Adult Uro Oncology

Question 1

<p>ProtecT trial</p>

Answer 1

<p>Randomized 1,643 men with screen-detected PCa to active monitoring, radical prostatectomy, or radiation therapy with curative intent. At a median of 10 years, no differences in PCa mortality were observed across groups (PCa deaths per 1,000 person years: active monitoring 1.5, surgery 0.9, radiation 0.7, p = 0.48).</p>

Question 2

<p>PIVOT trial</p>

Answer 2

<p>The Prostate Cancer Intervention Versus Observation Trial (PIVOT) found that radical prostatectomy did not improve overall or disease-specific mortality at a median follow-up of 12.7 years.1,3 However, surgery reduced the risk of progression (40.9% vs 68.4%; HR 0.39, 95% CI 0.32-0.48) and treatment for progression (33.5% vs 59.7%; HR 0.45, 95% CI 0.36-0.56) compared to watchful waiting.</p>

Question 3

<p>SPCG 4</p>

Answer 3

<p>The Scandinavian Prostate Cancer Group Study No. 4 (SPCG 4) reported an improvement in overall and disease-specific mortality for men undergoing radical prostatectomy compared to watchful waiting. The absolute OS benefit favoring prostatectomy was 12%, which translated to a median 2.9 years of life gained at median 23 years of follow-up</p>

Question 4

<p>Prostate cancer Active surveillance inclusion criteria</p>

Answer 4

<p>Men with very low risk and low risk PCa per AUA and NCCN guidelines (or clinically insignificant disease per Epstein criteria) are typically candidates for AS.
<br></br>
<br></br>These criteria include:
<br></br>1. Grade Group 1 (Gleason score ≤ 6)
<br></br>2. Clinical stage ≤ T2a
<br></br>3. PSA density < 0.15ng/mL/g
<br></br>4. < or ≤ 3 positive biopsy cores
<br></br>5. ≤ 50% cancer in each core</p>

Question 5

<p>PUNCH trial</p>

Answer 5

<p>randomized patients with high-risk, clinically localized prostate cancer to neoadjuvant chemohormonal therapy with docetaxel and ADT plus radical prostatectomy or radical prostatectomy alone. Results indicated no difference in 3-year biochemical progression free rates, the primary endpoint. However, neoadjuvant chemohormonal therapy was associated with improved MFS and OS compared to surgery alone</p>

Question 6

<p>RADICALS-RT trial</p>

Answer 6

<p>enrolled 1396 men with intermediate-to-high risk prostate cancer after radical prostatectomy, and randomized them to adjuvant vs. early salvage RT demonstrated no statistically significant difference with regards to biochemical progression-free survival and freedom from subsequent hormonal therapy between the treatment arms. Adjuvant radiotherapy was associated with an increased number of urinary and bowel adverse effects.</p>

Question 7

<p>Recommended dose for conventonial fractionated EBRT in prostate cancer</p>

Answer 7

<p>Recommended doses for conventionally fractionated radiation are 75.6 to 79.2 Gy for low-risk cancers and up to 81 Gy for intermediate- and high-risk prostate cancers</p>

Question 8

<p>What is EBRT</p>

Answer 8

<p>External Beam Radiation Therapy
<br></br>
<br></br>delivered using a linear accelerator (LINAC.) The LINAC generates a high energy electron beam that is passed through a tungsten target to generate a photon beam. These beams reach megavoltage energies (commonly 6-15 MV) capable of delivering ionizing radiation energies to targets deep in the body.</p>

Question 9

<p>What is 3DCRT</p>

Answer 9

<p>Dimensional Conformal Radiation Therapy.
<br></br>
<br></br>The process of using CT images to generate a 3-dimensional radiation plan to maximize radiation dose to the target volume while minimizing dose to neighboring organs at risk (OAR’s)</p>

Question 10

<p>What is IMRT</p>

Answer 10

<p>Intensity Modulated Radiation Therapy (IMRT) is a specialized form of EBRT. The process of generating an IMRT plan is similar to the generation of a 3DCRT plan. However, IMRT utilizes a process called inverse planning.</p>

Question 11

<p>RT for low risk prostate cancer</p>

Answer 11

<p>Eligible patients: Men with NCCN low-risk prostate cancer (T1-2a and Gleason score 6 and PSA < 10 ng/ml).
<br></br>
<br></br>In addition to AS and RP, radiation treatment options for low-risk prostate cancer include EBRT or brachytherapy monotherapy.</p>

