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Z - M2 Heme/Onc > Heme/Onc - Week 1 Review - Part 1 > Flashcards

Heme/Onc - Week 1 Review - Part 1 Flashcards

1
Q

6 Major Capabilities of Tumors

A

1) Resist Cell Death
2) Sustained Proliferation Signaling
3) Evade Growth Suppression
4) Activating Invasion Metastasis
5) Replicative Immortality
6) Angiogenesis Induction

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2
Q

Cancer Defintions - Hyperplasia vs. Hypertrophy vs. Neoplasia

A

Hyperplasia - Increased cell and tissue growth in normal arrangement
Hypertrophy - Increased Size
Neoplasia - New abnormal and uncoordinated growth - Malignant = invasion + metastasis

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3
Q

Tumor Nomenclature - Epithelial (Benign + Malignant + Example)

Tip - Two Varieties

A

1) Glandular Epithelium
Benign - Adenoma
Malignant - Adneocarcinoma
Ex. Lung Adenocarcinoma

2) Other Tissue
Benign - Papilloma
Malignant - Papillary Carcinoma

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4
Q

Tumor Nomenclature - Mesenchyme (Benign + Malignant + Example)

A

Benign - Lipoma
Malignant - Liposarcoma (Osteosarcoma)
Example - Connective Tissue = Sarcoma

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5
Q

Tumor Nomenclature - Lymphocyte (Benign + Malignant + Example)

A

Benign - No Benign Form
Malignant - Lymphoma/Leukemia
Example - Burkitt’s Lymphoma

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6
Q

Tumor Nomenclature - Melanocyte (Benign + Malignant + Example)

A

Benign - Nevus
Malignant - Melanoma
Example - Skin Cancer

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7
Q

Malignant Distinction (vs. Benign) - 5 Keys

A

1) Differentiation (Extent of Spread)
2) Rate of Growth
3) Local Invasion
4) Metastasis

CLASS KEY - Benign has capsule vs. malignant does not

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8
Q

Benign Tumor Features (5)

A

1) Well Differentiated
2) Cell Uniformity
3) Normal Nuclei/Chromatin
4) Normal Mitotic Rate
5) Tissue Architecture Preserved

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9
Q

Malignant Features (7)

A

1) Well/Poor/Undifferentiated (Can be all)
2) Loss of cell uniformity (pleomorphic = cells look different from one another)
3) Increased Nuclear Size/Cytosol Ratio
4) Hyperchromatic
5) Abnormal Mitosis
6) Loss of Architecture
7) Local Invasion/Metastasis

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10
Q

Tumor Invasion Pathway –> 3 Key Parts

A

1) Epithelial tumor down regulates E-Cadherin to dissociate
2) Cells attach to the lamina and destroy the BM Collagen Type IV via collagenases –> Allows escape to ECM
3) Attach to firbonectin in the ECM to spread

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11
Q

Metastatic Spread - Lymphatic vs. Hematogenous Rules

A

1) Lymphatic - Carcinoma (E.g. Breast)

2) Hematogenous - Sarcoma

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12
Q

Hematogenous Spread Rule Exceptions (4)

A

1) Renal Cell Carcinoma (Renal vein)
2) Hepatocellular Carcinoma (Hepatic Vein)
3) Follicular Carcinoma of the Thyroid
4) Choriocarcinoma

Carcinoma is normal lymphatic metastasis

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13
Q

Immunohistochemistry Stains - 5 Major Intermediate Filament Stains

A

1) Keratin - Epithelium (Carcinoma)
2) Vilnelin - Mesenchyme (Sarcoma0
3) Desmin - Muscle
4) GFAP - Neuroglia (GBM + Astrocytoma)
5) Neurofilament - Neurons

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14
Q

Immunohistochemistry Stain (What Organ) - Keratin

A

Epithelium (Carcinoma)

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15
Q

Immunohistochemistry Stain (What Organ) - Vilnelin

A

Mesenchyme (Sarcoma)

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16
Q

Immunohistochemistry Stain (What Organ) - PSA

A

Prostate Epithelium

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17
Q

Immunohistochemistry Stain (What Organ) - ER

A

Estrogen Receptor - Breast Epithelium

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18
Q

Immunohistochemistry Stain (What Organ) - Thyroglobulin

A

Thyroid Follicular Cells

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19
Q

Immunohistochemistry Stain (What Organ) - CHromogramin

A

Neuroendocrine Cells

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20
Q

S-100

A

Melanoma

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21
Q

B-Cell Lymphoma Translocations (4)

A

All switch with the IgH section of chromosome 14 - Results in Super-active proteins

t3: 14 - Bcl6 - Diffuse Large B-Cell Lymphoma - Excess Bcl6 prevents apoptosis
t8: 14 - c-myc - Burkitt Lymphoma - Oncogene
t11: 14 - Cyclin D1 - Mantle Cell Lymphoma
t18: 14 - Bcl2 - Follicular (Small B-Cell Lymphoma) - Prevents apoptosis

22
Q

t:18:14 - Protein + Disease

A

Bcl2 - Follicular Lymphoma

23
Q

t11:14 - Protein + Disease

A

Cyclin D1 - Mantle Cell Lymphoma

24
Q

t:8:14 - Protein + Disease

A

C-Myc - Burkitt’s Lymphoma

25
Q

t3:14 - Protein + Disease

A

Bcl6 - Diffuse Large B-Cell Lymphoma

26
Q

Ras Protein Family - Normal Function + Mechanism of Oncogenesis + Associated Malignancy

A

Normal Function - GPCR Linked - Needs to remove the GTP to turn off

Mechanism of Onc. - mutation prevents GAP proteins from turning GTP off - Amplificaiton of growth signals

Diseases - Most common ONCOGENE (p53 = most common overall)

