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Pathophys Semester II > Neoplasia PT-1 Test II > Flashcards

Neoplasia PT-1 Test II Flashcards

1
Q

Tumor Classification

A

Benign

Innocent Behavior

Localized Lesions

Without spread

PT survival

Surgically removable

Malignant

Aggressive Behavior

Metastasis

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2
Q

Connective tissue Tumors

A

Tissue Type - Benign Tumor - Malignant Tumor

Adult Fibrous Tissue - Fibroma - Fibrosarcoma

Embryonic fibrous tissue - Myxoma - Myxosarcoma

Fat - Lipoma - Liposarcoma

Cartilage - Chondroma - Chondrosarcoma

Bone - Osteoma - Osteosarcoma

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3
Q

Epithelium tissue Tumors

A

Tissue Type - Benign Tumor - Malignant Tumor

Blood Vessels - Hemangioma - Hemangiosarcoma, angiosarcoma

Lymph vessels - Lymphangioma - Lymphangiosarcoma

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4
Q

Muscle tissue Tumors

A

Tissue Type - Benign Tumor - Malignant Tumor

Smooth Muscle - Leimyoma - Leiomyosarcoma

Striated Muscle - Rhabdomyoma - Rhabdomyosarcoma

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5
Q

Epithelial tissue Tumors

A

Tissue Type - Benign Tumor - Malignant Tumor

Stratified Squamous - Papilloma/seborrheic keratosis - squamous cell carcinoma/epidermoid carcinoma

Glandular epethelium - Adenoma - Adenocarcinoma

Liver - Hepatic Adenoma - Hepatocellular carcinoma

Kidney - Renal Tubular Adenoma - Renal Cell Carcinoma

Bile Duct - Bile Duct Adenoma - Cholangiocarcinoma

Transitional Epithelium - Transitional Cell Papilloma - Transitional Cell Carcinoma

Testis - Benign teratoma - Choriocarcinoma

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6
Q

Neural tissue Tumors

A

Tissue Type - Benign Tumor - Malignant Tumor

Glial Cells - Glioma - Diffuse astrocytic and oligodendroglial tumors

Nerve cells - Ganglioneuroma - Neuroblastoma/Medulloblastoma

Meninges - Meningioma - Malignant meningioma

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7
Q

All Tumor Basic Components

A

Neoplastic Cells - constituting the tumor parenchyma

Supporting stroma - tumor blood and lymphatic vessels, ECM (collagen and hyaluronic acid) and stromal cell constituents;

Angiogenic Vascular cells

Infiltrating immune cells

Cancer-associated fibroblastic cells

*Important influence on the malignancy and outcome of treatment responses

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8
Q

Clinical Relevance of tumor microenvironment

A

Remodel the tumor environment to enhance therapy

Vascular Normalization;

Reduce pore size->improves perfusion->improves drug delivery

Stress alleviation strategy:

Decrease stromal expression of TGFB as well as other fibrosis-inducing molecules->improves drug delivery

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9
Q

Characteristics of Benign and Malignant neoplasms

A

Differentiation - How closely the cells histologically and functionally resemble their normal cell counterpart

Lack of differentiation is called anaplasia -> malignancy’s hallmark

Metaplasia - replacement of one cell type with another cell type

Dysplasia - Loss of cellular uniformity and architectural organization

Carcinoma in situ - Marked dysplastic changes involving the entire thickness of the epithelium

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10
Q

Local invasion and metastasis of Neoplasm

A

Local invasion

Most benign tumors develop a surrounding rim of condensed connective tissue or capsule (no Local Invasion), but Malignant Tumors are invasive and infiltrative destroying surrounding normal tissues with no capsule (Local invasion)

Metastasis

Single most important feature distinguishing benign from malignant. Invasion of lymphatics, blood vessels, or body cavities by tumor, followed by transport and growth of secondary tumor cell masses

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11
Q

Tumor Metastatic Tropism

A

Prostate cancer -> Bone marrow

Pancreas -> Liver

Breast -> Lungs & Bone Marrow

Colon -> Liver

Some Tumor cells have adhesion molecules, some have chemokine receptors. The microenvironment of an organ might not be suitable for every type of metastases.

