Molecular Oncology Testfragen

Question 1

tumors - which item is right?

a.
hepatocellular sarcomas originate from epithelial cells

b.
the grading systems of distinct human tumors use identical parameters

c.
the development of a colon carcinoma may take >20 years

d.
Schwannomas develop in breast and prostate, as well as in the PNS and CNS

e.
tumors consist solely of tumor cells

Answer 1

c.
the development of a colon carcinoma may take >20 years

Question 2

cancer cell senescence - which item is wrong?

a.
cancer develops in the elderly, because of the lack the regenerative capacity of stem cells

b.
senescence may be overcome by inactivation of the retinoblastoma (pRB) pathway

c.
senescent cancer cells display a secretory phenotype, which affects immune cells

d.
senescence goes along with telomere erosion, which will contribute to cell crisis

e.
senescence may be induced by impaired DNA repair and mitochondrial dysfunction

Answer 2

a.
cancer develops in the elderly, because of the lack the regenerative capacity of stem cells

Question 3

genome and epigenome - which item is wrong?

a.
driver mutations are mutations which are beneficial to tumor progression

b.
driver mutations occur in genes crucial for normal cellular functions

c.
passenger mutations are not contributing to tumor progression over long periods

d.
any mutation in a putative driver gene will inevitably lead to tumor formation

e.
mutations and epigenetic changes contribute to tumorigenesis

Answer 3

d.
any mutation in a putative driver gene will inevitably lead to tumor formation

Question 4

tumor evolution - which item is wrong?

a.
the malignant state is characterized by increased growth rate, increased vascularization, ulceration and high rates of necrosis

b.
tumorigenesis is a multistep process, which involves initiation, promotion and progression

c.
when a tumor undergoes evolution, it will always switch from a benign to a malignant phenotype

d.
compounds mediating tumor initiation encompass polycyclic aromatic hydrocarbons, X-ray and UV

e.
compounds mediating tumor promotion include hormones and phorbol esters

Answer 4

c.
when a tumor undergoes evolution, it will always switch from a benign to a malignant phenotype

Question 5

populations of tumor cells - which item is wrong?

a.
only a subgroup of the primary tumor cells is able to produce metastatic cells

b.
any kind of neoplastically transfomated cell will persist during tumor evolution

c.
only a subgroup of neoplastically transformed cells will allow for the formation of a primary tumor

d.
microenvironmental factors, such as the immune system may impose a positive selection on the tumor cells

e.
all tumors show substantial intratumoral heterogeneity. This describes the presence of cells with distinct sets of driver mutations in the same tumor

Answer 5

b.
any kind of neoplastically transfomated cell will persist during tumor evolution

Question 6

tumorigenesis_ which item is wrong?

a.
Additional crucial events in tumorigenesis, are the evasion of apoptosis which could result from the loss of functional Tp53.

b.
Tumorigenesis is a multistep process, in which the functional inactivation of tumor suppressors is a crucial event.

c.
Cancer-associated inactivation tumor suppressors mostly affects both alleles; i.e. as long as one functional copy is present, neoplastic transformation will not occur.

d.
Closely related tumors, such as lung carcinoma in smokers and non-smokers, show identical activities of oncogenic drivers.

e.
Deregulation of the cell cycle control is a crucial event in tumorigenesis. It may result from the loss or inactivation of the CDKN2A locus

Answer 6

d.
Closely related tumors, such as lung carcinoma in smokers and non-smokers, show identical activities of oncogenic drivers.

Question 7

types of mutations_which item is wrong?

a.
LOFs are a loss of function mutations

b.
GOFs are a gain of function mutations

c.
Deregulation of proto-oncogenes is by GOFs

d.
Deregulation of tumor suppressors occurs always by LOFs

e.
The term LOH describes the loss of one functional allele or chromosome

Answer 7

d.
Deregulation of tumor suppressors occurs always by LOFs

Question 8

oncogenic_pathways_which item is wrong?

