Final for Cancer Biology

Which of the following can cause mutations which contribute to development of cancers?

A. Chemicals in food. B. UV and ionising radiation. C. Viruses & bacteria D. A. and B.* None of the above

The resting, non-proliferative state/phase of a cell in the cell cycle is

A. G0.* G1 G2 S M

Some cancer cells escape crisis by

A. Over-expressing hTERT. B. Activating the ALT mechanism. C. Shortening their telomeres. D. A and/or B.* E. None of the above.

Which of the following pairs have been found to be collaborating oncogenes by in vitro or by in vivo experiments:

A. Ras and myc B. Abl and myc P53 and Rb C. All of the above D. All of the above E. (A and B ) Ras and myc, and; Abl and myc (A and B )*

Which of the following is/are characteristic of a cancer cell?

A. Replicates for an unlimited number of times. B. Grows and divides without stimulation by a growth factor. C. DNA damage does not halt cell division or stimulate apoptosis. D. Releases factors that cause nearby cells to become cancerous. E. A, B, and C.*

Inactivation of tumor suppressor genes can occur as the result of

A. Somatic mutation of both alleles. B. Promoter demethylation. C. Loss of heterozygosity. D. A and C.* E. None of the above.

Which of the following statements is TRUE?

Accumulation of oxidative damage does not contribute to senescence. Senescent cells are viable, but do not divide, and have reached the Hayflick limit* Senescent cells are undergoing cell death. Senescence is a key step in promoting neoplastic proliferation. None of the above.

Which of the following types of mutation cannot give rise to an oncogene?

Addition or deletion of a base producing a nonsense message and an inactive protein product.* A point mutation changing just one amino acid in the protein product. A translocation which puts the gene under the control of a strong promoter, producing over-expression. A point mutation which produces a stop codon, prematurely terminating the message and producing a truncated protein. All of them.

Which of the following types of mutations would NOT be advantageous for the survival of a cancer cell?

An inactivating mutation in a tumor suppressor gene An inactivating mutation in an oncogene* An inactivating mutation in a gene that promotes apoptosis All of the above None of the above

Which one of the following BEST defines an oncogene?

An oncogene codes for a cell cycle control protein. An oncogene codes for a mutated form of a protein that forms part of a signal transduction pathway. An oncogene codes for a protein that prevents the cell from undergoing apoptosis. An oncogene is a dominantly expressed mutated gene that gives a cell a growth or survival advantage.* None of the above defines an oncogene.

The cell's latent suicide program, resulting in rapid cell death, is called

Apoptosis.* Necrosis. Eradication. Ischemia Caspase.

Formation of reciprocal chromosomal translocation between human chromosomes 9 (abl) & 22 (bcr) genes results in hybrid genes (oncogene) that encode hybrid bcr-abl proteins associated with which of the following malignancy.

Breast Thyroid Nerve Leukemia (CML)* Melanoma

Loss of contact inhibition occurs in which the following type of cells:

Cancer* Normal Neural Hormone secreting Embryonic

Virtually all cell types in human can give rise to cancer but the most common human cancers are of epithelia (epithelial cell) origin and are known as:

Carcinomas* Sarcomas Melanoma All of the above None of the above

The virus known as RSV (Rous Sarcoma Virus) is associated with:

Chicken sarcoma* Bovine cancer Breast cancer D. Liver cancer Human carcinoma

Following serum starvation, if normal fibroblasts were treated with cycloheximide to shut down cellular protein synthesis, then, when exposed to fresh serum, the cells would

Continue to remain viable in a quiescent state. Express immediate early genes. Enter ia state of senescence. Die. None of the above.

The cyclin/cyclin-dependent kinase pair that is active during the G1 phase of the cell cycle is

Cyclin A/CDC2. Cyclin B/CDC2. Cyclin D/CDK4/6.* Cyclin E/CDK2. Cyclin A/CDK2.

Which of the following can act as tumor promoter?

Cytotoxic agents Mitogenic agents Chronic inflammation Infectious agents All of the above*

Process of migration of malignant/cancerous cells from the site of their origin to other part(s) of the body forming secondary tumors is called:

Diapedesis Metastasis* Proliferation Cellular over growth None of the above.