27
Q

C-Myc - Normal Function + Mechanism of Oncogenesis + Associated Malignancy

A

Normal Function - Nuclear transcription factor

Mechanism of Onc. - t8:14 Translocation

Diseases - Burkitt Lymphoma - (C-K) - EBV/HIV Associated

Also assocaited with nasopharyngeal carcinoma in Asian Males

28
Q

N-Myc - Normal Function + Mechanism of Oncogenesis + Associated Malignancy

A

Normal Function - Nuclear transcription factor

Mechanism of Onc. - Amplification

Diseases - Neuroblastoma (N-N)

29
Q

L-Myc - Normal Function + Mechanism of Oncogenesis + Associated Malignancy

A

Normal Function - Nuclear transcription factor

Mechanism of Onc. - Amplification

Diseases - Small Cell Lung Carcinoma (L-L)

30
Q

Platelet Derived GF - Normal Function + Mechanism of Oncogenesis + Associated Malignancy

A

Normal Function - To Much Stimulation

Mechanism of Onc. - Autocrine overstimulation (make to much and keep turning the same cell on)

Diseases - Astrocytoma + GBM

31
Q

HER/Neu GF - Normal Function + Mechanism of Oncogenesis + Associated Malignancy

A

Normal Function - Epidermal Growth Factor Receptor - Small GF Stimulus massive response

Mechanism of Onc. - Amplication (Key)

Diseases - Subset of Breast Cancer - Treat with Tranmusamab

32
Q

RET GF - Normal Function + Mechanism of Oncogenesis + Associated Malignancy

A

Normal Function - Neural - Growth Factor Receptor - Small GF Stimulus massive response

Mechanism of Onc. - Point Mutation

Diseases - Multiple Endocrine Neuoplasion = Thyroid Carcinoma + EGFR Lung Adenocarcinoma

33
Q

c-KIT GF - Normal Function + Mechanism of Oncogenesis + Associated Malignancy

A

Normal Function - Stem Cell Growth Factor Receptor - Small GF Stimulus massive response

Mechanism of Onc. - Amplification

Diseases - GI Stromal Tumor (GIST)

34
Q

ABL - Normal Function + Mechanism of Oncogenesis + Associated Malignancy

A

Normal Function - Tyrosine Kinase

Mechanism of Onc. - t9:22 - Translocation with BCR

Diseases - CML + Some Types of ALL

35
Q

Jax2 - Normal Function + Mechanism of Oncogenesis + Associated Malignancy

A

Normal Function - Tyrosine Kinase

Mechanism of Onc. - Amplification

Diseases - Polycythemia Vera + ET

36
Q

CCND1 (Cyclin D1) -Normal Function + Mechanism of Oncogenesis + Associated Malignancy

A

Normal Function - Cylcin - must be elevated for G1-S Phase Transition

Mechanism of Onc. - t:11:14

Diseases - Mantle Cell Lymphoma (Edge of Follicle)

37
Q

CDK4 - Normal Function + Mechanism of Oncogenesis + Associated Malignancy

A

Normal Function - Increased levels for G1-S Transition

Mechanism of Onc. - Amplification

Diseases - Melanoma

38
Q

t9:22 - Protein + Disease

A

BCR-Abl

CML + Adult ALL

39
Q

Rentinoblastoma Protein - Function + 2 Examples

A

Retinoblastoma is phosphorylated by cyclin - when phosphorylated it no longer blocks (EF2 and no longer prevents transcription)

E.g. To much cyclin = transcription because retinoblastoma is phosphorylated

E.g. knocked out = no inhibition of EF2 and transcriptions

40
Q

Retinoblastoma Mutations (2)

A

1) Autosomal Dominant - Promotes hypermethylation - High risk of developing retinoblastoma
2) Sporadic - Need 2 random mutations in same cell - very rare

41
Q

p53 - Function + Mechanism + Key Fact

A

1 Gene mutation in cancer (Ras = #1 oncogene)

Function - Inhibits G1-S Phase

Mechanism - Cell Cycle Arrest + Apoptosis + Senescence

42
Q

Li-Fraumeni Syndrome

A

Autosomal Dominant Predisposition to concer - p53 mutation

43
Q

Adenomatous Polyposis COli (APC) - Function + Neo-Genesis

A

Function - Tumor suppressor that destroys Beta-Catenin

Knock out APC - Beta Catenin build-up - increased transcription - Very common in colon cancer

44
Q

Familial Adenomatous Polyposis

A

Autosomal Dominant - APC Absent - Only need one mutation to loss it - 100% will develop colon cancer by age 35-40

45
Q

Neo-Angiogenesis - Pathway

A

VGEF (Proangiogenic) vs. Thrombospondind (Anti-Angiogeneic)

Hypoxia –> HIF-1Alpha - INcreases VGEF) - Aloows tumors to grow greater than 1-2 mm

46
Q

Von-Hippel-Lindaue Syndrome

A

Autosomal dominant - predisposes to development of hemangioblastomic and phechromocytomas

47
Q

Avoiding Immune Detection - Pathway

A

Normally - MHC-1 presents antigens from inside the cell that are not “self” - CD8 Cells destroy the cell

Tumor down regulate MHC-1 to avoid CD8 destruction but can be killed by NK Cells which recognize cells without MHC

48
Q

Key Tumor Antigens (3)

A

1) Mucin
2) CEA
3) CD20 - B-Cells

49
Q

Example of a Tumor Inducing Gain of Function Deletion

A

1) TALL - Deletion brings the TAL1 gene right next to a promotor - leads to ALL

50
Q

Lynch Syndrome

A

Familial Risk of Colon Cancer - Mutation in mismatch repair genes - loss of DNA Proof Reading - Microsatalite instability

Z - M2 Heme/Onc (10 decks)

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