Testis Cancer, Anatomy, Embryology Flashcards

1
Q

Gene that determines gonadal transition to a male

A

SRY

Under the influence of the SRY gene (sex-determining region of the Y chromosome), in the 7th to 8th week, cells in the genital ridge differentiate into seminiferous tubules containing spermatogonia and Sertoli cells. Without the SRY protein, ovarian follicles form.

The Sertoli cells begin to secrete Müllerian-inhibiting substance (MIS), acting locally and causing the Müllerian ducts to regress between 8-10 weeks, thus contributing to normal male phenotypic development.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Which cells produce testosterone?

A

Leydig cells

In the 9th-10th weeks, Leydig cells differentiate from genital ridge cells in response to SRY protein and are located between the seminiferous tubules. These cells begin to produce testosterone. There is a rise in both serum and testicular testosterone that peaks at 13 weeks before beginning to decline.

Between the 8th and 12th week, testosterone secretion stimulates the virilization of the wolffian ducts into the vas deferens, seminal vesicles, and ejaculatory ducts.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Table of timing of male gonadal development

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Normal adult testis size and volume

A

On average, the normal adult testis measures 4-5cm long, 3cm wide, and 2.5cm deep with volume ranging 12-30ml.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Three types of histologic cells in testis

A

Seminiferous tubules, Sertoli cells, Leydig cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Arterial blood supply to testis

A

Three:
1. Gonadal/Testicular
- Arises inferior to SMA, directly off of aorta
2. Cremasteric
- Arises from inferior epigastric artery
- Anastomoses with testicular artery within testis
3. Vasal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Left Testicle Lymphatic Drainage

A

The primary drainage pattern on the left is to the para-aortic and preaortic lymph nodes, followed by the interaortocaval nodes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Right Testicle Lymphatic Drainage

A

On the right side, primary drainage is to the interaortocaval nodes, followed by the precaval and preaortic nodes.

It is more common for the lymphatic drainage of the right testis, and rare with left-sided tumors, to cross the midline and exhibit bilateral lymph node metastases

Drainage is right to left!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Layers of the scrotum and spermatic cord encountered during surgical exploration, progressing from superficial to deep

A

Skin, dartos, external spermatic fascia, cremasteric fascia, cremasteric muscle, internal spermatic fascia, tunica vaginalis (parietal then visceral), tunica albuginea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

T staging of testicular tumors

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

N staging of testicular cancer

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

M staging of testicular cancer

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Serum Tumor Marker Staging

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Stage Grouping

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Risk Classification for Sem and Non-Sem

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Treatment options for stage IA and IB pure seminoma

A

(i) Surveillance (preferred)
(ii) Retroperitoneal Radiotherapy
(iii) Chemotherapy with carboplatin (1 or 2 cycles)

More than 80% of patients with stage I seminoma are cured with orchiectomy alone, therefore surveillance is the preferred approach, and the disease specific survival for stage I disease is 99% irrespective of the management strategy used.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

AUA Guideline Algorithm for treatment of early testicular cancer

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Surveillance for Stage IA and IB Seminoma

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Risk factors for predicting relapse

A

In an analysis of over 600 patients, rete testis invasion and tumors ≥ 4 cm were identified as risk factors for predicting relapse.

For patients with 0, 1, or 2 of these risk factors the recurrence rates were 12%, 16%, and 32%, respectively.

NCCN recommends against a risk-adapted approach and supporting surveillance as the preferred strategy for all stage I patients.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Stage I Seminoma Surveillance NCCN and AUA

A
21
Q

Types of testicular cancer

A

The vast majority are classified as germ cell tumors (95%), while the remaining are predominately sex cord/stromal tumors (mainly Leydig cell and Sertoli cell tumors). Germ cell tumors (GCT) are further designated as seminoma or non-seminoma germ cell tumors (NSGCT).

22
Q

Risk factors for developing testicular cancer

A

Cryptorchidism, personal or family history, intra-tubular germ cell neoplasia (ITGCN).

It is felt that most GCTs arise from ITGCN and its presence is a major risk factor as 50% of men with ITGCN will develop a GCT within 5 years.

23
Q

Histologic Subtypes of Testicular Cancer

A

Germ Cell Tumors:
- Seminoma
- Nonseminomatous Germ Cell Tumors: Embryonal, Choriocarcinoma, Teratoma, Yolk Sac (Endodermal Sinus Tumor)

24
Q

Does Seminoma produce AFP? bHCG?

