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Pathology dt2 > Practical: Oncology > Flashcards

Practical: Oncology Flashcards

1
Q

A carcinoma is, by defintion, a malignant tumor derived from

a. ectodermal cells
b. surface tissue
c. epithelium
d. parenchyme

A

c. epithelium

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2
Q

Whichc tumor differentiates towards mesenchymal tissues?

a. carcinoma
b. lymphoma
c. sarcoma
d. deminoma

A

c. sarcoma

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3
Q

Which microscopic abnormality is an important potential carcinoma precursor?

a. dysplasia of the epithelium
b. introduction of cytogenic stroma
c. metaplasia of the epithelium
d. loss of epithelial surface tissue

A

a. dysplasia of the epithelium

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4
Q

The term ‘dysplasia, referring to epithelial abnormalities’, means:

a. the presence of atypical mitoses, as a sign of malignancy
b. early genetic damage that does not result in morphologic deviations yet
c. loss of organized epithelial maturation, combined with invasive growth
d. loss of organized epithelial maturation, with deviations in nucleus size and shape

A

d. loss of organized epithelial maturation, with deviations in nucleus size and shape

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5
Q

Tumour grade as defined by a pathologist is a parameter of:

a. the extensiveness of the tumour
b. tumour aggressiveness
c. presence or absence of metastases
d. presence or absence of invasive growth

A

b. tumour aggressiveness

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6
Q

Clonality (=monoclonality) of a tumor refers to the fact that all tumour cells…

a. descend from a single cells
b. are genetically identical
c. are morphologically identical
d. contain the same combination of mutations

A

a. descend from a single cells

tumour is (mono-)clonal, which means that it originates from a single transformed call. an inscreasing number of variants is formed within one tumour by genetic instability

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7
Q

What is meant by ‘pleomorphism’ of tumour cells in oncology?

a. variation in tumour cell differentiation type
b. differences between cells of the primary tumour and cells from metastases
c. the frequent occurrence of mitosis figures
d. variation in growth and shape of tumour cells and their nuclei

A

d. variation in growth and shape of tumour cells and their nuclei

pleoforfe tumorcellen (melanoom)

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8
Q

Which growth property is defining for a malignant tumour (instead of a benign tumour)?

a. Expansive growth, with formation of a centre that compresses surrounding tissues
b. significant growth, causing the tumour to reach a size of more than 10 centimeters
c. invasion of surrounding tissues, causing destruction of said tissue
d. net tumour growth (more cell division than cell loss)

A

c. invasion of surrounding tissues, causing destruction of said tissue

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9
Q

Tumour STAGE refers to…

a. the extent to which the tumour has spread throughout the body and metastasized.
b. The phase of tumour progression towards the ending stage of an aggressive, anaplastic tumour
c. The general state of the patient, in which the general condition and local problems caused by the tumours are taken into account
d. Tumour aggressiveness and susceptiblity to therapy

A

a. the extent to which the tumour has spread throughout the body and metastasized.

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10
Q

What is meant by ‘differentiation’ in the context of tumour cells?

a. hormone production by a tumor
b. antibody production by a tumour
c. morphologic and function similarity of neoplastic cells to a (normal) cell type
d. genetic similarity of neoplastic cells to a (normal) cell type

A

c. morphologic and function similarity of neoplastic cells to a (normal) cell type

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11
Q

What is the correct term for the characteristic increase in dark staining of tumour cell nuclei?

a. anisokaryosis
b. polymorphism
c. hyperchromasia
d. metaplaia

A

c. hyperchromasia

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12
Q

“Double minutes” and “HSRs” (homogeneously staining regions) are distinctive for

a. amplifications
b. deletions
c. translocations
d. inversions

A

a. amplifications

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13
Q

What is meant by the growth fraction of a tumour?

a. all tumour cells are in the S- and M-phase of cell cycle
b. the average duration of the cells cycle in tumour cells, as a percentage of the cell cycle duration in corresponding normal tissues
c. the fraction of tumour cells that partakes in tumour proliferation
d. the tumour doubling time divided the tumour volume

A

c. the fraction of tumour cells that partakes in tumour proliferation

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14
Q

The tumour suppressor gene p53 encodes a protein that reduces the hazard of cancer in different ways. In which way precisely (1/more alternative)

a. induction of apoptosis, blockage of telomerase
b. induction DNA repair blockage of MHC class expression, induction of heterochromatin
c. induction of cell cycle arrest, induction of DNA repair, induction of apoptosis
d. induction of heterochromatin, induction of cell cycle arrest

A

c. induction of cell cycle arrest, induction of DNA repair, induction of apoptosis

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15
Q

What is LOW?

