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NONNEOPLASTIC & NEOPLASTIC DISEASES OF PROSTATE > CARCINOMA OF THE PROSTATE > Flashcards

CARCINOMA OF THE PROSTATE Flashcards

1
Q

the most common form of cancer in men

A

Adenocarcinoma of the prostate

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2
Q

Adenocarcinoma of the prostate is uncommon before the age

A

50

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3
Q

Pathogenesis of prostate carcinoma

A

androgens,
heredity,
environmental factors, and acquired somatic mutations

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4
Q

Androgens are of central importance because they

A

provide the “soil,” the cellular context

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5
Q

does not develop in

A

males who are castrated before puberty

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6
Q

cancers →often regress for a time in response to

A

surgical or chemical castration

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7
Q

tumors that recur in the face of anti-androgen therapies still depend on

A

gene products regulated by androgen receptors for their growth and survival

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8
Q

there is no evidence that

A

androgens initiate carcinogenesis, nor are androgen levels associated with prostate cancer risk

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9
Q

there is an increased risk among

A

first-degree relatives of patients
• Prostate cancer

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10
Q

Uncommon in

A

Asia

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11
Q

highest among

A

African-Americans and in Scandinavian countries

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12
Q

Genome-wide association studies have identified

A

a number of genetic variants that are associated with increased risk for developing prostate cancer. Although each variant carries only a small increased risk, the effect is multiplicative, such that men with multiple risk alleles may have up to a 5-fold increase in risk compared to the general population.

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13
Q

Environment

A

in Japanese immigrants to the United States the incidence of the disease rises as the diet in Asia becomes more westernized

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14
Q

Acquired genetic aberrations

A

as in other cancers, genetic aberrations are the actual drivers of cellular transformation

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15
Q

actual drivers of cellular transformation

A

genetic aberrations

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16
Q

The most common gene rearrangements in prostate cancer create fusion genes

A

TMPRSS2-ETS fusion genes

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17
Q

TMPRSS2-ETS fusion genes is found in

A

40% to 60% of prostate cancers

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18
Q

TMPRSS2-ETS fusion genes occur relatively early in

A

tumorigenesis

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19
Q

Other mutations commonly lead to activation of

A

the PI3K/AKT signaling pathway

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20
Q

Most common mutations include

A

are loss-of-function mutations involving the tumor suppressor PTEN

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21
Q

GROSS

A

Carcinomas detected clinically are usually not visible grossly.
• More advanced lesions appear as firm, gray-white lesions with ill-defined margins
• infiltrate the adjacent gland

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22
Q

LM

A

moderately differentiated adenocarcinomas with well-defined glands

23
Q

Glands in LM

A

typically are smaller than benign glands

24
Q

Glands are

A

lined by a single uniform layer of cuboidal or low columnar epithelium, lacking the basal cell layer seen in benign glands
are crowded together
characteristically lack branching and papillary infolding

25
Q

the cytoplasm of the tumor cells ranges from

A

pale-clear (as in benign glands) to a distinctive amphophilic (dark purple) appearance

26
Q

nuclei

A

are enlarged and often contain one or more prominent nucleoli

27
Q

some variation

A

in nuclear size and shape is usual

28
Q

… is not marked

A

pleomorphism

29
Q

.. are uncommon

A

mitotic figures

30
Q

With increasing grade

A

irregular or ragged glandular structures, cribriform glands,
sheets of cells, or
infiltrating individual cells are present

31
Q

Grade 1

A

→ the most well differentiated tumors,

32
Q

grade 5

A

→no glandular differentiation

33
Q

Most tumors are patterns

A

3, 4, or 5

34
Q

the majority of tumors contain

A

more than one pattern

35
Q

primary grade is assigned to

and a secondary grade to

A

the dominant pattern

the next most frequent pattern.

36
Q

The two numerical grades are then

A

added to obtain a combined Gleason score.

37
Q

Tumors with only one pattern are treated

A

as if their primary and secondary grades are the same →the number is doubled

38
Q

The most differentiated tumors have a Gleason score of

A

2 (1 +1)

39
Q

least differentiated tumors merit a score of

A

10 (5 +5)

40
Q

approximately 80% of cases in remaining tissue harbors→

A

high-grade prostatic intraepithelial neoplasia (HGPIN)

41
Q

high-grade prostatic intraepithelial neoplasia (HGPIN)

A

80% of cases in remaining tissue harbors

42
Q

Many of the molecular changes seen in invasive cancers are also seen in

A

HPIN

43
Q

Clinical Features

A

small, nonpalpable, asymptomatic lesions discovered on needle biopsy performed to investigate an elevated serum prostate-specific antigen (PSA) level

44
Q

Some 70% to 80% of prostate cancers arise in

A

the outer (peripheral) glands,

45
Q

subset of outer glands prostate cancers may be palpable as

A

irregular hard nodules on digital rectal examination.

46
Q

prostate cancer is less likely than BPH to cause ….. because..

A

urethral obstruction in its initial stages

of the peripheral location

47
Q

Locally advanced cancers often infiltrate

A

the seminal vesicles and periurethral zones of the prostate may invade the adjacent soft tissues,
the wall of the urinary bladder, or less commonly the rectum

48
Q

Bone metastases, particularly to… are frequent late in the disease and typically cause ..

that can be detected on ..

A

axial skeleton,

osteoblastic (bone-producing) lesions

radionuclide bone scans.

49
Q

most widely used test in the diagnosis and management of prostate cancer

A

The PSA (prostate specific antigen) assay

50
Q

PSA as a biomarker is that it is not cancer specific , may also increase in

A

BPH,
prostatitis,
prostatic infarcts,
instrumentation of the prostate, and ejaculation

51
Q

Conversely, … of patients with organ confined prostate cancer have PSA values below the cutoffs

A

20% to 40%

52
Q

The most common treatments for clinically localized prostate cancer are

A

radical prostatectomy and radiotherapy.

53
Q

The prognosis after radical prostatectomy is based on

A

the pathologic stage,
whether the margins of the resected specimens are free of tumor, and Gleason grade

NONNEOPLASTIC & NEOPLASTIC DISEASES OF PROSTATE (3 decks)

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