Routes of systemic spread of tumor emboli and tumor cells include which of the following?

Direct extension across organ and body cavities Hematogenous spread Lymphatic spread All of the above* None of the above

Which of the following types of cellular changes would be considered to be malignant?

Dysplasia Squamous cell carcinoma* Papilloma Fibroma Adenoma

Carcinomas are tumors arising from:

Epithelial tissue* Bone Muscle Connective tissue None of the above

All tumors are lethal:

False

Tumor promoting genes are known as proto-oncogenes.

False

Telomeres are complex molecular structures comprised of:

G-rich strand C-rich strand Telomere binding proteins that include: TRF1, TRF2, POT1 & other proteins All of the above* None of the above

Tumor suppressor genes are considered as growth controlling genes by which of the following functions they suppress formation of cancer:

Growth arrest Differentiation Apoptosis All of the above* None of the above

When a cancer cell becomes immortal, its growth is dependent on several factors in the host. Examples of some of these factors are:

Growth factors Supply of oxygen Host defense mechanism All of the aboce* None of the above

According to the American Cancer Society (ACS) which of the following type of cancer causes the highest rate of death in both (male and female) genders?

Lung cancer* Thyroid cancer Breast cancer Prostate cancer Pancreatic cancer

Cells deploy a wide variety of enzymes (mechanisms) to restore normal DNA structure. Which of the following mechanism is focused on detecting nucleotides of normal structure that have been incorporated into the wrong positions?

Mismatch repair (MMR) mechanism that involves MutS and MutL* De-alkylating mechanism Error-prone mechanism Nucleotide-excision repair (NER) mechanism None of the above

Which of the following intracellular pathways might be involved in human cell transformation:

Mitogenic signaling pathway controlled by Ras Cell cycle checkpoint controlled by pRB Alarm pathway controlled by p53 All of the above* None of the above

Which of the following are true for p53?

Most commonly mutated gene in cancers (Overall 50% of total When p53 is mutated, DNA-damaged cells are not arrested in G1 phase and DNA repair does not take place. Failure to arrest DNA-damaged cell by p53 in G1 phase is repeated in subsequent cell cycles permitting other mutations to accumulate, culminating in neoplastic transformation, tumor formation and cancer. All of the above* Non of the above

Sporadic cases of retinoblastoma require

One inactivating somatic mutation in one copy of Rb. Two somatic inactivating mutations, one in each of the two copies of Rb.* One somatic mutation in Rb, leading to its activation. Two somatic mutations in a copy of Rb, leading to its activation. None of the above.

In the Ames test which of the following is the indicator to suggest that the test compound is mutagenic:

Plant extracts Mouse liver cells Growth of mutant (His-) strain of Salmonella typhimurium in histidine deficient medium* All of the above None of the above

Origin of oncogenes in human cancers could include which of the following mechanism(s

Point mutation DNA rearrangement Gene amplification Chromosomal translocation All of the above*

Heterocyclic amines (HCA) are generally generated in meats that are cooked at high temperature. These molecules may interact with DNA and are known as

Promoters Adducts.* Initiators D. All of the above None of the above

Ras activation results in activation of which of the following effecter loops with their main downstream partners:

Ral-GEF Raf kinase PI3K All of the above effecter loops* None of the above

Which of the following gene(s) function both as caretaker and gate-keeper gene(s)?

Rb P53* APC (adenomatous polyposis coli) P53 and APC (adenomatous polyposis coli) None of the above.

Which of the following gene(s) is/are classified as tumor suppressors?

Rb p53 APC All of the above* None of the above

Which of the following signaling pathways is in the correct order

Receptor → Sos → Grb2 → Ras Receptor → Ras → Sos → Grb2 Receptor → Sos → Ras → Grb2 Receptor → Grb2 → Ras → Sos Receptor → Grb2 → Sos → Ras*

Which of the three domains of src protein has tyrosine kinase activity?