a. low output heterochromatin
b. linkage of hierarchy
c. low-grade oncogenic hyperplasia
d. loss of heterozygosity

A

d. loss of heterozygosity

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16
Q

Examples of substances that play a role in chemical carcinogenesis are ‘initiators’ and ‘promotors’

a. they are mutagenic and do not stimulate proliferation
b. they are not mutagenic but they do stimulate proliferation
c. they are mutagenic and stimulate proliferation
d. they are not mutagenic and do not stimulate proliferation

A

b. they are not mutagenic but they do stimulate proliferation

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17
Q

How would you describe the loss of differentiation in a malignant tumour?

a. clonality
b. mull phenotype
c. amorphy
d. anaplasia

A

d. anaplasia

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18
Q

An oncogenic mutation in as RAS gene leads to an increased activity of the RAS protein. What causes this increase in activity?

a. RAS protein is more abundant as a consequence of the amplification of the RAS gene
b. The RAS protein is always active as a consequence of point mutation in the RAS gene
c. Alternative splicing of RAS mRNA results in accumulation of RAS protein, because degradation of RAS in proteasome is inhibited
d. The Ras protein is targeted towards the cell nucleus because of a change in the signal peptide

A

b. they are not mutagenic but they do stimulate proliferation

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19
Q

An activating (gain of function) mutation in a certain gene contributes to the onset of cancer. to which gene group does this gene belong

a. proto-oncogens
b. tumour suprresor genes
c. genes that encode apoptosis-enhancing proteins
d. genes that encode DNA-repair or enzymes

A

a. proto-oncogens

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20
Q

Translocations play a rol in the onset of some hematologic malignancies. Which oncogenes are activated by such a translocation?

a. RAS and BRAF
b. ERB-B2 and RB
c. C-MYC and CL-2
d. EGFR and APC

A

c. C-MYC and CL-2

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21
Q

Invasive growth of malignant tumors required degradation of the extracellular matrix. Which enzymes are directly responsible for this process?

a. matrix metalloproteinases (MMPs)
b. ubiquitinases
c. the family of “scatter factors”
d. prostaglandins

A

a. matrix metalloproteinases (MMPs)

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22
Q

Studies into new ‘targeted’ therapies against cancer focus on the HIF-1 protein, amongst others. What aim does selective inhibition of HIV-1 in tumors serve?

a. Repair of the G1 checkpoint
b. Selective inhibition of DNA repair
c. Inhibition of matrix degradation and cell motility
d. Inhibition of angiogenesis in tumour stroma

A

d. Inhibition of angiogenesis in tumour stroma

23
Q

Of which proto-oncogenes is gene amplification the common mechanism, by which they contribute to oncogenesis?

a. RAS and BRAF
b. RB and ARF
c. N-MYC and ERB-B2
d. BCL-2 and APC

A

c. N-MYC and ERB-B2

24
Q

Some tumour suppressor genes encode proteins that fulfill a function in

a. passing on signals that stimulate proliferation
b. apoptosis inhibition
c. inducing an arrest in proliferation
d. the breakdown of extracellular matrix

A

c. inducing an arrest in proliferation

25
Q

Cyclin dependent kinases or CDKs are activated by

a. dimerisation
b. binding to histone proteins
c. binding to cyclins
d. cleavage of a small part of the molecule

A

c. binding to cyclins

26
Q

Severe loss of muscle mass (cachexia) is seen in patients with chronic inflammatory disease. It is presumably caused by.

a. Necrosis of muscle tissue
b. Elevated activity of tumour necrosis, TNF
c. Elevated activity of insulin and decreased glucagon activity
d. Decreased activity of adiponectin

A

b. Elevated activity of tumour necrosis, TNF

27
Q

A 67 year old man visits the GP after finding blood in his stool. The GP refers him to the gastro-enterologist. During colonoscopy, a polipous tumour of 1.5 cm is found in the sigmoideum. It is removed with a Loop Electrosurgical Excision Procedure. During microscopic examination, the pathologist concludes that the lesion was removed incompletely. The patient however refuses to undergo endoscopic follow-up. What do you see in the microscopy?

a. only normal colon mucosa
b. top: normal mucosa, bottom: adenoma
c. top: adenoma, bottom: normal mucosa
d. only adenoma

A

c. top: adenoma, bottom: normal mucosa

28
Q

What do you see in this image?

a. normal colon mucosa everywhere
b. normal mucosa and adenoma
c. only adenoma

A

b. normal mucosa and adenoma

stratified nuclei and reduced mucous fraction of the epithelium

29
Q

Loss of APC protein plays a role in the first phase on the onset of colon adenoma and colon carcinoma. Which function of APC is essential in this context?

a. binding of beta-catenin, resulting in destruction of van beta-catenin
b. binding of cylinder D1 in the cytoplasm
c. P53 activation, by means of phosphorylation
d. Targeting of the VHL protein for proteasomal degradation

A

a. binding of beta-catenin, resulting in destruction of van beta-catenin

30
Q

Six years later, the patient visits his GP once more: He had found blood in his stool again.