a.
The Pi3K/AKT/mTOR pathway may initiate tumorigenesis after loss of functional PTEN

b.
Increased expression of the transcription factor c-MYC may results in a metabolic switch

c.
Loss of functional APC may render the Wnt pathway oncogenic

d.
Overexpression of E2F will shut down the senescence pathway and cell cycle progression

e.
The MAPK pathway may contribute to tumorigenesis by overexpression of RTKs

Answer 8

d.
Overexpression of E2F will shut down the senescence pathway and cell cycle progression

Question 9

Tp53_which item is wrong?

a.
In dominant negative Tp53 allele will interfere with the function of Tp53 wild-type alleles

b.
The functional consequences of distinct Tp53 mutations are identical

c.
Tp53 impacts on cell cycle progression by regulation of p21

d.
Tp53 is a transcription factor which binds to DNA as a tetramer

e.
MDM2 is encoded by a Tp53 target gene and a negative regulator of Tp53

Answer 9

b.
The functional consequences of distinct Tp53 mutations are identical

Question 10

Which statement about BRCA1 is wrong?

a.
BRCA1 has been classified as a human oncogene

b.
BRCA1 mutations contribute to breast and ovarian cancer

c.
Deregulation of BRCA1 may result from promoter-hypermethylation

d.
Deregulation of BRCA1 may be caused by mutations in its promoter

e.
BRCA1 is crucial for genomic integrity

Answer 10

a.
BRCA1 has been classified as a human oncogene

Question 11

Which statement about CAFs/SASPs is wrong?

a.
Fibroblasts in an aged mirco-environment do not secrete cytokines and growth factors, which in turn leads to tumor growth

b.
Healthy fibroblasts in a young tissue secrete cytokines and growth factors, which provide a growth-restrictive micro-environment for premalignant cells

c.
SASP is a short-lived senescence-associated secretory phenotype of fibroblasts

d.
SASPs and immune-suppressive immune infiltrates accumulate in aged micro-environments

e.
CAFs are fibroblasts, residing in the tumor microenvironment

Answer 11

a.
Fibroblasts in an aged mirco-environment do not secrete cytokines and growth factors, which in turn leads to tumor growth

Question 12

Which statement about the tumor micro-environment TME is wrong?

a.
The TME supports metastasis

b.
The TME encompasses stromal and extracellular matrix components

c.
The TME prevents tumor-host interactions

d.
The TME promotes tumor progression

e.
The TME promotes tumor maintenance

Answer 12

c.
The TME prevents tumor-host interactions

Question 13

Which statement about the extracellular matrix (ECM) is wrong?

a.
In the context of softer tissue microenvironments increased stiffening of the ECM may promote efficient tumor progression

b.
The elastic properties of the ECM increase during aging in all tissues

c.
Components of the ECM are synthesized by CAFs

d.
Age-induced accumulation of SASP augments ECM stiffness in e.g. lung tumors

e.
Integrins act as receptors for certain ECM molecules

Answer 13

b.
The elastic properties of the ECM increase during aging in all tissues

Question 14

Which is not a feature of cancer stem cells (CSCs)?

a.
CSCs are non-tumorous stem cells found in the tumor niche

b.
CSCs show a low abundance in the tumor

c.
CSCs undergo MET when they occupy the metastatic niche

d.
CSCs display indefinite self-renewal

e.
CSCs undergoing symmetric cell division will generate two daughter CSCs

Answer 14

a.
CSCs are non-tumorous stem cells found in the tumor niche

Question 15

Micro-RNAs and neoplasms. What is wrong?

a.
microRNAs may contribute to angiogenesis and metastasis

b.
Mutations in the protein Dicer may be oncogenic

c.
Let-7 miRNA over-expression will lead to activation of the proto-oncogenes cMYC and RAS

d.
Mutation of Exportin 5 has been classified as a cancer–related

e.
Overexpression of miRNAs targeting the PTEN mRNA is oncogenic

Answer 15

c.
Let-7 miRNA over-expression will lead to activation of the proto-oncogenes cMYC and RAS

Question 16

Which statement about the metabolic switch in cancer cells is wrong?