SH1* SH2 SH3 All of the above None of the above

Which of the following are disadvantages of the gene transfection assay using the NIH 3T3 cells:

Some oncogenes may be specific for particular human cell types and so may not be detected with mouse fibroblasts. The NIH-3T3 cells are not 'normal' cells since they are a permanent cell line and genes involved in early stages of carcinogenesis may therefore be missed. The assay depends upon the transfected gene acting in a genetically dominant manner and so will not detect tumor suppressor (recessive) genes. All of the above* None of the above

When a normal cell and a cancer cell were fused, the resulting hybrids lost the ability to form tumors in mice. This suggests that

The cancer cell alleles are dominant over the normal cell alleles. The cancer cell alleles are recessive to the normal cell alleles.* The normal and cancer cell alleles are co-dominant. The original tumor formed as a result of infection by a tumor virus. E. None of the above.

When a normal cell and a cancer cell were fused, the resulting hybrid appeared normal and the hybrid cell lost the ability to form tumors in mice. This suggests that

The cancer cell alleles are dominant over the normal cell alleles. The cancer cell alleles are recessive to the normal cell alleles.* The normal and cancer cell alleles are co-dominant. The original tumor formed as a result of infection by a tumor virus. None of the above.

The critical decision point at which a cell determines its fate at the end of the G1 phase of the cell cycle is called

The transition point. The resolution point The commitment point. The restriction point.* The contraction point.

Development of anti-cancer therapies has been imperfectly served by the use of human cancer cell lines because:

They are 2-dimentioan and not 3-dimentional Their glucose supply in culture is not limiting They do not have stromal cells All of the above* None of the above

When an oncogene is transcribed and translated with another gene, the expressed product is:

Transcribed protein Fusion/hybrid protein* Fusion cell Cancer protein None of the above

A cancerous tumor eventually grows faster than surrounding tissues because a greater proportion of its cells are dividing. True or False?

True

Base-excision repair (BER) tends to repair lesions in the DNA that derive from endogenous sources, such as the reactive oxygen species and depurination events; whereas Nucleotide-excision repair (NER) focuses largely on repairing the lesions created by exogenous agents, such as UV photons and chemical carcinogens.

True

Based on several experimental evidence, it is considered that a common set of cellular proto-oncogenes might be activated either by retroviruses in animals or by nonviral mutational mechanisms during the formation of cancers in humans.

True

Because NF-κB promotes cancer-cell proliferation, prevents apoptosis, and increases tumor's angiogenic and metastatic potential, it is suggested to be a crucial linker for inflammation and cancer:

True

Cancer originating in one body organ takes its characteristics with it even if it spreads to another part of the body.

True

Defective check points mechanism allows errors in the cell duplication process to persist into the next generation that can lead to unregulated proliferation and the development of cancer

True

Following application of Ames test, it become obvious that not all mutagens were carcinogens; some were considered as tumor promoters. (True or False)

True

Human genome encodes at least 120 SH2 domains/groups. Each constitutes a domain of a larger protein & each has an affinity for binding a particular phosphotyrosine together with a flanking oligopeptide sequence. This SH2 domain binding enables the protein carrying it to associate with a partner protein that is displaying a specific phosphotyrosine plus flanking aa sequence, and forms a physical complex between these two proteins. Do you think, this could be the mechanism of various proteins to become localized to certain sites within the cytoplasm of a cell?

True

Interior of a cell (cytoplasm) contains a large number (~20,000) of proteins, and many of them are crucial components of the cytoplasmic regulatory circuit. Despite this complexity, a signaling process functions as a linear cascade; thus must recognize only those signals that come from upstream partner protein(s) and pass them onto its downstream partners. In doing so, it must largely ignore thousands of other proteins within the cell.

True

Is it true that endogenous biochemical processes may make greater contributions to genome mutations than do exogenous factors?

True

Is it true that quiescent (G0) cells contain an array of proteins that can quickly convey mitogenic signals from extracellular receptors to transcription factors operating in nucleus?

True

It is now known that a single mutation is not sufficient for the development of cancers, and may require collaboration between two or more mutant genes.

True

Jak-STAT Pathway allows signal transmission directly from interacellular domain (ICD) of the activated receptor to nucleus of a cell.

True

Micro RNAs (miRNAs) can act either as oncogenes or tumor suppressor genes. True or False.

True

Nectins and nectin-like molecules (glycoproteins) play a role in the process of contact inhibition

True

Patients with no or low N-myc amplification have better prognosis and minimal clinical events compared to patients with extensive N-myc amplification.

