polyposis coli (APC) gene: Mutations lead to familial adenomatous polyps (FAP).
Tumor protein TP53 (p53) gene: Normally activated in DNA-damaged cells promoting apoptosis; inactivation leads to cell survival.

Genetic Events Leading to Loss of Tumor Suppressor Gene Function

Loss of heterozygosity: The normal tumor suppressor gene copy is either inactivated or mutated.
Two-hit hypothesis: Cancer develops when sufficient mutations have occurred within a lifetime of mutations that lead to cancer development.

Hallmarks of Cancer

Cell acquires 8 essential alterations in cell physiology.
This occurs due to the multistep development of cancer.
Two additional characteristics enable cancer progression.

Enabling Replicative Immortality

Telomeres protect chromosome ends from deterioration or fusion.
Telomeres shorten with each division until cell division stops.
Normal cells cannot divide indefinitely.
Telomerase is an enzyme for telomere elongation, active in stem cells and most cancer cells.
In cancer cells, the enzyme rebuilds telomeres, enabling immortality, and the ability to divide indefinitely.

Risk Factors of Developing Cancer

High consumption of certain food substances (e.g., omega-6 fatty acids, grilled/preserved foods).
High calcium intake (> 2000 mg).
High-glycemic-index carbohydrates.
Ionizing radiation (e.g., X-rays, UV light).
Chemicals (e.g., tar from cigarettes).
Obesity.
Alcohol consumption.
Lack of exercise.
Bacterial and viral infections (e.g., Helicobacter pylori, HPV).
Hereditary predisposition (e.g., BRCA1 & BRCA2 for breast cancer).

Benign or Malignant Tumor?

Benign Tumors: Do not spread from their origin, but can crowd out surrounding cells (e.g., brain tumors, warts).
Malignant Tumors: Can spread to form secondary tumors (metastasis). Both types of tumors need nutrients for rapid growth.

Benign vs Malignant Tumor

Benign: well-differentiated cells, progressive and slow growth, usually encapsulated.
Malignant: undifferentiated cells, rapid growth, not encapsulated, invades surrounding tissues, and gains access to blood/lymph channels to spread.

Morphology of Cancer Cells

Anaplasia: Loss of cell differentiation.
Pleomorphism: Variations in cell and nuclei size and shapes.
Nucleoli: Larger than normal in most nuclei.
Chromatin/Chromosomes: Coarse and clumped.

Metastasis

Cancer cells can invade nearby tissues or metastasize (spread) to other organs.
Cancer cells may spread via three routes: venous system, lymphatic system, seeding.

Mechanisms of Tumor Metastasis

Cancer cells disrupt and invade extracellular matrix.
Release of proteolytic enzymes degrades extracellular matrix, allowing cancer cells to migrate.
Cancer cells penetrate basement membrane.
Cancer cells spread through blood vessels or lymphatics to other parts of the body.

Diagnosis of Cancer

Investigation of symptoms depends on cancer location.
Imaging techniques (MRI, X-ray, CT scan) are used for diagnosis.
Tumor markers are substances produced by cancer cells found in blood, spinal fluid, or urine; some are sensitive and specific for certain cancers (e.g., cervical cancer, and colorectal cancer).
Tumor tissue biopsy is used for identifying cancer stages (e.g., Papanicolaou or PAP smear for cervical cancer, colonoscopy for colorectal cancer).

Manifestations & Prognosis of Cancer

Cachexia: Severe malnutrition with anorexia, early satiety, and weight loss, present in 80% of cancer patients at death.
Anemia: Decrease in hemoglobin concentration in blood due to chronic bleeding, resulting in iron deficiency, malnutrition. Medical treatments or malignancy in blood-forming organs.
Prognosis is linked to cancer type, and tumor size, lymph node involvement, and metastasis.

Staging of Cancer

Staging: Determined by tumor size and extent of local invasion, spread to regional structures, and distant sites.
TNM system: Used to categorize tumors based on primary tumor (T), lymph node (N), and metastasis (M) factors.

Colorectal Cancer

Common cancer in men and women.
90% of colorectal cancers are preventable.
Risk factors: age over 50, obesity, family history, diets high in fat, low in fiber, smoking, high alcohol consumption, and lack of exercise.

Four Main Types of Leukemia

Acute Lymphoid Leukemia (ALL): Most common in children.
Acute Myeloid Leukemia (AML): Most common in adults, rapid dividing, myeloid cells.
Chronic Lymphoid Leukemia (CLL): Slow-growing, mature cells.
Chronic Myeloid Leukemia (CML): Affects myeloid cells, slow progression.

Nasopharyngeal Carcinoma (NPC)

Gender: Male more often than female.
Risk factors: Diet (salted cured fish), smoking, EBV infection, Family history and environment.

Breast Cancer

Estrogen receptor-positive breast cancer cells proliferate due to estrogen and are inhibited by tamoxifen.
Estrogen receptor-negative breast cancer cells proliferation is not controlled by estrogen, and not inhibited by tamoxifen.

Investigations of Breast Cancer

Mammogram: Breast imaging to look for tumors.
Biopsy: Fine needle aspirate (FNA) for testing.
Inherited mutations (BRCA, HER2)
Estrogen receptor (ER) positive: Hormonal therapy.
Breast lumps detected by mammograms.

Hormonal Therapy for Breast Cancer

Selective estrogen receptor modulators (SERMs): Examples include tamoxifen.
Aromatase inhibitors (AIs): Examples include anastrozole, exemestane, letrozole.
Estrogen receptor downregulators (ERDs): Examples include fulvestrant.

Treatment of Breast Cancer

Surgery: Lumpectomy, quadrantectomy, mastectomy, breast-conservative surgery.
Radiation therapy: Treats tumors.
HER2 +ve Breast Cancer: Trastuzumab, Laptinib

Targeted Cancer Therapy (TKI)

Tyrosine kinases: Protein activation by phosphorylation.
TKI: Inhibitory signaling pathways, promoting tumor survival and growth.
Examples: Imatinib, pazopanib, sunitinib. These medicines target signaling proteins in cancer cells and prevent signal transduction pathways to stop proliferation and growth.

Other Cancer Treatments

Conventional treatments: Surgery, radiation, chemotherapy, or a combination.
New possible treatments: Immunotherapy, cancer-fighting vaccines, stem cell research, and gene therapy.

Notable Side Effects of Chemotherapy

Severe Emesis: Acute and delayed nausea/vomiting.
Photosensitivity: Increased sensitivity to light.
Pulmonary toxicity: Lung damage.
Neurotoxicity: Nerve damage.
Hepatotoxicity: Liver damage.
Ulcers: Sores in the lining of the digestive tract.
Renal toxicity: Kidney damage.
Hemorrhagic cystitis: Blood in the urine.

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Description

Test your knowledge on cancer metastasis pathways and the staging system used to evaluate cancer progression. This quiz covers important concepts such as the role of lymph nodes, the TNM system, and classification of tumor sizes. Improve your understanding of how cancer spreads within the body.