a.
The preferred expression of PKM2 is one aspect of altered cancer metabolism

b.
The metabolic switch of cancer cells may result in a process called aerobic glycolysis

c.
The switch to a lactogenic phenotype was described as a metabolic adaptation

d.
The metabolic switch is associated with an altered redox balance

e.
The metabolic switch has been proven to be the cause of cancer

Answer 16

e.
The metabolic switch has been proven to be the cause of cancer

Question 17

Which statement about HIF1alpha is wrong?

a.
HIF1alpha is a transcription that regulates the expression of glycolytic enzymes and glucose transporters

b.
HIF1apha regulates the expression of the kinase PDK1, which controls the activity of the pyruvate dehydrogenase complex (PDC)

c.
HIF1alpha is an obligatory antagonist of the transcription factor c-Myc

d.
HIF1alpha is hydroxylated and poly-ubiquitinated under normoxic conditions

e.
The expression level of HIF1alpha is negatively correlated with the oxygen concentration

Answer 17

c.
HIF1alpha is an obligatory antagonist of the transcription factor c-Myc

Question 18

Which statement about OXPHOS in cancer cells wrong?

a.
The reduction equivalents obtained in the citric acid cycle (TCA) may enter OXPHOS

b.
In order to shut down OXPHOS cancer cells switch from carbohydrate to fatty acid metabolism

c.
Cancer stem cells carry out very little OXPHOS, because of immature mitochondria

d.
Lactate may enter OXPHOS with the help of the mMCT transporter and the LDH

e.
During differentiation cancer cells may acquire an OXPHOS phenotype

Answer 18

b.
In order to shut down OXPHOS cancer cells switch from carbohydrate to fatty acid metabolism

Question 19

Which statement about ROS is wrong?

a.
The NADPH-dependent regeneration of the reduced form of glutathione (GSH) is antagonizing the accumulation of ROS

b.
Excess ROS will destroy many biomolecules, including DNA and RNA

c.
ROS are reactive oxygen species that might originate from the activity of the OXPHOS complexes I and III

d.
Due to the production of 2-hydroxyglutarate (2-HG) accumulation of ROS is prevented in cells with mutant isocitrate dehydrogenase 1 (IDH1)

e.
Intermediate ROS levels are more beneficial for cancer cells than very low ROS levels

Answer 19

d.
Due to the production of 2-hydroxyglutarate (2-HG) accumulation of ROS is prevented in cells with mutant isocitrate dehydrogenase 1 (IDH1)

Question 20

Which statement about metabolic compartments is wrong?

a.
The knowledge about anabolic and catabolic cancer cells may be used in clinical settings: Metformin and arsenic are envisaged to disrupt the crucial pathways

b.
One parameter determining whether cancer cells is an anabolic or a catabolic cells is its distance to the vasculature

c.
Anabolic cancer cells completely metabolize glucose by means of glycolysis, TCA and OXPHOS to generate high amounts of ATP

d.
Catabolic cancer cells take up glucose, lactate and free fatty acids (FFAs) from the extracellular space and use these compounds to drive the TCA cycle and OXPHOS

e.
The term “metabolic compartment” describes the presence of anabolic and catabolic cancer cells in close neighborhood in the same tumor

Answer 20

d.
Catabolic cancer cells take up glucose, lactate and free fatty acids (FFAs) from the extracellular space and use these compounds to drive the TCA cycle and OXPHOS

Question 21

Neoplasms of the hematopietic lineage – what is wrong?

a.
Leukemia is the cancer of blood cells

b.
Lymphoma is the cancer of the lymphocytes. The cancers are classified as Hodgkin’s and non-Hodgkin’s lymphomas

c.
The suffix acute and chronic consider the rapid versus slow increase of abnormal hematopoietic cells and the need of immediate versus delayed treatment

d.
Leukemia cells are exclusively found in the bone marrow

e.
Myeloma is the cancer of the plasma cells, which are derived from bone marrow

Answer 21

d.
Leukemia cells are exclusively found in the bone marrow

Question 22

Leukemia and lymphoma symptoms – what is wrong?

