Pathology: Neoplasia Block I

Front 1

Autonomous growth of a clonal cell population that may produce a puposeless mass

Back 1

Neoplasm

Front 2

The suffix ______ always denotes a tumor or mass lesion which is most often benign and rarely, uncertain.

Back 2

Oma

Front 3

Malignant neoplasms carry the suffix _______ if they are of epithelial origin.

Back 3

Carcinoma

Front 4

Malignant neoplasms carry the suffix _______ if they are of mesenchymal origin.

Back 4

Sarcoma

Front 5

This suffix is often added to imply origin from an embryonic or primitive cell type. Most such tumors are encountered in children and their growth is usually fast or aggressive

Back 5

Blastoma

Front 6

Early on, neoplasms show what kind of cell differentiation?

Back 6

Early on, neoplasms have architecture and cellular features very close to the normal tissue and are well differentiated.

Front 7

As the neoplasm progresses to malignant, what kind of cell differentiation is seen?

Back 7

The tissue architecture and cellular features become less and less identifiable and poorly differentiated.

Front 8

________ is the most common genetic disorder.

Back 8

Cancer

Front 9

Abnormalities in which two things cause cancer?

Back 9

1) Abnormalities in DNA of genes that control cellular proliferation
2) And genes that control genetic stability

Front 10

Cyclins, RAS, N-myc, and Her2-neu genes belong to which class of genes that may lead to carcinogenesis?

Back 10

Proto-Ocogenes

Front 11

P53, Retinoblastoma (RB) or APC genes belong to which class of genes that may lead to carcinogenesis?

Back 11

Growth inhibiting tumor supressor genes

Front 12

BLC2 gene belongs to which class of genes that may lead to carcinogenesis?

Back 12

Genes that regulate programmed cell death (apoptosis)

Front 13

BRCA1 and BRCA2 genes belong to which class of genes that may lead to carcinogenesis?

Back 13

Genes that regulate repair of damaged DNA.

Front 14

Mutant alleles of proto-onco genes are ________.

Back 14

Dominant- they transform cells despite the presence of their normal counterpart.

Front 15

Mutants of tumor supressor genes are _______.

Back 15

Recessive- both normal alleles of tumor supressor genes must be damaged for transformation to occur.

Front 16

The ultimate outcome of all growth promoting stimuli is _______________________.

Back 16

The entry of quiescent cells into the cell cycle.

Front 17

Name the three stages a cell can exist in:

Back 17

(1) Quiescent/Stable
(2) Permanent
(3) Continuously Cycling Labile Cells

Front 18

RAS is inactive in its ____ bound state.

Back 18

GDP

Front 19

Activated RAS recuits RAF and stimulates which pathway to transmit growth promoting signals to the nucleus?

Back 19

MAP-Kinase

Front 20

About 30% of all human tumors contain mutated versions of ____ ________.

Back 20

Ras Proteins

Front 21

Mutation of _____ ______ is the single most common abnormality of dominant oncogenes in human tumors.

Back 21

Ras Genes

Front 22

In some cases, oncogenes are activated via _____ as in CML and ABL-BCR hybrid gene.

Back 22

Translocation

Front 23

This gene encodes a transmembrane glycoprotein receptor with intrinsic tyrosine kinase activity. It is amplified in about 25-30% of breast cancers.

Back 23

Her2 Gene

Front 24

This gene is amplified in breast cancer and its overexpression leads to an increase in mitogenic cell signaling and increased cell proliferation:

Back 24

HER2 Gene

Front 25

This drug is a good example of targeted immunotherapy, targets the HER2 oncogene receptor:

Back 25

Herceptin

Front 26

_______ and ______ play a significant role in regulating the G1-S checkpoint of the cell cycle.

Back 26

RB and cyclins.

Front 27

The phosphorylation of RB is inhibited by cyclin inhibitors (CKIs) because they inactivate ______.

Back 27

Cyclin-CDK Complexes

Front 28

Name the four genes that regulate phosphorylation of RB:

Back 28

1. RB1
2. CDK4
3. Cyclin D proteins
4. CDKN2A

Front 29

Virtually all cancel cells show dysregulation of the _______ checkpoint. How is it regulated?

Back 29

G1-S- regulated by phosphorylation of RB

Front 30

This tumor supressor gene product is critical to maintaining the integrity of the genome. It is the single most common target for genetic alterations in human cancer.

Back 30

P53

Front 31

Prevents apoptosis by blocking the channel-forming activity of bax, a pro-apoptotic member of the bcl2 family. This blocking of apoptosis allows lymphocytes to accumulate and allows other mutations to supervene, which may lead to formation of lymphoma:

Back 31

Bcl-2

Front 32

Bax dimerization leads to channel formation in the mitochondrial membrane and subsequent release of ___________. What is the significance of this step?

Back 32

Cytochrome C- release of cytochrome C appears to be a critical step in apoptosis.

Front 33

What are the two tumor supressor pathways that regulate cell senescence?

Back 33

P53 and RB tumor supressor pathways

Front 34

_______ is due to the shortening of chromosomal telomeres due to the inability of DNA polymerases to completely replicate the ends of chromosomal DNA that occurs as normal cells undergo repeated rounds of DNA replication in cell cycles.

Back 34

Crisis

Front 35

________ _________ lengthens the telomeric DNA by adding DNA repeats to the chromosome ends. It is absent in most somatic cells and present in the vast majority of human tumors.

Back 35

Telomerase activity.

Front 36

Name the three types of carcinogens:

Back 36

1. Chemical (Aflatoxin, Asbestos)
2. Physical (UV, X-Rays)
3. Biological (Viral)

Front 37

A healthy liver is the major player in the defense against _______ ________ and exposure is almost always associated with hepatic injury as well.

Back 37

Chemical Carcinogen

Front 38

The model system for ______ carcinogenesis is the two step process if initiation and promotion.

Back 38

Chemical Carcinogenesis

Front 39

This condition results in faulty repair of DNA damage caused by high energy photons in physical carcinogenesis.

Back 39

Xeroderma Pigmentosum

Front 40

Papova, Herpes, Hepatitis, Pox and Adeno are all viruses in which class?

Back 40

Onco-DNA viruses- They're all viral carcinogens

Front 41

Transform cells by integrating their oncogenic DNA directly into the host cell genome.

Back 41

Onco-DNA viruses

Front 42

This virus causes squamous papilloma (warts) and squamous cell carcinoma

Back 42

HPV

Front 43

This virus causes lymphomas

Back 43

EBV (Epstein-Barr Virus)

Front 44

This virus causes hepatocellular carcinoma

Back 44

HBV (Hepatitis B)

Front 45

This virus causes Kaposi's sarcoma, lymphoma

Back 45

KSHV (Kaposi's Sarcoma Herpes Virus)

Front 46

This RNA virus causes T cell leukemia

Back 46

HTLV-1

Front 47

These early gene products block apoptosis and remove restraints to cell proliferation.

Back 47

E6 and E7 Proteins

Front 48

This cancer syndroms is autosomal dominant, leads to predisposition to rare types of cancer such as retinoblastoma and familial adenomatous polyposis of colon.

Back 48

Inherited Cancer Syndromes

Front 49

Name five types of inherited cancer syndromes:

Back 49

1. Retinoblastoma
2. Multiple endocrine neoplasia
3. Neurofibromitosis
4. Von Hippel-Lindau Syndrome
5. FAPC