Testicular Cancer Flashcards

1
Q

Presentation

A

IF localized –> nodule, painless mass, dull ache or heavy sensation (30%), gynecomastia, testicular atrophy, infertility
*Sometime testis is just enlarged and indurated, and you don’t necessarily feel a mass
Lower abdominal pain

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2
Q

Tumor markers to test for as part of initial workup

A

bHCG + AFP + LDH

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3
Q

Term for premalingant condition associated with testicular cancer

A

Germ-cell neoplasia in situ (GCNIS)

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4
Q

Primary distinction between germ cell tumors

A

Seminoma histologies
Nonseminomatous histologies

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5
Q

nonseminomatous histologies

A

Embryonal cell
Choriocarcinoma
Yolk sac
Teratoma
Stroma tumors (sertoli, leydig)

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6
Q

biomarker associated with yolk sac histology

A

AFP

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7
Q

biomarker associated with choriocarcinoma + level typically

A

beta-HCG
*Extremely high levels

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8
Q

most aggressive subtype

A

choriocarcinoma

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9
Q

Serum tumor markers used in testicular cancer

A

LDH
AFP
beta-HCG

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10
Q

Chemo regimens used for testicular cancer

A

EP
BEP
VIP
TIP

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11
Q

what is EP regimen

A

etoposide/cisplatin

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12
Q

what is BEP regimen

A

belomycin/etoposide/cisplatin

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13
Q

Stage IIB/C seminoma management (RP lymphadenopathy)

A

Inguinal orchiectomy + chemo (regimen determined based off risk level)

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14
Q

response assessment

A

tumor markers + CT-abdomen pelvis

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15
Q

surveillance

A

Tumor markers, CXR, CT abdomen/pelvis

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16
Q

Seminoma origin

A

Originates in the germinal epithelium of the seminiferous tubules. Thus tumor originates in the testes. These are slow growing and more indolent and curable than nonseminomatous.

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17
Q

5 year survival of testicular cancer

A

Over 95 percent. Testicular cancers are among the most curable solid neoplasms; the five-year survival rate is

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18
Q

Pathway of treatment (surgery vs. chemo)

A

For men who present with clinically advanced disease, we perform a radical orchiectomy prior to chemotherapy whenever possible. Despite this, there are some men who present with life-threatening advanced disease who undergo systemic chemotherapy prior to orchiectomy (“delayed orchiectomy”).

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19
Q

meaning of “germ cell tumor”

A

tumor arising from germ cell, so either testicular or ovarian

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20
Q

Primary class of chemo used for testicular

A

platinum-based chemotherapy

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21
Q

High risk features of NSGCT

A

1) LVI
2) Predominance of an embryonal carcinoma component
3) T3/ T4
*Rework question

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22
Q

RPLND means

A

retroperitoneal lymph node dissection

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23
Q

Difference in management between seminomatous and nonseminomatous testicular cancer

A

Only differs for localized. For men with advanced testicular germ cell tumors (GCTs), management is the same

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24
Q

how management of advanced testicular tumor is determined

A

risk stratification

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25
Q

most sensitive means for detecting relapse in men with NSGCT

A

Tumor markers

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26
Q

Management differences in advanced NSGCT in general

A

Different number of cycles of BEP

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27
Q

Pure seminoma biomarkers

A

AFP normal
bHCG can be elevated
LDH can be elevated

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28
Q

Stage IIA NSGCT management after radical orchiectomy IF markers negative

A

Nerve sparing RPLND or primary chemo with BEP

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29
Q

term for testicle removal surgery

A

radical inguinal orchiectomy

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30
Q

What are the most common histologies w/ testicular cancer in order for prevalence

A
  • most commonly seminoma
  • Embryonal cell and yolk sac equally distributed
  • choriocarcinoma very rare.
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31
Q

What are the stages?

A

Stages I, II, and III (there is no stage IV)

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32
Q

Stage II means

A

1) Retroperitoneal lymph node involvement
2) STMs can only be mildly elevated

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33
Q

Stage III means

A

Lymphadenopathy anywhere else other than retroperitoneal

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34
Q

RF’s

A
  • Cryptorchidism (Undescended) (prepubertal orchidectomy decreases risk of testicular cancer)
  • Infertility
  • FH of testis cancer
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35
Q

Genetic fingerprint of germ cell tumors

A

Isochromosome 12p
*Testis GCTs invariably have increased copies of genetic material from 12p

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36
Q

What are the germ cell tumors

A

Seminoma
Embryonal carcinoma
Choriocarcinoma
Yolk sac tumor
Teratoma
Spermatocytic tumor

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37
Q

What are the sex cord/gonadal stroll tumors?

A
  • Leydig cell tumor
  • Sertoli cell tumor
  • Granulosa cell tumor
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38
Q

Benign causes of AFP elevation

A

Liver disease, toxicity

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39
Q

AFP half-life + clinical relevance of half-life

A

1 week
*So if not falling by 50% following orchiectomy, this may indicate residual cancer

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40
Q

Upper limit of normal for AFP + clinical relevance

A

20
*Ignore slightly elevated AFP, very nonspecific. Pay more attention to the pattern.