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12
Q

Portal Circulation and Liver Metastasis

A

Circulation layouts may also influence metastatic site.

Primary Colon Cancer mainly metastasizes to the Liver due to the Portal Vein drainage from the colon directly into the liver.

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13
Q

Environmental risk factors in cancer

A

Infectious agents

Smoking

Alcohol

Diet

Obesity

Reproductive history

Environmental carcinogens

Aging

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14
Q

Acquired predisposing factors in Cancer

A

Chronic Inflammation - Highest cancer risk with infectious causes

Precursor Lesions - Cancer rarely can rise in the previous benign tumors

Immunodeficiency states - Particularly T cell

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15
Q

Hallmarks enabling Characteristics of Cancer

A

Avoiding immune destruction

Evading Growth suppressors

Enabling replicative immortality

Tumor-promoting inflammation

Activating invasion and metastasis

Genomic instability

Inducing angiogenesis

Resisting cell death

Deregulating cellular energetics

Sustaining proliferative signaling

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16
Q

Cell-mediated immunity in cancer cells

A

Avoid Cytotoxic T cells CD8+, NK, and Macrophages by the following;

Failure to produce Tumor antigen

Mutations in the MHC genes prevent presentation of antigen

Production of immunosuppressive proteins or inhibitory cell surface protein

17
Q

Evading growth suppressors

A

Tumor suppressor genes slow down cell division and repair DNA mistakes/activate apoptosis.

Cancer can arise by inactivation of Tumor suppressor gene

Loss of Heterozygosity - mutation of both alleles of tumor suppressor genes are needed for carcinogenesis.

18
Q

Tumor Suppressor Gene RB

A

RB gene mutation leads to cell cycling if the mutation spreads to both homologues loss of growth control occurs and can lead to childhood tumor retinoblastoma

19
Q

Tumor Suppressor Gene P53

A

P53 prevents the growth of genetically defective cells by;

Sensing DNA damage

Arresting cell cycle

If DNA can be repaired, the cell undergoes S phase

If not p5s induces apoptosis

P53 is mutated in more than 50% of all human cancers

20
Q

Enabling Replicative immortality

A

Telomerase is activated in most tumor cells preventing cell senescence/apoptosis.

21
Q

What is Therapy-Induced inflammation?

A

Necrosis of malignant cells -> release of necrotic products and DAMPs-> activates inflammatory cells.

Cytokines activate pro-survival genes in residual cancer cells-> cancer cells become resistant to following rounds of therapy.

22
Q

Activating Invasion & Metastasis

Invasion of the ECM

A

Detachment and loosening of the intracellular Junctions

ECM degradation due to proteases

Migration: Tumor cells have increased locomotion due to cytokines and motility factors

23
Q

Activating Invasion & Metastasis

Vascular spreading and homing of Tumor Cells

A

STEPS

  1. Clonal expansion, growth, diversification, angiogenesis
  2. Metastatic subclone
  3. Adhesion to and invasion of basement membrane
  4. Passage through the ECM
  5. Intravasation (into blood vessel)
  6. Interaction with host lymphoid cells
  7. Tumor cell embolus
  8. Adhesion to basement membrane
  9. Extravasation (Out of the Vessel)
  10. Metastatic deposit
  11. Angiogenesis,
  12. Growth
24
Q

What theories explain how metastasis occurs?

A

Clonal Evolution model

Rare variant clones in the primary tumor occur and spread.

Metastatic Signature

Some tumors have a high frequency of cells that metastasize

Metastatic Signature with Variants

Some Tumors have a high frequency of cells that have a high probability of metastasizing, some of them become variants and go.

Tumor Stromal Response

The tumor Stromal which forms encourages favorable conditions for metastasic variant formation and eventual metastasis.

