Neoplasia Flashcards

1
Q

What are two basic components of tumour

A
  1. the parenchyma, made up of transformed or
    neoplastic cells, and
    (2) the supporting, host-derived, nonneoplastic stroma, made up of connective tissue, blood
    vessels, and host-derived inflammatory cells
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2
Q

benign tumor arising in fibrous tissue is a

A

Fibroma

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3
Q

What is the term for a malignant tumor of mesenchymal origin?

A

Sarcoma

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4
Q

What are carcinomas?

A

Malignant epithelial tumors.

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5
Q

What is an adenocarcinoma?

A

carcinoma with glandular patterns.

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6
Q

What is a teratoma?

A

mixed tumor containing cells or tissues from more than one germ cell layer.

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7
Q

What is a hamartoma?

A

disorganized mass of tissue native to the site, often considered developmental rather than neoplastic.

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8
Q

What is a choristoma?

A

A congenital anomaly with a mass of normal tissue in an abnormal location.

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9
Q

What is the difference in differentiation between benign and malignant tumors?

A

Benign tumors show complete differentiation, resembling their tissue of origin, while malignant tumors may show differentiation or anaplasia, characterized by loss of specialized features.

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10
Q

How is anaplasia reflected in malignant tumors?

A

It involves large, variably shaped nuclei, disorganized cell growth (dysplasia), secretion of fetal proteins, mucin production in adenocarcinomas, and ectopic hormone secretion by non-endocrine tumors.

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11
Q

List examples of ectopic hormones secreted by tumors

A

Lung carcinoma cells may secrete ACTH, parathyroid-like hormone, insulin, and glucagon

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12
Q

: What is dysplasia, and how does it differ from anaplasia?

A

Dysplasia is disorganized cell growth, often seen in preneoplastic conditions, but it is potentially reversible. Anaplasia is irreversible and indicates malignant transformation.

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13
Q

How does the rate of growth differ between benign and malignant tumors?

A

Benign tumors: Grow slowly and steadily.
Malignant tumors: Grow rapidly, with rates influenced by blood supply, hormonal factors, and differentiation. Poorly differentiated tumors grow faster.

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14
Q

What factors influence tumor growth rate

A

Hormonal stimulation: Some tumors, like uterine leiomyomas, grow faster with hormonal changes.
Position: Tumors in restricted spaces (e.g., pituitary tumors in the sella turcica) have limited growth.

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15
Q

Describe the local invasion characteristics of benign and malignant tumors.

A

Benign tumors: Are localized and encapsulated; they do not invade surrounding tissues.
Malignant tumors: Invade and infiltrate surrounding tissues by breaking through the basement membrane and extracellular matrix.

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16
Q

What are the key steps involved in tumor invasion?

A

Detachment: Tumor cells lose adhesion due to E-cadherin inactivation.
Degradation: Proteolytic enzymes like matrix metalloproteinases (MMPs) degrade ECM components.
Attachment: Tumor cells bind ECM proteins such as collagen and laminin.
Migration: Tumor cells move through degraded ECM using cytokines and growth factors.

17
Q

Q: What is metastasis, and how is it achieved?

A

Metastasis is the spread of tumor cells to distant sites. It involves:

Invasion of the basement membrane.
Entry into blood or lymphatic vessels.
Formation of tumor emboli by aggregating with platelets and leucocytes.
Exit at a distant site (extravasation) and colonization.

18
Q

What determines organ-specific metastasis?

A

Tumour cells express certain chemokind receptors (e.g., CXCR4, CCR7) that bind ligands expressed by certain organs, directing metastasis to those sites.

19
Q

How do malignant tumors achieve angiogenesis

A

Malignant tumors secrete vascular endothelial growth factor (VEGF) and other factors that stimulate blood vessel formation to support rapid growth and metastasis.

20
Q

What are the hallmarks of malignancy

A

Invasion and infiltration of surrounding tissues.
Ability to metastasize.
Loss of differentiation (anaplasia).
High mitotic activity.
Resistance to apoptosis.

21
Q

Explain how tumors interact with the extracellular matrix (ECM) during invasion.

A

Tumors degrade the ECM using enzymes (e.g., MMPs), attach to ECM proteins, and modify ECM components to promote migration and resistance to apoptosis.

22
Q

What is the clinical relevance of tumor grading and staging?

A

Staging (TNM): Describes tumor size (T), nodal involvement (N), and metastasis (M), critical for prognosis and treatment planning

23
Q

Define preneoplastic conditions and explain their significance.

A

Preneoplastic conditions are acquired states that increase the likelihood of malignancy. Chronic inflammation associated with these conditions exposes cells to inflammatory products, leading to somatic mutations. Removal of the inflammatory cause can reverse tissue damage.

24
Q

Define preneoplastic conditions and explain their significance.

A

Preneoplastic conditions are acquired states that increase the likelihood of malignancy. Chronic inflammation associated with these conditions exposes cells to inflammatory products, leading to somatic mutations. Removal of the inflammatory cause can reverse tissue damage.

25
Q

Provide examples of preneoplastic conditions and their associated cancer risks.

A

Squamous metaplasia and dysplasia of bronchial mucosa in smokers: Risk of lung cancer.
Endometrial hyperplasia or dysplasia from excessive estrogen: Risk of endometrial carcinoma.
Leukoplakia of oral cavity, vulva, or penis: Risk of squamous cell carcinoma.
Villous adenoma of the colon: Risk of colorectal carcinoma.

26
Q

What are proto-oncogenes, and how do they contribute to cancer?

A

A: Proto-oncogenes are normal genes that promote cell growth and division. Mutations or activation of proto-oncogenes, such as RAS or EGFR, can convert them into oncogenes, leading to uncontrolled cell proliferation.

27
Q

What role does the TP53 gene play in cancer suppression?

A

The TP53 gene produces the p53 protein, which regulates the cell cycle, DNA repair, and apoptosis. Mutations in TP53 lead to loss of this tumor suppressor function, allowing damaged cells to proliferate unchecked.

28
Q

What role does the TP53 gene play in cancer suppression?

A

The TP53 gene produces the p53 protein, which regulates the cell cycle, DNA repair, and apoptosis. Mutations in TP53 lead to loss of this tumor suppressor function, allowing damaged cells to proliferate unchecked.

29
Q

What is the significance of the RB gene in cancer?

A

The RB gene regulates the G1-S phase transition by binding E2F transcription factors. Mutations in both copies of RB disable this control, leading to unregulated DNA replication and tumorigenesis.