Question 12

<p>RT for intermediate risk prostate cancer</p>

Answer 12

<p>Eligible Patients: T2b-T2c or T1-T2a with Gleason score 7 or PSA 10-20 ng/ml.
<br></br>Radiation Treatment
<br></br>
<br></br>Options: EBRT +/- short course androgen deprivation therapy, brachytherapy monotherapy, combination brachytherapy and EBRT +/- short course androgen deprivation therapy.</p>

Question 13

<p>Ascende-RT trial</p>

Answer 13

<p>compared 46 Gy of pelvic EBRT with dose-escalation by 3DCRT (DE-EBRT) boost to 78 Gy or with an LDR boost.
<br></br>
<br></br>Men with both NCCN intermediate- (N==122, 30.7%) and high-risk disease (N=276, 69.3%) were eligible and received 1 year of ADT with 8 months delivered neoadjuvantly. With a median follow-up of 6.5 years there was a significantly greater risk of bPFS in men treated with DE-EBRT vs brachytherapy boost among the total population (HR=2.04, p=0.004) and among men with NCCN intermediate-risk disease (p=0.003). No benefit in prostate cancer specific or all-cause mortality could be observed.</p>

Question 14

<p>RT for High/very HR prostate cancer</p>

Answer 14

<p>Eligible Patients: T3-T4 or Gleason score 8-10, or PSA > 20 ng/ml.
<br></br>
<br></br>Radiation Treatment options: EBRT + long course ADT or combination brachytherapy and EBRT + ADT.</p>

Question 15

<p>Adjuvant RT post prostatectomy</p>

Answer 15

<p>Eligible Patients: pT3 disease, positive margins at prostatectmy.
<br></br>Radiation treatment options: EBRT to the prostatic fossa..
<br></br>
<br></br>Evidence shows improved Biochemical reurrence free survival and OS</p>

Question 16

<p>Salvage RT post prostatectomy</p>

Answer 16

<p>Eligible Patients: detectable and rising PSA (≥ 0.1 ng/ml) without radiographic evidence of nodal or distant metastasis.
<br></br>Radiation treatment options: EBRT +/- ADT.
<br></br>
<br></br>those most likely to benefit include those with Gleason less than 7, with pre-RT PSA less than 2ng/mL, negative SVI, positive margins, and those with PSA doubling times greater than 10 months.
<br></br>
<br></br>-prostatic fossa/pelvic lymph node RT with short-term ADT confers better biochemical control.</p>

Question 17

<p>List trials of adjuvant vs salvage radiation post prostatectomy</p>

Answer 17

<p>https://university.auanet.org/core/img/223_table7_2021.png</p>

Question 18

<p>ProPSMA trial</p>

Answer 18

<p>prospective multi-institutional study in which patients with high risk prostate cancer (PSA>20, clinical stage T3-4, Grade Group 3-5) were randomized to gallium-68-PSMA-PSMA-11 PET/CT vs conventional imaging (bone scan and CT scan)
<br></br>
<br></br>PSMA PET-CT was more sensitive (85% [74-96] vs. 38% [24-52]) and specific (91% [85-97] vs 98% [95-100]) than convention first-line imaging for the detection of nodal or metastatic disease.</p>

Question 19

<p>Guideline recommendation for prostate cN1 nodes on conventional imaging</p>

Answer 19

<p>systemic treatment with ADT +/- radiation therapy to the primary
<br></br>
<br></br>Currently, surgical management of cN1 patients should be restricted to patients enrolled in clinical trials</p>

Question 20

<p>PROMIS trial</p>

Answer 20

<p>576 men underwent a 1.5 Tesla mpMRI followed by both TRUS biopsy and a template mapping prostate biopsy. For clinically significant cancer, mpMRI was more sensitive (93%; 95% CI 88-96%) and less specific (41%; 95% CI 36-46%). The authors concluded that using mpMRI to triage men might allow 27% of patients to avoid a primary biopsy and 5% fewer clinically insignificant cancers would be detected</p>

Question 21

<p>PRECISION Study</p>

Answer 21

<p>500 men without a history of a prostate biopsy and a clinical suspicion for prostate cancer were randomized to undergo mpMRI with targeted biopsy versus standard TRUS prostate biopsy. Clinically significant prostate cancer was detected in 38% of the mpMRI targeted biopsy group as compared to 26% of the TRUS biopsy group (p=0.005) and fewer men in the mpMRI targeted biopsy group received a diagnosis of clinically insignificant cancer</p>

Question 22

<p>ExoDx</p>

Answer 22

<p>a urine-based 3-gene exosome (ERG, PCA3, and SPDEF) expression assay validated for the risk of clinically significant PCa in men without a prior biopsy.</p>

Question 23

<p>miR</p>

Answer 23

<p>a urine-based test interrogates small noncoding RNAs (sncRNA) isolated from urinary exosomes. This test was developed and validated to stratify patients with prostate cancer into risk categories</p>