25
Q

Genomic Instability

A

Genomic instability can occur due to inherited mutations or DNA damage. Genomic instability is evident in all hereditary cancers.

Breast Cancer

Can be caused by inherited or sporadic mutations in BRCA1 or BRCA2

Ovarian, prostate, Pancrease, and stomach cancers

Can be caused by inherited or sporadic mutations in BRCA2

26
Q

Inducing angiogenesis

A

Small localized tumors can trigger angiogenesis by releasing a signaling molecule, this will stimulate tumor growth through endothelial cell production of growth factor, and influence metastatic potential.

Ex. Hypoxia in tissue-> upregulation of VEGF -> favor angiogenesis

(Tumor needs O2 and nutrients to continue growing)

27
Q

Resisting Cell Death

A

Normal cells have a predominance of proapoptotic proteins and are considered Primed for cell death if needed.

Tumor cells have a predominance of antiapoptotic proteins making them Unprimed.

28
Q

Deregulating cellular Energies

A

In normal Cells

ATP produced via Oxidative phosphorylation and glucose is metabolized to Pyruvate.

Pyruvate reduced to lactate in Anaerobic environment producing less ATP.

In Cancer Cells

85% of Pyruvate pyruvate in malignant cells are fermented into lactate and only 5% of Pyruvate enters TCA cycle. This means that the tumors excrete enough lactase to change the PH of their microenvironment. They make less ATP, but do it extremely fast.

29
Q

Sustaining Proliferative Signaling

A

Normal Cells proliferate by binding Growth Factor to cell surface receptor and activating signal transduction proteins to initiate DNA transcription.

In Cancer

Mutations convert Proto-oncogenes into oncogenes that promote autonomous (abnormal) growth.

30
Q

Growth Factor receptors

A

Tyrosine kinase-mediated signal transduction causes cellular growth apoptosis and cell migration

Mutations or abnormal signaling can inappropriately activate neoplastic growth etc.

31
Q

MYC Oncogenes

A

Malignant transformation can occur after growth factor receptor constitutive activation caused by either mutations or overexpression (MYC Oncogenes)

MYC Oncogene - is most commonly involved in Human Tumors.

There are MYC translocations in Burkitt lymphoma

Burkitt lymphoma - An aggressive type of B-cell lymphoma most often in children and young adults.

MYC overexpression leads to malignancy.

32
Q

Steps of Chemical Carcinogenesis

A
  1. Initiation - Introduction of mutations in the Genome. Either Direct-acting agents (No metabolic conversion needed) or Indirect-acting agents (Metabolic conversion needed.)
  2. Promotion - Induce tumors in previously initiated cells by stimulating proliferation (short-lived, reversible, and non-tumorigenic by themselves).
33
Q

Events in the Initiation step of Chemical Carcinogenesis

A
  1. Carcinogen or Metabolic Electrophilic Intermediates are either Detoxified and excreted or they are not.
  2. Binding to DNA; Adduct formation - one of 3 things occur, Cell repairs, Cell destroyed, or this leads to the Final Event,
  3. Permanent. DNA Lesion: Initiation of Cell
34
Q

Events in the Promotion step of Chemical Carcinogenesis​

A
  1. Cell proliferation: Altered differentiation
  2. Preneoplastic Clone

Proliferation and additional mutations lead to event 3

  1. Malignant Neoplasm
35
Q

Radiation Carcinogenesis

UV Radiation

A

UV Sunlight - Most toxic type of UV radiation comes from UV light-induced photoproducts.

Formation of either Cyclobutane Pyridine Dimers (CPDs) or (6-4) pyrimidine-pyrimidone photoproducts (6-4PPs)

These cause Kinks in the DNA strands.

36
Q

Radiation Carcinogenesis

Ionizing Radiation

A

Ionizing radiation consists of the upper end of UV through x-ray, gamma ray and beyond.

Ionizing radiation either directly damages the DNA or indirectly does so by increasing ROS in a cell.

Pathophys Semester II (14 decks)

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