a.
Leukemia may be associated with neurological symptoms

b.
Most cases of Leukemia and Lymphoma are caused by previous EBV infections

c.
Both leukemia and lymphoma patients experience weakness and fatigue

d.
Leukemia patients experience fever, chills and night sweats

e.
Lymphoma patients complain about troubles breathing or chest pain

Answer 22

b.
Most cases of Leukemia and Lymphoma are caused by previous EBV infections

Question 23

Mantle cell lymphoma (MCL) – what is wrong?

a.
The mutation of the kinase ATM is a frequent driver mutation in MCL

b.
The t(11,14) translocation is a frequent driver mutation in MCL, which inserts the Cyclin D1 gene into an IgH locus

c.
The processes during neoplastic transformation of MCL cells reflect the genomic re-arrangement and hyper-mutation in the germinal centers

d.
MCL is a rare, benign form of Hodgkin’s lymphoma

e.
MCL arise from B cells present in the mantle zone of secondary lymphoid organs

Answer 23

d.
MCL is a rare, benign form of Hodgkin’s lymphoma

Question 24

Burkitt’s lymphoma (BL) – what is wrong?

a.
The risk of transplanted patients to develop BL is increased, which is related to the application of immune-suppressants

b.
The sporadic variant is also called non-African variant

c.
Three variants of BL have been described, all of which are induced by the HIV

d.
The t(8;14) translocation, which leads to an over-expression of c-myc, is frequently observed in BL patients

e.
The classical BL variant is the African, endemic variant

Answer 24

c.
Three variants of BL have been described, all of which are induced by the HIV

Question 25

Chronic myeloproliferative disorders (CMD) – what is wrong?

a.
Mutations in receptor tyrosine kinases, such as c-Kit, are frequently observed in CMD patients

b.
All JAKs possess receptor interacting domains, as well as a kinase domain and a pseudo-kinase domain

c.
The oncogenic potential of JAK V617F is due to a mutation in the kinase domain JH1

d.
A single point mutation in the JAK2-gene is sufficient to activate the oncogenic potential of this Janus kinase

e.
The JAK2 V617F mutant may trigger neoplastic transformation of myeloid cells

Answer 25

c.
The oncogenic potential of JAK V617F is due to a mutation in the kinase domain JH1

Question 26

C-Myc dysregulation – what is wrong?

a.
The epigenetic deregulation of the c-myc promoter has been observed in hematopoietic cancers

b.
C-Myc self-induction was shown to contribute to hematopoietic neoplasms

c.
The t(8;14) translocation generates a fusion protein consisting of a c-myc moiety fused to the heavy chain of an immunoglobulin

d.
All three c-myc translocations, t(8;14), t(2;8) and t(8;22) insert the c-myc proto-oncogene into an immunoglobulin locus

e.
Increased stability of the c-myc mRNA has been associated with c-myc deregulation in B cells

Answer 26

c.
The t(8;14) translocation generates a fusion protein consisting of a c-myc moiety fused to the heavy chain of an immunoglobulin

Question 27

C-Abl and leukemia – what is wrong?

a.
The BCR-ABL fusion provides the ABL tyrosine kinase with an oligomerization domain

b.
Leukemia with a BCR-ABL driver mutant are successfully treated with the kinase inhibitor Imatinib

c.
In the Philadelphia chromosome [t(9;22)] the C-terminal moiety of the c-abl proto-oncogene is inserted into a locus coding for the breakpoint cluster region BCR

d.
BCR-ABL increases survival and acts in an anti-apoptotic fashion

e.
The the c-abl proto-oncogene is located on human chromosome 22 and encodes a receptor tyrosine kinase

Answer 27

e.
The the c-abl proto-oncogene is located on human chromosome 22 and encodes a receptor tyrosine kinase

Question 28

PML-RARalpha and leukemia – what is wrong?

a.
The PML-RARa translocation is a frequent driver mutation in APL (acute promyelocytic leukemia)

b.
PML-RARa replaces the wild-type RARa on RA-responsive elements, which leads to continuous expression of the respective promoters

c.
PML-RARa interacts with the transcriptional regulator Pu.1 on promoters regulating the differentiation of macrophages or B cells

d.
The t(15;17) translocation fuses the N-terminus of PML to a large moiety of the transcription factor RARa, including the DNA binding domain of RARa

e.
PML-RARa prevents the activation by the transcription factor Pu.1. This leads to a differentiation block, which can be relieved by arsenic

Answer 28

b.
PML-RARa replaces the wild-type RARa on RA-responsive elements, which leads to continuous expression of the respective promoters

Question 29

Hematopoietic stem cells (HSCs) and leukemia stem cells (LSCs) – what is wrong?

a.
A quiescent HSC and an active HSC co-localize in the niche. The active HSC generates the common progenitors of the lymphoid and myeloid lineage

b.
LSCs display self-renewal and generate all cells of the neoplasm

c.
LSCs may only develop from the common lymphoid stem cells

d.
HSCs are able to reconstitute a functional hematopoietic system after transplantation

e.
Normal HSCs and neoplastically transformed LSC reside in niches in the bone marrow

Answer 29

c.
LSCs may only develop from the common lymphoid stem cells

Question 30

Cell replacement therapy – what is wrong?

a.
The recipient of a cell replacement therapy receives a 3-day chemotherapy and total body irradiation

b.
The chance for the functional integration of the transplanted bone marrow cells in the HSC niche of a recipient is approx. 98%

c.
The umbilical cord is an alternative source for stem cells which might be used in replacement therapies concerning the hematopoietic system

d.
Mobilization of donor cells can be mediated by G-CSF, which disrupts the CXCR4/SDF1a retention axis

e.
In cell replacement therapy a mixture of HSCs, progenitors, mesenchymal stem cells and endothelial stem cells is aspirated from the bone marrow of the donor

Answer 30

b.
The chance for the functional integration of the transplanted bone marrow cells in the HSC niche of a recipient is approx. 98%

Question 31

Relations between viruses and cancer. – what is wrong?

a.
The beta-herpes simplex virus CMV typically induces warts

b.
The Epstein-Barr virus (EBV) is a DNA tumor virus and induces Burkitt’s lymphoma

c.
The hepatitis B virus (HBV) induces chronic hepatitis and hepatocellular carcinoma

d.
Oral cancer may be induced by papilloma viruses

e.
Chronic HPV infection may lead to cervix carcinoma

Answer 31

a.
The beta-herpes simplex virus CMV typically induces warts

Question 32

EBV – what is wrong?

a.
The oncogenic factors in EBV encompass EBNA and LMP proteins

b.
Activation of LMP1 and LMP2 leads to complete B cell transformation

c.
EBNA2 drives cellular proliferation through c-Abl

d.
EBNA2 cooperates with EBNA-LP for induction of LMPs

e.
LMP1 activates NFkB transcription

Answer 32

c.
EBNA2 drives cellular proliferation through c-Abl

Question 33

HPV – what is wrong?

a.
The oncogenic proteins in HPV are E1, E5, E6 and E7

b.
E1 is a replication protein and target of effector caspases

c.
E5 contributes to immortalization

d.
E7 binds to Tp53, which in turn increases the stability of the genome

e.
E6 leads to higher activity of the telomerase and reduces rate of cell death

Answer 33

d.
E7 binds to Tp53, which in turn increases the stability of the genome

Question 34

HTLV1- what is wrong?

a.
The Tax protein encodes a transcription factor with basic leucine zipper motif

b.
The repair function in HTLV-1 infected cells is grossly disturbed, which leads to chromosomal abnormalities

c.
The Tax protein is the crucial oncogenic protein encoded by HTLV1

d.
The typical retroviral genes gag, pol and env, two LTRs and three additional genes are present in the HTLV1 genome

e.
HTLV1 is a retrovirus consisting of an envelope and a capsid, which contains to identical copies of RNA

Answer 34

a.
The Tax protein encodes a transcription factor with basic leucine zipper motif

Question 35

General processes associated with viral infection - what is wrong?

a.
In the non-permissive state, viruses rather act as molecular parasites

b.
Infection with DNA tumor viruses will inevitably lead to cancer

c.
In the permissive state, viruses lyse/kill the infected cells

d.
Viral tumorigenesis is a by-product (=complication) of virus-transmission

e.
Proteins encoded by DNA tumor viruses interact with the tumor suppressors, in particular Tp53 and RB