True

Rounded refractile cells, anchorage independent growth, immortality, and inability to halt proliferation in response to deprivation of growth factors are some of the properties of virally transformed cells.

True

Some tumor suppressor genes (TSGs) are involved in regulation of cell cycle.

True

Some viruses can alter expression of cell's copy of one of the proto-oncogenes, such viruses are termed as the oncogenic viruses.

True

The cell cycle is a programmed series of events that enables a cell to duplicate its contents and generate 2 daughter cells. This process is controlled by check points in the cycle to ensure that a new step in the cycle is not undertaken until the preceding step has been completed. However, many types of cancer cells have inactivated one or more of these checkpoint controls to propel their neoplastic growth.

True

The src proteins alter several target molecules, resulting in the transmission of signals to the nucleus that help regulate the cell

True

Tumors arising in epithelia of lung, uterus and cervix may contain both squamous-carcinoma and adeno- carcinoma cells.

True

Unactivated proto-oncogenes are normal versions of transforming genes that are present in normal cells.

True

Which of the following gene(s) is/are abnormally activated in conversion of a normal cell to a cancerous cell?

Tumor metastasis gene(s) Proto-oncogene(s)* Tumor suppressor gene(s) Transposon(s) Angiogenesis gene(s)

Which of the following is characteristic of a malignant rather than a benign tumor?

Undergoes metastasis.* Develops blood supply. Cells divide an unlimited number of times. Grows without needing a growth signal. None of the above.

When a cell is at G0 or early G1 phase, pRb is

Undetectable. Unphosphorylated or the least phosphorylated Hyperphosphorylated. Overexpressed. E. None of the above.

Cancer is characterized by its:

controlled cell growth Incorrect functioning of major and vital organs Altered energy metabolism All of the above* None of the above

Which of the following can be possible carcinogen(s):

nizing radiation (UV light, X-rays) Chemicals (tar from cigarette, polyphenolic compounds) Microbial toxins such as fungal toxins All of the above* None of the above

Can defects in DNA repair mechanism(s) in a cell lead to increased cancer susceptibility?

true

Complement-mediated killing of a cell occurs after an antibody has reacted with its target on cell surface and complement components have created the membrane attach complex (MAC)

true

During the process of metastasis of cancer, extravasation is facilitated by clot formation

true

Effective therapy of cancer depends of its accurate diagnosis and disease stratification which in recent years is based on functional genomic analysis (Gene signature stratification).

true

In an experiment, expression of a large array of "immediate early genes" (IEGs) was induced within first two hrs after serum starved cells (G0) were exposed to fresh serum. This expression of IEGs occurred even when protein synthesis was blocked by cycloheximide during this induction period. Did it indicate that transcription factors which regulate expression of these genes were already present in serum starved cells?

true

Many chemotherapeutic drugs cause damage to chromosomes in cells. Since many cancer cells lack key G2/M Checkpoint controls, they advance into mitosis without having chromosomal damage repaired. This causes them (such cells) to enter into "mitotic catastrophe" resulting in aneuploidy, polyploidy, formation of micronuclei, and eventually death.

true

Most familial cancer syndromes are related to Tumor Suppressor Genes (TSGs)

true

Most familial cancer syndromes are related to Tumor Suppressor Genes, whereas only a very few familial cancer syndromes are related to Oncogenes.

true

Neoangiogenesis represents an attractive target for the development of novel anti-cancer agents, because the targeted cells are various normal stromal cell types participating in angiogenesis rather than the ever changing cancer cells.

true

Normal and cancer cells use the same or identical biochemical circuitry; however, the actual difference is that cancer cells have adapted ways to make modifications to the control machinery operating within them to slow their growth and progression.

true

Normal and neoplastic epithelial tissues are formed from interdependent cell types

true

Stromal cells are active contributors to tumorigenesis; and macrophages represent important participants in activating the tumor associated stroma that provide heterotypic support for tumor growth

true

The process of tumorigenesis is a multistep pathway and involves accumulation of genetic alterations as the process of tumor initiation and progression proceeds.

true

Tumors are complex tissues that depend on intercommunications between various cell types. Most tumors are as complex histologically as normal tissues in which they arise.

true

Tyrosine phosphorylation controls location and action of many cytoplasmic signaling proteins

true