He has started to defecate irregularly. Because he is increasingly worried, he agrees to undergo a colonoscopy. At the site where the adenoma was removed earlier, a dish-shaped tumour of 4 cm is found, with a central crater. After confirming the diagnosis with endoscopic biopsies, a surgical resection was performed. During pathologic evaluation, it was shown that the tumour had already grown through the muscularis propria, into the subserosal adipose tissue. The tumour is also found in 2 out of 10 lymph nodes obtained during resection.

The post-operative course remained uncomplicated and the patient is now treated with adiuvant chemotherapy.
What do you see in this image?
(Q32)

A

Only normal colon mucosa

31
Q

What do you see in this image?

a. only normal colon mucosa
b. top: normal mucosa, bottom: adenoma
c. Top: adenoma, bottom: normal mucosa
d. only adenoma

A

b. top: normal mucosa, bottom: adenoma

32
Q

Which number is placed in the carcinoma in this image?

a. 1
b. 2
c. 3
d. 4

A

d. 4

33
Q

What do you see at the arrows in this picture?

a. transition from adenoma towards adenocarcinoma
b. ulceration of adenocarcinoma at its surface
c. lymphangioinsivasive growth of the adenocarcinoma
d. necrosis of the adenocarcinoma at the edges of the tumour

A

c. lymphangioinsivasive growth of the adenocarcinoma

34
Q

What do you se e at the arrows in this image?

a. transition from adenoma towards adenocarcinoma
b. invasive growth of the adenocarcinoma into the submucosa
c. invasive growth of the adenocarcinoma into the muscular Propria
d. invasive growth of the adenocarcinoma into the perirectal adipose tissue

A

c. invasive growth of the adenocarcinoma into the muscular Propria

35
Q

Which number separates the adenocarcinoma from NORMAL colon mucosa?

a. 1
b. 2
c. 3
d. 4

A

b. 2

36
Q

Three years after treatment, a solitary tumour of the liver with a diameter of 2.5 cm is found during follow-up. Further research yields no further abnormalities.

The tumour was resected surgically.

What do you see in this image?

a. Top: liver tissue, bottom: metastasis of adenocarcinoma
b. Top: metastases adenocarcinoma, bottom: liver tissue
c. only metastasis of adenocarcinoma

A

a. Top: liver tissue, bottom: metastasis of adenocarcinoma

37
Q

What do you see at the arrow in this picture?

a. vena centralis in liver tissue
b. portal triad (kiernans trangle) in liver tissue
c. micrometastasis of adenocarcinoma in liver tissue
d. small focus of necrosis in liver tissue

A

b. portal triad (kiernans trangle) in liver tissue

38
Q

What do you see at the arrow in this picture?

a. necrotic focus in liver tissue
b. necrotic focus in adenocarcinoma
c. apoptotic cell mass in adenocarcinoma
d. liver tissue amidst adenocarcinoma

A

b. necrotic focus in adenocarcinoma

39
Q

What is the name of reactive mesenchymal tissue, which was induced by this adenocarcinoma?

a. scar tissue
b. granulation tissue
c. cytogenic stroma
d. demoplastic stroma

A

d. demoplastic stroma

40
Q

Can you explain the origin of the black material at the border of this resection of a liver metastasis, originating from a colon carcinoma?

a. charred tissue, caused by cauterization of wound borders during tumour resection
b. bacterial contamination following sample acquisition, which happened prior to fixation
c. ink, applied by the pathologist in order to perform histologic radicality analysis

A

c. ink, applied by the pathologist in order to perform histologic radicality analysis

41
Q

Why would you resect a liver metastasis of a colon carcinoma surgically? Is this even helpful in metastasized disease?

A

Actually it is, although only under specific circumstances. A retrospective study showed that a significant increase in survival was obtaind by resection of metastases. Recent studies focus on laporascopic tumour resection of liver metastases: This meta-analysis is a fine example.

Outcomes of laparoscopic hepatic resection for colorectal cancer metastases.
Nguyen KT, Geller DA.