Answer 35

b.
Infection with DNA tumor viruses will inevitably lead to cancer

Question 36

Which of the following tumors is not observed in the human brain? - What is wrong?

a.
Medulloblastoma

b.
Ependymomy

c.
Retinoblastoma

d.
Meningioma

e.
Astrocytoma

Answer 36

c.
Retinoblastoma

Question 37

Which of the following symptoms is generally not associated with human brain? -What is wrong ?

a.
fever

b.
Seizures

c.
Nausea and vomiting

d.
Mental changes

e.
Subfalcine Herniation

Answer 37

a.
fever

Question 38

Differences between primary and secondary GBMs – what is right? (1 out of 5 is right!)

a.
Due to their less invasive character, secondary GBMs might be cured by surgical resection

b.
Chemotherapy with the alkylating reagent Temozolomide is applied before surgical intervention in secondary GBMs

c.
Radiotherapy is preferentially applied in the presence of TTP-fields in primary GBMs

d.
Mutations in the gene coding for the isocitrate dehydrogenase IDH1 are helpful tools to distinguish between primary and secondary GBMs

e.
Primary GBMs develop from a WHO grad I glioma, secondary GBMs from a WHO grade II or III glioma

Answer 38

d.
Mutations in the gene coding for the isocitrate dehydrogenase IDH1 are helpful tools to distinguish between primary and secondary GBMs

Question 39

MGMT protein and GBM therapy – What is wrong?

a.
MGMT codes for a protein which removes alkyl groups from the base guanine

b.
MGMT induces cytotoxic effects which ultimately may result in apoptosis of glioma cells

c.
Hypermethylation of the mgmt promoter is the most unfavorable condition in GBM patients under TMZ therapy

d.
The alkylation of the base guanine in the O6-position is mediated by the drug TMZ

e.
The expression of MGMT is regulated by the methylation of the mgmt-promoter

Answer 39

c.
Hypermethylation of the mgmt promoter is the most unfavorable condition in GBM patients under TMZ therapy

Question 40

The 1p/19q-status in oligodendrogliomas – what is wrong?

a.
Oligodendrogliomas with loss 1p/19q respond better to chemotherapy as those with no loss

b.
the majority of oligodendrogliomas shows a combined loss of 1p/19q

c.
LOH of 19q is most likely based on a translocation involving chromosome 19

d.
Clinical trials studying whether the 1p/19q status might serve as a good prognostic marker are very contradictory

e.
Loss of 1p indicates that alleles on the short arm of chromosome 1 are lost

Answer 40

d.
Clinical trials studying whether the 1p/19q status might serve as a good prognostic marker are very contradictory

Question 41

GBM mouse models – what is wrong?

a.
GBM formation from human cells may be studied in zebrafish embryos

b.
heterotopic GBM models: researchers inoculate human GBM cells in organs distinct from brain; often this is done subcutaneously

c.
orthotopic GBM models: researchers xenotransplant human GBM cells into one hemisphere of the mouse brain

d.
Analyses addressing the co-operation between non-tumor cells and GBM cells work well in orthotopic but not in autochthonous mouse models

e.
autochthonous mouse models are genetically engineered mice, which may be used for analyses of GBM induction and progression

Answer 41

d.
Analyses addressing the co-operation between non-tumor cells and GBM cells work well in orthotopic but not in autochthonous mouse models

Question 42

Which statement is not related to genetic pathways to glioblastoma (GBM)?

a.
G-CIMP GBMs display aberrant DNA methylation at specific loci causing disruption of CTCF binding sites

b.
deregulation of ATRX is observed in secondary GBMs and pediatric GBMs

c.
.Several mutations occur before a GBM becomes detectable. The temporal sequence of these events is purely random

d.
primary GBMs show a deregulation of EGFR and the CDKN2A locus

e.
pediatric GBMs show B-RAF deregulation

Answer 42

c.
.Several mutations occur before a GBM becomes detectable. The temporal sequence of these events is purely random

