Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

AUC Molecules to Medicine > Exam 4 > Flashcards

Exam 4 Flashcards

You may prefer our related Brainscape-certified flashcards:
Organic Chemistry 101 flashcards
1
Q

Neoplasia

A

New, uncontrolled growth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Dysplasia

A

Disordered growth with atypia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Hamartoma

A

Wrong tissue, right place. Benign mass

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Choristoma

A

Right tissue, wrong place. Benign mass

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Pleomorphism

A

Cells vary in shapes and are not uniform

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Hyperchromasia

A

Darkly staining chromatin (clumping)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Anaplasia

A

Lack of differentiation between cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Ten Hallmarks of Cancer

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Desmin Stain

A

Views Muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

S100 Stain

A

Views nerves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

CD31 stain

A

Views Blood Vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Adenocarcinoma

A

Malignant tumor of glandular tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Squamous Cell Carcinoma

A

Characterized by keratin pearls/whirls. Very pink

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Breast Cancer

A

Carcinoma, most common cancer among women

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Anaplastic Tumor

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Lymph Channel Spread of Neoplasms

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Tumor Grading

A

How differentiated is the tumor?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Tumor Staging

A

How far spread is the tumor?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Proto-oncogene carcinogenesis

A

Growth-promoting mutation, gain of function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Tumor suppressor gene carcinogenesis

A

Growth-inhibiting mutation. Loss of function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Apoptotic Carcinogenesis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

DNA Repair Carcinogenesis

A

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

23
Q

ERBB1

A

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

24
Q

Her2Neu/ERBB2

A

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

25
Q

FGFR

A

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

26
Q

RET receptor

A

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

27
Q

Cyclin B

A

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

28
Q

Cyclin D

A

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

29
Q

Cyclin E

A

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

30
Q

Cyclin A

A

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

31
Q

KRAS

A

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

32
Q

RAF/BRAF

A

Mutations cause hairy cell leukemia and melanoma

33
Q

PI3K

A

Mutations cause breast carcinoma

34
Q

PTEN

A

A suppressor which causes endometrial carcinoma when mutated

35
Q

MYC

A

Amplified in many cancers

36
Q

C-MYC

A

Activated by chromosomal a translocation in Burkitt’s lymphoma

37
Q

N-MYC

A

Amplified in neuroblastoma

38
Q

Philadelphia Chromosome

A

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

39
Q

Burkitt Lymphoma

A

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

40
Q

Follicular Lymphoma

A

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

41
Q

Acute Promyelocytic Leukemia

A

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

42
Q

Synovial Sarcoma

A

X:18 SYT-SSX Translocation

43
Q

Renal Cell Carcinoma

A

X:17 Xp11 translocation

44
Q

Ewing Sarcoma

A

11:22 EWS-FLI1 (transcription factor) translocation

45
Q

P53

A

A gene whose expression induces apoptosis

46
Q

RB

A

A gene whose expression stops progression through G1-S checkpoint

47
Q

Retinoblastoma

A

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.

48
Q

MDM2

A

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

49
Q

APC

A

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.

50
Q

BRCA1 and BRCA2

A

Tumor suppressor genes implicated in breast cancer.

51
Q

NF1

A

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

52
Q

Bcl-2 and Bcl-xL

A

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

53
Q

Bax and Bak

A

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

54
Q

HNPCC (Lynch Syndrome)

A

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

AUC Molecules to Medicine (1 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions