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Genetics > Exam 3: Cancer III > Flashcards

Exam 3: Cancer III Flashcards

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Biology 101 flashcards
1
Q

(retro)viruses introduce

A

genomic instability; an additional way to introduce instability in genomes

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2
Q

retroviruses cause cancer by (2)

A
  1. mutating and rearranging proto-oncogenes

2. inserting strong promoters near proto-oncogenes (overexpression)

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3
Q

why might a virus be associated with a specific type of cancer? if it is inserting at random in the genome, why does that lead to one type of cancer?

A

critical word is: if. a virus has certain repeated sequences in it’s genetic code and our genome has similar sequences in parts of it. similarity in those regions of our genome and viral sequences makes a virus more likely to insert in those regions. virus is finding the parts of our genome that is more conducive to its integration and those parts of the genome contain genes that promote cervical, penile, and vulvar cancers.

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4
Q

monoclonal antibodies production

A

take a protein (cell surface protein on lymphoma) you want to develop ab against, make lots of it, and inject in an animal. animal creates abs and take their spleen cells and fuse them w. myeloma cells and convert them into immortalized cells and purify the cells that make mass amts of abs and insert into humans

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5
Q

monoclonal antibodies target _

A

cancer cell specific antigens

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6
Q

monoclonal antibodies induce _

A

an immunological response against the target cancer cell

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7
Q

what can be coupled to an antibody

A

a toxin, radioisotope, cytokine or ther active conjugate

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8
Q

antibody therapy for cancer: direct tumor cell killing can be elicited by

A

receptor agonist activity, such as an antibody binding to a tumor cell surface receptor and activating it

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9
Q

antibody therapy for cancer: direct tumor cell killing activation leads to

A

apoptosis

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10
Q

antibody therapy for cancer: direct tumor cell killing can also be mediated by

A

receptor agonist activity, such as an antibody binding to a cell surface receptor and blocking dimerization, kinase activation and downstream signaling, leading to reduced proliferation and apoptosis

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11
Q

antibody therapy for cancer: immune-mediated tumor killing can be carried out by

A

the induction of phagocytosis, complement activation, antibody-dependent cellular cytotoxicity, genetically modified T cells etc w/ T cells

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12
Q

antibody therapy for cancer: vascular and stromal cell ablation can be induced by

A

vasculature receptor antagonism or ligand trapping, stromal cell inhibition; MAC, MHC, NK

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13
Q

what type of drug is rituximab

A

chimeric monoclonal antibody

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14
Q

mode of action for rituximab

A

targets protein CD20 for elimination; these cells are found on the surface of immune system B cells

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15
Q

rituximab is used to treat

A

treat diseases which are characterized by excessive numbers of B cells, overactive B cells, or dysfunctional B cells ie lymphomas, leukemias, transplant rejection, and autoimmune disorders

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16
Q

ADCC

A

a rituximab proposed mech: attracts natural killer cells, T cells and macrophages (recognizing and killing antibody-labeled target cells, leading to cell lysis)

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17
Q

CDC

A

a rituximab proposed mech: binding of the antibody recruits complement proteins, which punch holes in the cell membrane, flooding the cell and leading to cell lyisis

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18
Q

a rituximab proposed mech: apoptosis

A

binding of the antibody signals the cell to self-destruct

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19
Q

cancer immunotherapy

A

the science of mobilizing the immune system to kill cancer

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20
Q

researchers are racing to expand the use of immunotherapy to benefit more cancer patients but it remains unclear why

A

only a subset of individuals respond to treatment and how to better achieve sustained remissions

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21
Q

cancer immunotherapy -these lines of research, along with growing evidence that the _ plays a defining role in immunotherapy response, are charting innovative paths toward truly _ medicine

A

gut microbiome; personalized medicine

22
Q

why CRISPR is called molecular scissors

A

hijack bacteria ability to store a virus’s invader dna in its own dna. makes a copy of the viral dna to give to protein (cas9) that will cut any future invasions with the copy/match to that stored dna; programmable protein to use as a tool to cut dna based on instructions (rna) that matches to invading dna

23
Q

CRISPR can be used as a tool to

A

edit genes and create designer immune cells programmed to hunt out and kill (ex drug resistant leukemia)

24
Q

PD-1 blockade therapy

A

cancer cells can sense they are being attacked from T cells by recognizing a certain cytokine produced from the T cell. upon recognition, the cancer cell expresses and reactivates PD-L1 on its surface which turns off T cells attacking the tumor. blockade of PD-L1 with therapeutic antibodies takes away the signal preventing T cells from attacking the cancer and leads to tumor infiltration

25
Q

CAR-T therapy has remarkable responses for patients with

A

B cell malignancies

26
Q

how does CAR-T therapy work

A

(T cells gene-engineered with chimeric antigen receptors) get pts blood with T cells, insert CAR gene that targets cancer cells into them (antigen), grow them, insert CAR T cells back into pt