Question 24

<p>MPS</p>

Answer 24

<p>MPS (MyProstateScore, formerly Michigan Prostate Score (MiPS)): combination of serum PSA, urinary PCA3 and TMPRSS2:ERG validated to assess the risk of incident PCa and clinically significant PCa. In validation it was shown to improve upon the performance of PSA or PCA3 alone in detecting aggressive PCa</p>

Question 25

PCA3

Answer 25

a non-coding mRNA in urine, may help identify incident and clinically significant PCa

Question 26

Select MDX

Answer 26

a urine-based risk assessment that measures DLX1 and HOXC6 against KLK3 mRNA levels in post-DRE urine validated for the risk of clinically significant PCa (≥3+4) in men without a prior biopsy

Question 27

4K score

Answer 27

a blood-based validated risk assessment for clinically significant PCa in men at risk for PCa.

Question 28

PHI

Answer 28

blood-based risk assessment using PSA, percent free PSA, and [-2]proPSA to estimate the risk of clinically significant PCa

Question 29

Confirm MDX

Answer 29

is an epigenetic test of the PCa-associated genes GSTP1, APC, and RASSF1. It is assessed on non-cancerous biopsy tissue and is validated to predict the absence of PCa on subsequent biopsy (rules out need for further biopsy)

Question 30

OncotypeDx

Answer 30

17-gene expression panel validated to predict the risk of adverse pathology at surgery and the risk of metastasis and death after treatment. It can be used to inform the decision between active surveillance and definitive therapy

Question 31

Prolaris

Answer 31

a 31-gene expression panel validated to predict the risk of disease-specific mortality with conservative management and the risk of metastatic disease after treatment. It can be used following biopsy to better determine whether a patient should receive active surveillance or definitive therapy.

Question 32

ProMark

Answer 32

an 8-protein proteomic assessment validated to assess the risk of adverse pathology. May be utilized for low or very low risk patients post biopsy to select active surveillance versus definitive therapy

Question 33

Decipher

Answer 33

a 22-gene genomic classifier that is validated to predict the risk of metastasis to select patients who are better treated with definitive therapy

Question 34

PCPT trial

Answer 34

Prostate cancer prevention trial

Ca was detected by biopsy (which included end-of study biopsies) in a remarkable 24.4% of the study participants, and finasteride decreased the overall relative risk of PCa by 25%.

Question 35

REDUCE trial

Answer 35

Reduction by dutasteride of Prostate cancer Events

xamined the effects of dutasteride in a higher risk cohort (PSA 2.5-10 ng/ml and negative prior biopsy), with a similar relative risk reduction of 25% and an absolute reduction of 5.1%.73

Question 36

SELECT Trial

Answer 36

randomized 35,533 men at low risk for PCa to regimens of either vitamin, or combinations of these agents.

No significant differences were found in rates of PCa across the intervention groups. Therefore, Selenium or Vitamin E is not recommended for the prevention of PCa.

Question 37

Most potent stimulator of the androgen receptor

Answer 37

dihydrotestosterone which is the principal androgen in the prostate cell

Question 38

Mechanisms of castration resistant prostate cancer

Answer 38

1. Ability of CaP cells to use intracellular androgens via de novo synthesis or get it exogenously from the adrenal galnds and tumor microenvironment

2. Increased AR expression

3. AR gene mutation that allow the receptor to be activated by other ligands other than other androgens

4. Alterations of AR signaling to promote tumor growth

5. Synthesis of AR variants (AR-V7)

Question 39

Treatment options for mCSPC (3)

Answer 39

1. ADT alone
2. Docetaxel + ADT (CHAARTED, STAMPEDE)
3. AA + ADT

Question 40

CHAARTED TRIAL

Answer 40

790 men w/ newly dx mCSPC randomized to ADT vs. ADT+ 6 cycles of docetaxel. At median f/u of 53.7 mos, the median OS was 47.2 mos versus 57.6 mos in favor of the ADT + docetaxel arm (HR 0.72, (0.59-0.89), P=0.0018).

There was a benefited seen in men withhigh vol dz but not in low vol dz

Question 41

STAMPEDE Trial

Answer 41

Multi-arm, multi-stage of ~ 3000 men, wherein the addition of docetaxel to ADT improved OS. In the subset of 1086 men with metastatic disease, the median OS for men undergoing ADT alone was 45 mos compared to 60 mos in the ADT plus docetaxel arm (HR 0.76 (0.62-0.92), P=0.005).
Also significant reduction of death in ADT + Doce arm long term

ADT + Abiraterone: demonstrated that at a median follow-up of 40 months, abiraterone in addition to ADT led to an OS benefit in a group of 1,917 men. A 37% relative improvement in survival was noted with a HR of 0.63 (95% CI, 0.52-0.76, P < 0.0001).

