GCD Exam 1 – Chapters 2-4: Nature of Cancer, Tumor Viruses, and Cellular Oncogenes

Flashcards covering the nature of cancer, tumor viruses, and cellular oncogenes from Chapters 2–4, focusing on definitions, mechanisms, and key examples.

What realization about tumors followed from the idea that all cells descend from the fertilized egg (the nineteenth-century view)?

Tumors are growths derived from normal tissues, not foreign bodies; cancer is a disease of malfunctioning cells.

Differentiate benign and malignant tumors.

Benign tumors are localized and noninvasive; malignant tumors are invasive and can metastasize; metastases are responsible for most cancer deaths.

Into how many major origin groups are most tumors classified, and what are they?

Four: epithelial, mesenchymal, hematopoietic, and neuroectodermal.

What are carcinomas and their two main categories?

Carcinomas are epithelial cancers; squamous cell carcinomas arise from protective epithelia and adenocarcinomas arise from secretory epithelia.

Name the nonepithelial malignant tumor types and their origins.

Sarcomas (mesenchymal), hematopoietic cancers (blood cell precursors), and neuroectodermal tumors (nervous system components).

What does 'anaplastic' mean in tumor terminology?

Dedifferentiated cells with loss of tissue-specific traits; origin may be hard to identify.

Describe the concept of cancer development as a progression.

Cancers develop progressively with gradations from benign to metastatic.

What distinguishes hyperplasia from metaplasia in benign tissues?

Hyperplasia: too many cells but normal appearance; metaplasia: normal cells displaced by other normal cell types.

Where are metaplastic changes most frequent?

Transition zones between two epithelial populations.

Define dysplasia and its significance.

Cytologically abnormal cells; a transitional state between benign and premalignant.

What are adenomas (adenomatous growths) and why are they considered benign?

Dysplastic epithelial tumors that are benign because they respect the basement membrane boundary.

What defines malignant tumors beyond the basement membrane breach?

Invasion of underlying tissues and potential for metastasis (requiring invasion, motility, and adaptation).

What does monoclonality mean in the context of tumors?

Most human tumors are monoclonal, descended from a single ancestral cell.

What explains country-by-country variations in cancer incidence?

Environment and lifestyle are dominant determinants, more so than heredity.

Which agents were implicated as cancer causes in laboratory studies?

Chemical and physical agents such as tobacco, coal dust, and X-rays.

What did the Ames test demonstrate about carcinogens?

Many carcinogens act as mutagens; some carcinogens are non-mutagenic (tumor promoters).

Who was Peyton Rous and what was the significance of RSV?

Peyton Rous discovered that viruses could induce tumors in chickens; RSV transforms cultured cells, showing cancer can be studied at the cellular level.

List key characteristics of RSV-transformed cells in culture.

Altered morphology, lack of contact inhibition, anchorage independence, growth without growth factors, immortalization, and tumorigenicity.

What are the genomes of RNA and DNA tumor viruses respectively?

RNA tumor viruses: single-stranded RNA (ssRNA); DNA tumor viruses: double-stranded DNA (dsDNA).

How do DNA tumor virus genomes persist in host cells?

They integrate into host-cell chromosomal DNA.

What is the role of reverse transcription in RNA tumor viruses?

RNA viruses can make double-stranded DNA copies (proviruses) that integrate into the host genome.

Define proto-oncogene.

A normal cellular gene with the potential to become an oncogene.

What is the significance of the src gene in RSV research?

src is the transformation-associated gene; v-src is the viral oncogene; c-src is the normal cellular proto-oncogene.

What evidence supports that proto-oncogenes can be activated without viruses?

DNA transfection experiments showed that oncogenes can arise in cells independently of viral infection; human tumor DNA can transform cells across species.

What is insertional mutagenesis in retroviruses?

Nontransforming retroviruses cause tumors by integrating near proto-oncogenes and activating them via viral promoters.

How can proto-oncogenes be activated in the absence of viruses?

Through gene amplification, point mutations altering protein structure, and chromosomal translocations.

Give an example of a chromosomal translocation affecting an oncogene and its consequence.

Burkitt’s lymphoma: myc is placed under a foreign promoter, leading to overexpression.

What is the Bcr-Abl fusion and its clinical relevance?

A fusion protein from chromosomal translocation that drives chronic myelogenous leukemia (CML).

What is the consequence of truncating the EGF receptor?

Leads to unremitting growth-promoting signaling.

What three activation mechanisms for the myc oncogene are discussed?

Provirus integration, gene amplification, and chromosomal translocation.

What is the overall conclusion of Chapter 4 about how cancers arise?

Most cancers arise from mutations in normal growth-controlling genes (proto-oncogenes) that become oncogenes, activated by viruses or somatic mutations; transfection experiments confirmed this concept.