27
Q

antibody therapy for cancer

A

monoclonal antibodies

28
Q

rituximab origin

A

approved by the USFDA in 1997 to treat B-cell non-Hodgkin lymphomas resistant to other chemotherapy regimens

29
Q

ultimate end goal of rituximab

A

elimination of B cells (including the cancerous ones) from the body, allowing a new population of healthy B cells to develop form the lymphoid stem cells

30
Q

the cancer immunotherapy revolution

A

newly approved immunotherapies include drugs that can manipulate components of the immune sys and methods to genetically engineer pts own T lymphocytes to recognize and attack their tumors

31
Q

researchers are racing to expand the use of immunotherapy bc

A

to benefit more cancer pts; clinical trials underway to see if combination therapy works. unraveling the cellular and molecular basis of treatment resistance should facilitate rational design of new mechanism-based studies and advances in genome sequencing are identifying predictive biomarkers and facilitating the design of personalized vaccines that target pt-specific tumor neoantigens

32
Q

antibody constructs and potential uses in oncology

A

if you can pinpoint a specific protein to a cancer (primarily in a cancer), can develop an ab against it as an effective tool to target those cancer cells for elimination

33
Q

canine lifetime health project

A

observational study (no intervention); pet dogs boast important virtues as a genetic model. there are lots of them and they suffer from many of the same diseases that humans do

34
Q

important of purebred dogs

A

(heavily inbred) tend to have less genetic variation than humans, allowing scientists to sniff out harmful gene mutations more easily

35
Q

significance of golden retrievers

A

popularity and vulnerability to cancer (60%); gather information ie epidemiology on golden retrievers and cancer occurence. environmental and health data for the occurence of cancer

36
Q

how is the canine lifetime health project conducted

A

each year, owners and their participating dog’s vet fill out comprehensive questionnaires; the vet also collects biological samples (hair, nails, blood, urine, and feces) and the dog undergoes a complete physical exam

37
Q

KC researchers testing dog vaccine for use against child brain cancer

A

to battle glioblastoma a particular aggressive form on brain cancer; using data that already exist on the treatment’s safety and effectiveness in dogs

38
Q

medicare will reimburse next-generation genomic sequencing test implications

A

medicare is paying for next-generation genomic sequencing tests which means private insurance is soon to follow; genomic sequencing is becoming a widespread tool that most people will have access to

39
Q

precision genetic testing in cancer diagnosis and therapy as well as FDA approved genetic diagnostic tools

A

different sequencing platforms that will give you a clinical report to make decisions on. sequence genes, look for chromosomal rearrangements, etc and provide high resolution genomic analysis on well known and described genes in promoting cancer. also, these companies will look at other genes in the background as well as specific genes (whole genome sequencing)

40
Q

real life results of FDA approved genetic diagnostic tools: simplified test results provide clear information about

A

companion diagnostic alterations and their associated targeted therapies. also provide clinically significant alterations and available clinical trials specific to each pts cancer

41
Q

FDA-approved therapies

A

list of FDA-approved companion diagnostics to identify pts who may benefit from associated therapies

42
Q

potential resistance to therapy interventions

A

pts may be resistant to therapy based on genomic profile or if some of the cells that are not killed by the chemotherapy mutate (change) and become resistant to the drug. and, altogether, cancer cells may develop a mechanism that inactivates the drug

43
Q

professional services with precision genetic testing

A

interpretive content that can be used for pt management in accordance w/ professional guidelines in oncology

44
Q

the cancer genome atlas (TCGA)

A

research program (comparison study) that identifies the genomic changes in more than 20 different types of human cancer. TCGA will help us to understand what turns a normal cell into a cancer cell

45
Q

TCGA: by comparing DNA from normal and cancer tissue, we have already learned that: (2)

A
  1. there are certain areas of the genome commonly affected in several types of cancers
  2. specific changes, aka signatures, allow us to tell one type of cancer from another
46
Q

what do signature help physicians identify

A

signatures help physicians identify specific types of cancer, which may respond differently to various treatments or have different prognosis

47
Q

what pathways are changed when areas of our genome are affected

A

changes in our genome affect genes that control pathways in cells that cause cells to divide and survive when they normally would die

48
Q

shared target genes in various types of cancers

A

attempt to identify underlying patterns that can be exploited for therapeutic intervention; naive as we can not point to one mechanism all we know is that they share the property of genomic instability (induced accumulation of variation)

49
Q

pan-cancer analysis

A

driver genes (genes that promote progression of cancer) across diff kinds of cancers; look at how many genes were activated/deactivated and if they are candidate genes which leads to better assessment of underlying biology

50
Q

approx one-half of advanced (metastatic) melanomas harbor a mutation in the

A

BRAF gene; targeted therapy as a result of testing for BRAF mutations

51
Q

acute promyelocytic leukemia (APL) is an abnormal accumulation of _ and is characterized by a _

A

abnormal accumulation of promyelocytes (immature granulocytes) characterized by a chromosomal translocation

52
Q

which type of mutation in telomerase could be associated with cancer cells?

A

mutations that increase the expression of telomerase

Genetics (37 decks)

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