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41
Q

beta-hCG produced by which tumors?

A

All GCT’s, but extremely elevated in choriocarcinoma

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42
Q

beta-hCG half life

A

Less than 3 days

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43
Q

False positives for beta-hCG

A
  • Reports that marijuana consumption leads to elevated HCG
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44
Q

Utility of LDH

A
  • prognostic/staging of disseminated nonseminomas
  • Not used to monitor response to treatment
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45
Q

Risk determined by

A
  • Tumor marker levels
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46
Q

AFP level indicating good, intermediate, and poor risk

A

Good = less than 1000
Intermediate = 1000-10,000
Poor = Greater than 10k

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47
Q

B-hCG level indicating good, intermediate, and poor risk

A

Good = less than 5000
Intermediate = 5000-50,000
Poor = Greater than 50k

48
Q

LDH level indicating good, intermediate, and poor risk

A

Good = less than 1.5x ULN
Intermediate = 1.5-10x ULN
Poor = Greater than 10x ULN

49
Q

When sperm banking is needed

A
  • prior to chemo/RT, *doesn’t need to happen before orchiectomy
50
Q

Primary determinant of risk of relapse

A

Lymphovascular invasion

51
Q

What is Stage 1S

A
  • No radiographic evidence of tumor spread but tumor markers stay elevated after orchiectomy
52
Q

Treatment of Stage 1S

A

Same as stage III, assume metastatic

53
Q

Tumors in which Stage 1S occurs

A

nonseminoma

54
Q

Stage I seminoma treatment

A

*Individualized, patient preference but surveillance is guideline preferred
*Surveillance
Vs
Single agent carboplatin (1 or 2 doses)
Vs
RT to retroperitoneum (fallen out of favor due to increased risk of secondary cancer – why do this if you can cure primary?)

55
Q

Management of Stage II seminoma

A

RT or chemo (BEPx3 or EPx4)
IF bulky RP disease –> chemo preferred

56
Q

Stage I NSGCT management

A

Surveillance (preferred)
OR
RPLND
OR
BEP x 1

57
Q

Surveillance schedule

A
  • intense
  • monthly visits required for tumor markers
58
Q

Stage II NSGCT management

A

IIA: RPLND or BEP
IIB/C or IIA w/ SI: BEP x3 or EPx4

59
Q

Caveat about RPLND with Stage II

A
  • you may not necessarily avoid chemo (if nodes are malignant, will need chemo)
60
Q

What is VIP?

A
  • etoposide (VePesid)
  • ifosfamide
  • cisplatin
  • meson
61
Q

2nd line chemo regimens

A

TIP
VeIP
High dose carboplatin and etoposide

62
Q

Bleomycin pneumonitis presentation

A

Dry cough, rales, dyspnea,

63
Q

What are bleomycin precautions?

A

1) Avoiding high partial pressure O2 in hospital or during surgery
2) Minimizing intraoperative IV fluids

64
Q

CXR caveat to know of with bleomycin

A
  • can cause pseudonodules (inflammatory nodules that are benign)
65
Q

Primary cisplatin toxicities

A
  • renal toxicity
  • ototoxicity
  • peripheral neuropathy
66
Q

When EP is used instead of BEP

A
  • Elderly
  • poor renal function
  • lung disease
  • serious athlete (lung function)
67
Q

Chemo for good-risk disease

A

BEPx3

68
Q

Chemo for intermediate or poor risk disease

A

BEPx4

69
Q

Criteria for intermediate/poor risk disease

A
  • AFP greater than 1000
  • B-hCG greater than 5K
  • LDH greater than 1.5x ULN
  • mets to organs other than the lungs
  • mediastinal primary NSGCT
70
Q

What is TIP?

A

Taxol
Ifosfamide
Cisplatin

71
Q

Second line systemic therapy options

A

VeIP x4
OR
TIP x 4
OR
HDCT x 2

72
Q

Growing teratoma concept

A

Masses that are growing during chemo are often teratoma. Need surgery.
*Tumor markers will go down
*Rare but commonly tested

73
Q

Management of seminoma with residual mass

A

Surveillance (most are benign)
IF greater than 3cm – get PET/CT

74
Q

Management of NSGCT with residual mass after completion of chemotherapy

A

Surgical resection
***never observation
**No role for PET/CT unless pure seminoma

75
Q

Carboplatin vs cisplatin efficacy for NSGCT’s

A

Carboplatin is less effective

76
Q

In research, why do testicular cancer patients do better at high volume institutions?

A

***Patients get more chemotherapy and it is on time. Fewer dose reductions. You shouldn’t dose reduce in cancer being treated with curative intent (for low counts or mild AKIs).

77
Q

Teratoma PET avidity

A

Teratomas don’t light up on PET

78
Q

Management of NSGCT patient with extensive lung mets

A
  • Brain MRI (patients with extensive lung mets are at higher risk for brain mets)
79
Q

Management of bleomycin lung toxicity? Rechallenge?