A

NO AFP
5% produce bHCG (because 5% contain syncytiotrophoblasts, which secrete bHCG)

25
Q

Most common GCT in children/infants?

A

Yolk Sac (Endodermal Sinus Tumor)

26
Q

Do Yolk Sac tumors produce AFP? bHCG?

A

Generally will produce AFP
NEVER bHCG

27
Q

Classic pathologic finding of Yolk Sac Tumors?

A

Schiller-Duval bodies

28
Q

Does choriocarcinoma produce AFP? bCHG?

A

NEVER AFP
Yes bHCG, usually high

29
Q

Do pure teratomas produce AFP? bHCG?

A

Pure teratoma will produce neither, but pure teratoma is very rare in adults

30
Q

What to do for evaluation of initial presentation of testicular mass?

A

Testicular US
- Homogeneous mass more likely to be seminoma
- Heterogeneous mass more likely to be NSGCT

No role for further imaging OF THE TESTIS at time of presentation

Microlithiasis: just recommend routine self-exam

Obtain tumor markers at time of diagnosis, prior to any intervention (AFP, LDH, bHCG)

31
Q

AFP:
- Half life?
- Which testicular cancers produce?
- Why else elevated?
- What is a true elevation?

A

5-7 days

NOT PRODUCED by seminoma

Normal <10

Elevated in 50-80% of NSGCT

Embryonal carcinoma and yolk sac tumors produce AFP, seminoma and choriocarcinoma do not.

AFP may also be elevated in patients with liver disease, hepatocellular carcinoma, and stomach/pancreas/biliary duct/lung cancers.

Mildly elevated AFP may not represent germ cell tumor, thus the decision to treat a patient should not be made for an AFP level < 20.

32
Q

bHCG:
- Half life?
- Which testicular cancers produce?
- Why else elevated?
- What is a true elevation?

A

Half life 24-36 hours

Elevated in 20-60% of NSGCT and 15% of seminomas

bHCG is elevated in embryonal carcinoma/choriocarcinoma/seminoma. Elevations may also be observed in liver, biliary, pancreas, stomach, lung, breast, kidney, and bladder cancers as well as secondary to marijuana use.

Significant hypogonadism may also cause low level elevation of HCG and these patients can be challenged with testosterone injections which normalize their HCG levels.

33
Q

LDH:
- Half life?
- Which testicular cancers produce?
- Why else elevated?
- What is a true elevation?

A

Half life is 24 hours

Non-specific marker of GCT

Patients should not be treated due to elevated LDH alone

34
Q

Role of miRNA in testicular cancer?

A

miR-371a-3p is the promising blood-based biomarker

Reliably detects all macroscopic GCT histologies, except for teratoma

miR-371a-3p holds promise in the following clinical scenarios:
1) patients with inconclusive testicular masses 2) surveillance after orchiectomy for early detection of relapse
3) response monitoring during chemotherapy 4) management of post-chemotherapy residual masses
5) surveillance after curative intent

short half-life of <24 hours

35
Q

Staging: Tis

A

Germ Cell Neoplasia in Situ

36
Q

Staging: T1

A

Confined to testis
NO LVI
Can be into epididymis
Can involve tunica albuginea but not vaginalis

37
Q

Staging: T2

A

Testis with or without epididymal involvement
+LVI OR into tunica vaginalis

38
Q

Staging: T3

A

Into spermatic cord
+/- LVI

39
Q

Staging: T4

A

Into scrotum
+/- LVI

40
Q

Staging: Clinical Nodes
N1

A

1-5 lymph nodes, all less than 2cm

41
Q

Staging: Clinical Nodes
N2

A

> 5 LNs (less than 5 cm)
OR
LN 2-5 cm in size

42
Q

Staging: Clinical Nodes
N3

A

LNs >5cm

43
Q

Staging: M1a

A

Distant mets
- Nonregional LNs
OR
- Pulmonary nodules/mets

44
Q

Staging: M1b

A

Distant mets OUTSIDE of nonregional LNs or lung

45
Q

Staging: Serum Tumor Markers
S1

A

AFP - <1k
bHCG - <5k
LDH - <1.5x normal

46
Q

Staging: Serum Tumor Markers
S2

A

AFP - 1k-10k
bHCG - 5k - 50k
LDH - 1.5 -10x normal

47
Q

Staging: Serum Tumor Markers
S3

A

AFP - >10k
bHCG - >50k
LDH - >10x normal

48
Q

Role of PET CT in testicular cancer

A

ONLY in seminoma to assess response to chemotherapy/determine if residual masses are active cancer
6-8 weeks after treatment