Question 43

What is not related to the GBM subtypes? (1 out of 5 is wrong)

a.
The classical (proliferative) and the neural GBM are characterized by EGFR mutations and/or amplifications

b.
The mesenchymal GBM is the GBM subtype in which mutations of the tumor suppressor NF1 appeared to be crucial

c.
Mutations of the gene coding for the IDH1 (iso-citrate dehydrogenase) are frequent in the pro-neural GBMs

d.
Mutation or loss of the tumor-suppressor Tp53 is shared by all GBM subtypes

e.
The pro-neural GBM shows several similarities to the genetic signature of secondary GBMs

Answer 43

d.
Mutation or loss of the tumor-suppressor Tp53 is shared by all GBM subtypes

Question 44

Which parameter is not related to invasiveness and migration of GBM cells?

a.
The Pi3K/AKT pathway is important for migration

b.
The production of MMPs by GBM and non-GBM cells is crucial for invasive growth

c.
The most important down-stream effector of integrins is the small GTPase K-Ras

d.
Degradation of the extracellular matrix (ECM) is associated with migration

e.
Integrins bind to proteins in the cell’s neighborhood and signal via FAK

Answer 44

c.
The most important down-stream effector of integrins is the small GTPase K-Ras

Question 45

What is not a function of GAMs (Microglial/tumor-associated macrophages)?

a.
GBMs produce versican, which in turn acts on the GAMs

b.
GAMs secrete TGFbeta, which then binds to GBM cells

c.
GAMs are recruited to the tumor lesion by several glioma cell-derived factors

d.
GAMs secrete factors, which de-activate the MMPs released by GBM cells

e.
GAMs are endowed with a M2-associated secretome, facilitating angiogenesis

Answer 45

d.
GAMs secrete factors, which de-activate the MMPs released by GBM cells

Question 46

Melanoma clinic – What is wrong?

a.
Pigment- (melanin-) free forms of skin cancer are always derived from the epithelial cells

b.
Melanoma is an aggressive fatal form of skin cancer originating from the melanocytes

c.
Metastatic melanoma is associated with high rates of relapse and mortality

d.
Early stages of melanoma may be cured by complete resection of the lesion

e.
Though melanoma is the type of cancer highly related to life style, familial cases of melanoma are additionally known

Answer 46

a.
Pigment- (melanin-) free forms of skin cancer are always derived from the epithelial cells

Question 47

Pigmentation – what is wrong?

a.
The synthesis of the brown and the black eumelanin starts with the amino acid tryptophan

b.
melanin is produced by the melanocytes, which reside in deeper layers of the epidermis

c.
Melanosomes are transported from melanocytes to keratinocytes, and from keratinocytes to keratinocytes

d.
melanin is deposited in the epidermis, where it protects the skin from UVA and UVB

e.
Melanin is packed in vesicles in the melanocytes. These cells possess filopodia that are involved in the transfer of melanin to neighboring cells.

Answer 47

a.
The synthesis of the brown and the black eumelanin starts with the amino acid tryptophan

Question 48

Types of melanomas – what is wrong?

a.
The CSD melanoma is related to life style and particularly frequent in the Caucasian population

b.
The CSD, non-CSD, acral and mucosal melanomas are more frequently observed in the clinic than the uveal melanoma

c.
Melanoma diagnosis is based on thickness and penetration depth, mitotic rate, ulceration and local metastasis

d.
Mucosal melanoma are observed in various regions of the body, including the gingiva, gastrointestinal tract and the genital mucosa

e.
The acral melanoma develops on palms and soles. The nail bed is excluded, as it does not possess pigment cells

Answer 48

e.
The acral melanoma develops on palms and soles. The nail bed is excluded, as it does not possess pigment cells

Question 49

Melanoma stages – what is wrong?

a.
Radial melanoma are often unsymmetrical und uneven, show color changes, but are still (mainly) confined to the epidermis

b.
In contrast to the melanoma cells from the vertical growth phase, the cells from the radial growth are not tumorigenic in experimental models

c.
Overexpression of the kinase AKT may drive melanoma from the radial into the vertical growth phase

d.
Dysplastic nevi possess irregular borders and are considered pre-cancerous

e.
melanocytic nevi are sharply-circumscribed benign lesion which frequently show the B-RAF V600E mutation

