Exam 1 Ch 54 Cancer Basic Principles Flashcards

1
Q

Which oncogenes code for growth factor receptors?

A

HER2 and RET

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2
Q

K-RAS and N-RAS are ongenes for cytoplasmic relays in stimulatory signaling pathways. What are their functions?

A

They code for guanine nucleotide-proteins with GTPase activity

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3
Q

What is the function of the oncogene BCR-ABL?

A

A gene for cytoplasmic kinases

-codes for non-receptor tyrosine kinases

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4
Q

What are 2 oncogenes for transcription factors that activate growth-promoting genes?

A

c-MYC and N-MYC

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5
Q

What are the three genes for proteins in the cytoplasm?

A

APC-step in signaling pathway
NF-1- codes for protein that inhibits stimulatory Ras protein
NF-2- codes for protein that inhibits stimulatory Ras protein

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6
Q

What oncogene can halt cell division and induce apoptosis?

A

p53

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7
Q

What oncogene is the master brake for the cell cycle?

A

RB1

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8
Q

Cells of ________ show diminished control of growth, BUT ___________ local tissue or spread to other parts of the body.

From Cancer Intro Lecture

A

Cells of Benign Tumors show diminished control of growth, BUT do NOT invade local tissue or spread to other parts of the body.

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9
Q

What are the 7 Key Characteristics of Cancer cells?

From Cancer Intro Lecture

A

1) Proliferate rapidly
2) Diminished growth control
3) Self-sufficient in growth signals
4) Insensitive to anti-growth signals
5) Stimulate local angiogenesis
6) Often able to evade apoptosis
7) Invade local tissues & Spread/metastasize to other parts of body

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10
Q

What is Desmoplasia?

From Cancer Intro Lecture

A

Dense collagenous stromal response often induced by malignant neoplasms, especially carcinomas (epithelial malignancies)

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11
Q

What is cancer?

From Cancer Intro Lecture

A

Malignant Neoplasm
Out of control growth of abnormal cells
Cancer cells grow, rapidly divide and do not die in an orderly fashion

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12
Q

What is Neoplasm?

From Cancer Intro Lecture

A

New Growth
Any abnormal new growth of tissue
Benign and malignant

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13
Q

The two main components of a malignant tumor are cancer cells and stroma. What are the components of stroma?

A

Connective tissue and blood vessels. All connective tissue consists of three main components: fibers (elastic and collagenous), ground substance and cells (fibroblasts, adipocytes, immune cells (macrophages, mast cells, leukocytes))

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14
Q

What are the morphological alterations seen in cancer cells?

A
  • variation in size and shape of cells and their nuclei
  • hyperchromatic nuclei due to increased DNA
  • increased nuclear to cytoplasmic ratio
  • large, irregular and/or multiple nuclei in neoplastic cells
  • atypical, increased, and/or aberrant mitotic activity
  • tumor giant cells
  • disorganized tissue architecture
  • ischemic necrosis
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15
Q

What is the difference between a low grade and high grade cancer?

A

A low grade cancer cancer contains cells that are well differentiated (less aggressive, better prognosis), whereas a high grade cancer has poorly differentiated cells (more aggressive, worst prognosis)

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16
Q

Describe the use of cancer staging, the TNM staging system, and state whether all cancers follow this.

A

Cancer staging reflects the amount and location of cancer in the body (extend and spread)
The TNM system describes Tumor size, lymph Node enlargement, and hematogenous Metastases.
Each cancer has its own staging system. For many cancers, the TNM combinations are grouped into five less-detailed stages (0-IV).

17
Q

List the three types of cancer nomenclature based on origin discussed in lecture, and how these different types of cancer differ.

A
  1. Carcinoma: epithelial; most common type; arises from cell that cover external and internal body surfaces (e.g. breast, lung, colon)
  2. Sarcoma: mesenchymal; arise from cells found in supporting tissue (e.g. bone, muscles, cartilage)
  3. Lymphoma: lymph nodes and immune system
    These types of cancer differ in genetics, growth rate, and response to therapy
18
Q

Which enzymes discussed in lecture are involved in epigenetic modification that target anticancer agents, and what modifications do they carry out?

A

DNA methyltransferase methylates DNA at CpG dinucleotides, and histone deacetylases (HDACs) repress transcription. Anticancer agents inhibit these genes and target their modifications. E.g. hypermethylation at CpG dinucleotides found near tumor suppressor genes can switch off these genes promote cancer development.

19
Q

What are the two basic mechanisms through which chemopreventive agents work?

A
  1. By inhibiting steps leading to cancer

2. By increasing protective processes