Exam 3: Cancer I

Question 1

significance of palladin

Answer 1

palladin encodes an essential component of a cell’s cytoskeleton; when mutated palladin contributes to the spread of pancreatic cancer

Question 2

pancreatic cancer is inherited as an _ trait in a family that possesses a mutant palladin gene

Answer 2

autosomal dominant trait; single aa change (highly conserved gene) that segregated with the cancer = autosomal dominant

Question 3

how palladin was discovered

Answer 3

used many pedigrees to find a gene that is mutated in a familial form of pancreatic cancer

Question 4

cancer is a group of diseases characterized by

Answer 4

cell proliferation

Question 5

tumor formation: a distinct mass of

Answer 5

abnormal cells

Question 6

benign tumor

Answer 6

the tumor remains localized

Question 7

malignant tumor

Answer 7

tumor cells invade other tissues

Question 8

metastasis

Answer 8

the tumor cells induce secondary tumors

Question 9

abnormal proliferation of cancer cells produces a tumor that

Answer 9

crowds out normal cells

Question 10

genetic evidence for cancer

Answer 10

carcinogens, chromosomal abnormalities, inheritance

Question 11

Knudson’s multistep model of cancer

Answer 11

requires several mutations

Question 12

the clonal evolution of tumors

Answer 12

tumor cells acquire more mutations that allow them to become increasingly more aggressive in their proliferative properties

Question 13

knudson’s 2 hit hypothesis

Answer 13

knudson proposed it requires more than one mutation to result in cancer (multistep process) you first get a somatic mutation, then a second mutation in that same cell that induces uncontrolled mitosis

Question 14

sporadic cancer

Answer 14

first somatic mutation and rarely, a single cell undergoes two somatic mutations but it does in the case of sporadic cancer resulting in a single tumor (2 hits required)

Question 15

hereditary cancer

Answer 15

a predisposed person inherits one mutation or one gene that is an oncogene/an activator (only one hit required) now have 50% greater chance of having a second mutation

Question 16

_ are required to produce cancerous cells

Answer 16

multiple mutations

Question 17

through clonal evolution, tumor cells acquire _

Answer 17

multiple mutations that allow them to become increasingly aggressive and proliferative (fast cell growth and instability of the genome = accumulation of mutations)

Question 18

main point of the various kinds of drivers of tumorigenesis/oncological progression of different kinds of cancers

Answer 18

looking for a description of the genetic steps to the different types of cancers/end result; various different pathways leads to the progression of a cancer and different phylogenetic mechanisms and/or different combinations of genetic mutations get to the point of cancer progression

Question 19

_ is the singular key event in cancer

Answer 19

genomic instability; leads to accumulation of more mutations (activating oncogenes and inactivation tumor suppressors)

Question 20

genomic instability leads to

Answer 20

mutations that activate all of the secondary hallmark events

Question 21

in hereditary cancers, the establishment of _ is probably the initiating event which then facilitates the establishment of _

Answer 21

genomic instability; establishment of all the other hallmarks

Question 22

in sporadic cancers (non-hereditary), _ may be the the initiating event which leads to DNA damage and DNA replication stress which, in turn, leads to _

Answer 22

deregulation of growth-regulating genes; leads to genomic instability and selective pressure for tumor suppressor p53 inactivation

Question 23

secondary hallmarks

Answer 23

oxidative stress and proteotoxic stress

Question 24

metabolic stress

Answer 24

ex is obesity; incr metabolic stress

Question 25

evading immune surveillance

Answer 25

surviving protection mechanisms

Question 26

angiogenesis/blood supply

Answer 26

blood supply to tumors

Question 27

activated growth signalling

Answer 27

continuous supply of growth signalling molecules

Question 28

evading apoptosis

Answer 28

getting around protection mechanisms

Question 29

evading cell death and senescence

Answer 29

avoid telomere shortening; unlimited ability to reproduce

Question 30

cancer is a _ disease but most are not inherited

Answer 30

genetic disease

Question 31

factors contributing to cancer (4)

Answer 31

1. tobacco use
2. obesity
3. alcohol
4. UV radiation
   * environmental contributions*

Question 32

we do not understand why there are different rates for the different types of cancers, either genetically or environmentally so what has been implemented?

Answer 32

cancer registries; we have to know what the targetable genes for cancer are. collecting information and characterizing all cancers by looking at drivers of cancer and looking for commonalities there to show a weak point that can be targeted for intervention

Question 33

although all cancers are heterogeneous, there are many shared lesions within pathways. Why would this be?

Answer 33

this would be bc clonal mutations are shared by all cells in a tumor, as clonal evolution allows tumor cells to acquire multiple mutations that allow them to become increasingly aggressive and proliferative, and then the tumor cells may harbor subclonal mutations that incur genomic differences

Question 34

tumor heterogeneity refers to

Answer 34

Tumor heterogeneity refers to observations that although cancer formation is believed to be a clonal process beginning with a single transformed cell, not all malignant cells within a tumor are the same.

Question 35

oncogenes

Answer 35

mutated, dominant-acting stimulatory genes that cause cancer

Question 36

proto-oncogenes

Answer 36

responsible for basic cellular functions in normal cells; when mutated, they become oncogenes

Question 37

difference btwn oncogenes and proto-oncogenes

Answer 37

oncogenes are important during early embryological development when we have fast dividing cells and are supposed to be turned off after a certain developmental milestone. proto-oncogenes are not yet turned on to cause cancer but when a certain point of genomic instability is reached, it allows reactivation of oncogenes

Question 38

loss of heterozygosity

Answer 38

is a gross chromosomal event that results in loss of the entire gene and the surrounding chromosomal region; contributes to loss of tumor suppressor genes

Question 39

oncogenes acquire mutations that allow

Answer 39

them to be reactivated

Question 40

proto-oncogenes normally produce

Answer 40

factors that stimulate cell division

Question 41

mutant alleles (oncogenes) tend to be _

Answer 41

dominant; one copy of the mutant allele is sufficient to induce excessive cell proliferation (single hit)

Question 42

tumor-suppressor genes normally produce

Answer 42

factors that inhibit cell division

Question 43

mutant alleles (tumor suppressor genes) are _

Answer 43

recessive; both alleles must be mutated to produce excessive cell proliferation (double hit)

Question 44

both oncogenes and tumor suppressor genes contribute to cancer but differ in their

Answer 44

modes of action and dominance

Question 45

people heterozygous for a tumor-suppressor gene are predisposed to cancer, why?

Answer 45

there is some genomic instability here, one tumor suppressor gene is already inactivated, and this incr the chance knocking out the other so one hit instead of 2 is needed; often a deletion (common part of chromosome is lost)

Question 46

normal function of p53

Answer 46

regulates cell division, apoptosis, DNA repair, and other functions