A
  • stop the drug, switch to EP (drop bleomycin)
  • never rechallenge (pulmonary fibrosis can be fatal)
  • high dose steroids
80
Q

presentation of bleomycin pulmonary toxicity

A
  • can start off as penumonitis, but can progress to fibrosis
81
Q

Significance of rising tumor markers at the end of treatment

A

chemorefractory disease

82
Q

chemo in locally advanced testicular cancer is followed by

A

RPLND

83
Q

Why RPLND is done at the end of treatment with GCTs

A

(teratoma will need to be resected because it is not chemo sensitive)

84
Q

what is growing teratoma syndrome?

A
  • residual mass (typically RP) increasing in size despite normalized or decreasing tumor marker levels
85
Q

Presentation of leydig cell tumor

A
  • gynecomastia, impotence, loss of libido
86
Q

Paraneoplastic phenomena of testicular cancer

A
  • hyperthyroidism (TSH and hCG have a common alpha subunit
  • limbic encephalitis (anti-Ma2 antibodies
87
Q

How is staging done in testicular cancer

A

radical inguinal orchiectomy (imaging is not reliable)

88
Q

Relationship between microlithiasis and testicular cancer

A
  • strong association but not causal
89
Q

Problem with CT abdomen for staging

A

High false negative rates in retroperitoneum w/ occult micrometastases (ie not sensitive for disease in the retroperitoneum)

90
Q

Where relapse typically occurs

A

Retroperitoneal lymph nodes

91
Q

Tumor markers in pure seminomas

A
  • AFP never elevated (seminomas don’t produce AFP)
  • BetaHCG typically normal but can be elevated in 20%
92
Q

Precursor lesion to testicular cancer

A

Testicular germ cell neoplasia in situ (GCNIS

93
Q

TNM staging components for NSGCT’s

A

TNM + S (tumor markers)

94
Q

N3 disease

A

lymph node mass larger than 5 cm in greatest dimension

95
Q

N2 disease

A

lymph node mass larger than 2 cm but not larger than 5 cm in greatest dimension

96
Q

N1 disease

A

lymph node mass 2 cm or smaller in greatest dimension and less than or equal to five nodes positive

97
Q

T4 disease

A

Tumor invades scrotum

98
Q

T3 disease

A

Tumor directly invades spermatic cord soft tissue

99
Q

T2 disease

A

Lymphovascular invasion OR Tumor invading hilar soft tissue or epididymis or penetrating visceral mesothelial layer covering the external surface of tunica albuginea with or without lymphovascular invasion

100
Q

Prognostic/risk stratification model used in testicular cancer

A

International Germ Cell Cancer Collaborative Group (IGCCCG)

101
Q

Risk groups for NSGCTs in IGCCCG model

A

good-, intermediate-, and poor-risk

102
Q

What is Stage 1S disease?

A

NSGCT limited to the testis on clinical staging but who have persistent elevation of tumor markers

103
Q

Relevance of spermatocytic features on path

A

Presence virtually eliminates the chance of recurrence. Positive prognosticator.

104
Q

Dominant pathology of testicular cancer in older men

A

LYMPHOMA

105
Q

Clinical features of embryonal cell histology

A
  • Higher risk of relapse.
  • early progression and development of metastatic disease
106
Q

Microscopic findings with embryonal cell

A

hemorrhage or necrosis within the tumor

107
Q

which testicular cancers produce AFP?

A
  • yolk sac very high
  • embryonal but less so than yolk sac
  • pure choriocarcinoma and pure seminoma do not produce AFP
108
Q

why do you never biopsy testicular?

A

Seeding of biopsy track

109
Q

Backbone of chemotherapy in testicular cancer

A

Etoposide, cisplatin

110
Q

Primary long term toxicities of chemotherapy in testicular

A

SMNs + CV disease

111
Q

Meaning of SMNs

A

secondary malignant neoplasms

112
Q

Why surgery/RPLND is never done in seminoma post chemotherapy

A

Desmoplastic reaction

113
Q

Does primary site affect outcome in seminoma?

A

NO

114
Q

Second line for advanced NSGCT

A

Conventional-dose chemotherapy (CDCT) w/ TIP for 4 cycles (or VeIP for 4 cycles)
High-dose chemo (HDCT) w/ sequential (2-3) ASCT

115
Q

Intermediate risk NSGCT per IGCCCG

A

ALL OF THE FOLLOWING
Testicular or retroperitoneal primary tumors
No metastases to organs other than the lungs and/or lymph nodes
Serum AFP 1000 to 10,000 ng/mL* or
Serum beta-hCG 5000 to 50,000 milli-international units/mL* or
LDH 3 to 10 times the upper limit of normal*

116
Q

Poor risk NSGCT per IGCCCG

A

Any of the following:
Mediastinal primary with or without metastases
Metastases to organs other than the lungs and/or lymph nodes
Serum AFP >10,000 ng/mL*
Serum beta-hCG >50,000 milli-international units/mL*
LDH more than 10 times the upper limit of normal*

117
Q

Good risk NSGCT per IGCCCG

A

All of the following:
Testicular or retroperitoneal primary tumors
No metastases to organs other than the lungs and/or lymph nodes
Serum AFP <1000 ng/mL, beta-hCG <5000 milli-international units/mL, and LDH <3 times the upper limit of normal*