42
Q

The family of the patient now starts to worry if this form of colon cancer may be hereditary. Two nephews of the patient were diagnosed with colon cancer as well, respectively at the age of 56 and 49. The mother of these two nephews died of an endometrial carcinoma at the age of 56. The hereditary non-polyposis colorectal cancer syndrome (HNPCC) is a consequence of mutations in genes that encode:

a. DNA mismatch repair proteins
b. apoptosis-inducing proteins
c. CDK inhibitors
d. Proteins that monitor chromosome segregation

A

a. DNA mismatch repair proteins

43
Q

Genetic analysis for elevated risk is possible for…

a. Familiar adenomatous polyposis (FAP)
b. hereditary non-polyposis coli colorectal cancer (HNPCC)
c. Both FAP and HNPCC
d. Neither FAP, nor HNPCC

A

c. Both FAP and HNPCC

44
Q

Most cases of cancer predisposition syndromes are based on…

a. an inactivating mutation of one of the tumour suppressor genes in the germ line
b. an inactivating mutation of a proto-oncogen in the germ line
c. an activating mutation of a tumour suppressor gene in the germ line
d. an activating mutation of a proto-oncogene in the germ line

A

a. an inactivating mutation of one of the tumour suppressor genes in the germ line

45
Q

The vast majority of cancer predisposition syndromes is caused by mutations in tumour suppressor genes. But which tumour predisposition syndrome is the consequence of an oncogene mutation int eh germ line?

a. familiar melanoma, by an INK4A mutation
b. familiar colon carcinoma, by an APC mutation
c. Li-Fraumeni syndrome, by a P53 mutation
d. MEN-2 (multiple endocrine neoplasia type 2)

A

d. MEN-2 (multiple endocrine neoplasia type 2)

46
Q

Which statement about a chronic H. pylori infection is true? A chronic H. pylori infection elevates the risk of…

a. gastric carcinoma, but not gastric lymphoma
b. gastric lymphoma, but not gastric carcinoma
c. both gastric carcinoma and gastric lymphoma
d. neither gastric carcinoma, nor gastric lymphoma

A

c. both gastric carcinoma and gastric lymphoma

47
Q

which of these lymph nodes shows signs of reactive hyperplasia?

a. left lymph node
b. right lymph node

A

Left lymph node: reactive hyperlasia

Right lymph node: malignant lymphoma

48
Q

Wich of the two follicle centres belongs to the lymph node with reactive hyperplasia, and how do you see this?

a. left lymph node
b. right lymph node

A

Left: reactive hyperplasia with abundant starry-sky macrophages
Right: malignant lymphoma, NO starry-sky macrophages

49
Q

How do you interpret this BCL2 staining?

a. malignant lymphoma, the large majority of cells in the follicles are BCL-2 positive
b. malignant lymphoma, the large majority of cells in the follicles are BCL-2 negative
c. reactive hyperplasia, the large majority of cells in the follicles are BCL-2 positive.
d. reactive hyperplasia, the large majority of cells in the follicles are BCL-2 negative.

A

How do you interpret this BCL2 staining?

a. malignant lymphoma, the large majority of cells in the follicles are BCL-2 positive
b. malignant lymphoma, the large majority of cells in the follicles are BCL-2 negative
c. reactive hyperplasia, the large majority of cells in the follicles are BCL-2 positive.
d. reactive hyperplasia, the large majority of cells in the follicles are BCL-2 negative.

50
Q

How do you interpret this BCL2 staining?

a. malignant lymphoma, the large majority of cells in the follicles are BCL-2 positive
b. malignant lymphoma, the large majority of cells in the follicles are BCL-2 negative
c. reactive hyperplasia, the large majority of cells in the follicles are BCL-2 positive.
d. reactive hyperplasia, the large majority of cells in the follicles are BCL-2 negative.

A

d. reactive hyperplasia, the large majority of cells in the follicles are BCL-2 negative.d. reactive hyperplasia, the large majority of cells in the follicles are BCL-2 negative.

51
Q

The following protein stimulates the extrinsic apoptosis pathway:

a. cytochrome c
b. BCL-2
c. IAp
d. TNF

A

d. TNF

52
Q

Which two direct consequences are caused by mitochondrial damage?

a. loss of oxidative phosphorylation and cytoplasmatic release of cytochrome c
b. loss of gluconeogensesis and lipolysis
c. activation of BCL-2 and BCL-x
d. loss of glycolysis and activation of caspase 8

A

a. loss of oxidative phosphorylation and cytoplasmatic release of cytochrome c

53
Q

Name an EARLY step in the initiation of apoptosis caused by damage to the DNA or endoplasmic reticulum (ER) stress

a. activation of BCL-2 and BCL-x
b. Activation of Bax and Bak
c. activation of Fas and FADD
d. Activation of caspase 3 and DNase

A

b. Activation of Bax and Bak

Pathology dt2 (39 decks)

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