Exam 4

Question 1

Neoplasia

Answer 1

New, uncontrolled growth

Question 2

Dysplasia

Answer 2

Disordered growth with atypia

Question 3

Hamartoma

Answer 3

Wrong tissue, right place. Benign mass

Question 4

Choristoma

Answer 4

Right tissue, wrong place. Benign mass

Question 5

Pleomorphism

Answer 5

Cells vary in shapes and are not uniform

Question 6

Hyperchromasia

Answer 6

Darkly staining chromatin (clumping)

Question 7

Anaplasia

Answer 7

Lack of differentiation between cells

Question 8

Ten Hallmarks of Cancer

Answer 8

Irrigateds (Invasion/metastasis, replicative immortality, resisting death, inducing angiogenesis, genomic instability, avoids immune destruction, tumor promoting inflammation, evades growth suppressors, deregulates energetics, sustains proliferation signals)

Question 9

Desmin Stain

Answer 9

Views Muscle

Question 10

S100 Stain

Answer 10

Views nerves

Question 11

CD31 stain

Answer 11

Views Blood Vessels

Question 12

Adenocarcinoma

Answer 12

Malignant tumor of glandular tissue

Question 13

Squamous Cell Carcinoma

Answer 13

Characterized by keratin pearls/whirls. Very pink

Question 14

Breast Cancer

Answer 14

Carcinoma, most common cancer among women

Question 15

Anaplastic Tumor

Answer 15

A tumor that lacks differentiation, obscuring origin. Often malignant and aggressive with a poor prognosis

Question 16

Lymph Channel Spread of Neoplasms

Answer 16

Most often by carcinomas. Renal cell, Hepatocellular, Follicular carcinoma of the thyroid, and choriocarcinoma are the most common types.

Question 17

Tumor Grading

Answer 17

How differentiated is the tumor?

Question 18

Tumor Staging

Answer 18

How far spread is the tumor?

Question 19

Proto-oncogene carcinogenesis

Answer 19

Growth-promoting mutation, gain of function

Question 20

Tumor suppressor gene carcinogenesis

Answer 20

Growth-inhibiting mutation. Loss of function

Question 21

Apoptotic Carcinogenesis

Answer 21

Mutation in genes that regulate cell death. Can be gain of function or loss of function.

Question 22

DNA Repair Carcinogenesis

Answer 22

Genomic instability mutation, increases likelihood of all mutations. Loss of function

Question 23

ERBB1

Answer 23

Can cause breast cancer, lung adenocarcinoma, stomach cancer, ovarian cancer, and uterine cancer when turned on non-stop. Mutation of ERBB1 causes lung adenocarcinoma

Question 24

Her2Neu/ERBB2

Answer 24

Can cause breast cancer, lung adenocarcinoma, stomach, ovarian, and uterine cancer with a bad prognosis in breast cancer when turned on non-stop

Question 25

FGFR

Answer 25

Mutation causes breast, lung, brain, stomach, and more cancers

Question 26

RET receptor

Answer 26

MEN 2A and MEN 2B, familial medullary thyroid carcinoma

Question 27

Cyclin B

Answer 27

Binds to CDK 1 to progress the cell from G2 to M phase

Question 28

Cyclin D

Answer 28

Binds to CDK 4/6 to progress the cell from G1 to the restriction point

Question 29

Cyclin E

Answer 29

Binds to CDK 2 to progress the cell from G1 to S phase

Question 30

Cyclin A

Answer 30

Binds to CDK 2 to progress the cell from S to G2 phase

Question 31

KRAS

Answer 31

Mutations call 90% of all pancreatic adenocarcinoma, 50% of all colon, endometrial, and thyroid cancers

Question 32

RAF/BRAF

Answer 32

Mutations cause hairy cell leukemia and melanoma

Question 33

PI3K

Answer 33

Mutations cause breast carcinoma

Question 34

PTEN

Answer 34

A suppressor which causes endometrial carcinoma when mutated

Question 35

MYC

Answer 35

Amplified in many cancers

Question 36

C-MYC

Answer 36

Activated by chromosomal a translocation in Burkitt’s lymphoma

Question 37

N-MYC

Answer 37

Amplified in neuroblastoma

Question 38

Philadelphia Chromosome

Answer 38

CML — BCR-ABL1 fusión gene from a 9:22 translocation. Creates a fusion gene with continuous activation of intracellular tyrosine kinase.

Question 39

Burkitt Lymphoma

Answer 39

8:14 c-MYC translocation, causes lymphocyte proliferation and has amplification

Question 40

Follicular Lymphoma

Answer 40

14:18 Bcl-2 (anti-apoptosis) Translocation causing overexpression

Question 41

Acute Promyelocytic Leukemia

Answer 41

15:17 PML- RAR alpha, a transcription factor translocation

Question 42

Synovial Sarcoma

Answer 42

X:18 SYT-SSX Translocation

Question 43

Renal Cell Carcinoma

Answer 43

X:17 Xp11 translocation

Question 44

Ewing Sarcoma

Answer 44

11:22 EWS-FLI1 (transcription factor) translocation

Question 45

P53

Answer 45

A gene whose expression induces apoptosis

Question 46

RB

Answer 46

A gene whose expression stops progression through G1-S checkpoint

Question 47

Retinoblastoma

Answer 47

Cancer almost exclusively in children <5 yo. Detected by white reflex. Caused by mutations in the RB gene, deactivating it and causing E2F to be over expressed.

Question 48

MDM2

Answer 48

A gene which keys p53 levels low in any given cell. Overexpression prevents p53 from inducing apoptosis

Question 49

APC

Answer 49

Polyubiquinates Beta-catenin in colon. Mutation causes increased levels of Beta-catenin, which in turn causes increased transcription of c-MYC and leads to colon polyps and cancer.

Question 50

BRCA1 and BRCA2

Answer 50

Tumor suppressor genes implicated in breast cancer.

Question 51

NF1

Answer 51

Tumor suppressor gene that normally inactivated RAS proto-oncogene. Mutation causes dysfunctional NF1, hyperactive RAS, and tumor formation leading to Neurofibromatosis.

Question 52

Bcl-2 and Bcl-xL

Answer 52

Sequesters pro-apoptotic proteins to encourage cell proliferation. P53 binds these proteins and releases the pro-apoptotic proteins

Question 53

Bax and Bak

Answer 53

Pro-apoptotic proteins typically sequestered by Bcl-2 and Bcl-xL. Released by P53.

Question 54

HNPCC (Lynch Syndrome)

Answer 54

Autosomal dominant, most common cause of hereditary colon cancer. Defect in DNA mismatch repair genes, causing micro satellite instability.