Answer 49

b.
In contrast to the melanoma cells from the vertical growth phase, the cells from the radial growth are not tumorigenic in experimental models

Question 50

Melanoma metastasis – what is wrong?

a.
Increasing vascularization and angiogenesis are pre-requisites for metastasis and are related to secretion of VEGF

b.
Melanoma cells capable of metastasis have undergone immortalization by activation of TERT

c.
Melanoma cells which disseminated from the vertical growth phase of a primary tumor will inevitably generate metastases within the next 2 years

d.
Dissemination of melanoma cells from the primary tumor is associated with a down-regulation of E-cadherin and concomitant up-regulation of N-cadherin

e.
The angiogenic switch during melanoma metastasis involves the laminin receptor and MMPs

Answer 50

c.
Melanoma cells which disseminated from the vertical growth phase of a primary tumor will inevitably generate metastases within the next 2 years

Question 51

Melanoma risk factors – What is wrong?

a.
The CDKN2A locus encodes the tumor-suppressors p16INK4a and Tp53

b.
Mutations in the CDKN2A locus are associated with an increased tumor risk, including melanoma

c.
The activation of the telomerase TERT is a crucial step during early and intermediate stages of melanoma development

d.
One of the most crucial drivers for the neoplastic transformation of pigment cells in the B-RAF V600E mutation

e.
The HBOC and Lynch cancer families display an increased melanoma risk

Answer 51

a.
The CDKN2A locus encodes the tumor-suppressors p16INK4a and Tp53

Question 52

Melanoma susceptibility – What is wrong?

a.
The CDKN2A locus is the high-penetrance melanoma susceptibility locus, the CDK4 gene is the rare high-penetrance melanoma susceptibility gene

b.
The receptor tyrosine kinase c-Kit is a major regulator of melanocyte migration, survival and differentiation

c.
Mutations in two subunits of the RNAP II transcription factor TFIIH (the 2 helicases), are associated with increased melanoma risk

d.
Most melanomas show oncogenic activity of several kinases, including RAS and ERK

e.
Overexpression or amplification of c-Kit may function as driver mutation in melanoma. Such melanomas respond to Imatinib

Answer 52

d.
Most melanomas show oncogenic activity of several kinases, including RAS and ERK

Question 53

RAF – what is wrong?

a.
RAF proteins possess a RAS-binding domain (RBD), which binds selectively to activated RAS (= RAS-GTP)

b.
A single point mutation will activate the oncogenic potential of A-, B-and C-RAF

c.
The kinase activity of B-RAF V600E is increased, because the interaction between the auto-inhibitory domain CR1 and the kinase domain is abrogated

d.
The B-RAF V600E mutant is the most frequent RAF mutation seen in melanoma

e.
The activity of RAF proteins is regulated by a “lock-down” mechanism, which is disrupted by the V600E mutation in B-RAF

Answer 53

b.
A single point mutation will activate the oncogenic potential of A-, B-and C-RAF

Question 54

Alpha-MSH receptor (=MC1R) – what is wrong?

a.
DNA damage drastically impairs the production of MSH and MC1R signaling

b.
The MC1R gene is polymorphic: variants of MC1R appear associated with familial melanoma risk

c.
The MC1R is G-protein coupled receptor which signals via cAMP

d.
The activated MC1R induces the expression of MITF via a G-protein cascade

e.
The MC1R gene is a major factor determining skin pigmentation

Answer 54

a.
DNA damage drastically impairs the production of MSH and MC1R signaling

Question 55

MITF (microphthalmia-associated transcription factor) – what is wrong?

a.
MITF is a bHLH transcriptions factor, which is mutated in patients with Waardenburg Syndrome (e.g. white forelock)

b.
Activated MITF translocates into the nucleus, where it up-regulates genes involved in pigment synthesis

c.
MITF is a key player in melanocytic development

d.
MITF decreases genes involved in melanoblast survival, lineage commitment, and proliferation

e.
MITF is activated by c-Kit and alpha-MSH. Overactive MITF may function as an oncogene and contribute to melanoma

Answer 55

d.
MITF decreases genes involved in melanoblast survival, lineage commitment, and proliferation