The STAMPEDE randomized trial arm H included a comparison of ADT vs ADT plus external beam radiotherapy in 2061 men with newly diagnosed metastatic prostate cancer. Three-year survival was noted to be 81% with radiotherapy and 73% in the control group among men with low volume metastatic disease burden by CHAARTED criteria (HR 0.68, 95% CI 0.52-0.90, P=0.007).

Question 42

GETUG-AFU 15 trial

Answer 42

Randomized, open-label phase 3 study of 385 patients that did not demonstrate statistically significant improvement in survival with the addition of docetaxel. Median survival was 58.9 mos in the ADT with docetaxel group, and 54.2 mos in the ADT alone group (HR 1.01, 95% CI 0.75-1.36).

Question 43

LATTITUDE study

Answer 43

1,199 men with de novo mPC and with 2 of 3 high risk features (visceral disease, Gleason score of ≥ 8, presence of ≥ 3 lesions on bone scan) were randomized to ADT with abiraterone or placebo. Interim analysis showed a marked benefit in the abiraterone plus ADT group with a prolongation of radiographic progression-free survival and a 38% reduction in the risk of death compared to ADT and placebo.

Question 44

Enzamet Trial

Answer 44

randomized 1125 mCSPC patients to receive ADT plus standard nonsteroidal anti-androgens or ADT plus enzalutamide. The three year OS was 80% in the enzalutamide group and 72% in the control group. At a median follow-up of 34 months, the HR for death was 0.67 (95% CI 0.52 -0.86, P=0.002) in favor of the enzalutamide group

Caveat: good number experienced AE especially if they received Docetaxal.

Question 45

MOA and dosing of Docetaxal

Answer 45

Microtubule inhibitor

75 mg/m2/dose IV x 1 on day 1 of 21 day cycle; total 6 cycles

Question 46

MOA and dosing of Abiraterone

Answer 46

Nonsteroidal inhibitor of CYP17A1

1000 mg PO daily with prednisone 5 mg PO daily

Question 47

MOA and dosing of Apalutamide

Answer 47

Nonsteriodal anti-androgen

240 mg PO daily

Question 48

MOA and dosing of Enzalutamide

Answer 48

Androgen receptor signaling inhibitor

160 mg daily

Question 49

MOA and Radiation dose for mCSPC

Answer 49

Causes DNA damage.

2.75 gy x 20 Fractions

Question 50

Titan Trial

Answer 50

phase 3 TITAN randomized trial of 1052 men compared ADT plus apalutamide to ADT plus placebo. An interim analysis showed OS at 24 mos was 82.4% in the apalutamide arm compared to 73.5% in the placebo arm. The HR for death was 0.67 (95% CI 0.51-0.89, P=0.005). The rate of AEs was similar in the apalutamide and placebo arms

Question 51

HORRAD Trial

Answer 51

randomized 432 patients with PSA >20 ng/mL and primary bone metastases on bone scan between 2004 and 2014 to ADT with EBRT or ADT alone. The median PSA was 142 ng/mL with 67% of the patients having ≥ 5 bone metastases. With a median follow up of 47 months, no significant diff in overall survival (45 months in EBRT + ADT group and 43 months in the ADT group (p=0.4). There was an improvement in PSA progression in the radiotherapy group HR: 0.78; 95% CT: 0.63-0.97m p=0.02)

Question 52

Treatment options for nmCRPC

Answer 52

Observation if PSADT > 10 mos and with hormone therapy when PSADT < 10 mos

ADT + AA ( Enza, Apal, Daro)

Question 53

Definition of nmCRPC

Answer 53

defined as the patient with a rising PSA despite castrate levels of testosterone following androgen deprivation therapy and no radiographic evidence of metastases on conventional imaging with CT or MRI abdomen/pelvis and bone scan

Question 54

PROSPER Trial

Answer 54

1401 patients w/ nmCRPC and a PSA DT of 10 mos or less (mean PSA DT 3.7 mos) were randomized 2:1 to receive enza plus ADT or placebo plus ADT. The median MFS was 36.6 mos in the enza group vs 14.7 mos in the placebo group (HR 0.29, CI 0.24-0.35; p<0.001).

Median OS was 67 months

Question 55

SPARTAN TRIAL

Answer 55

1207 patients with nmCRPC and a PSA DT of 10 months or less were randomized 2:1 to receive apalutamide plus ADT or placebo plus ADT. Median MFS was 40.5 months in the apalutamide group as compared with 16.2 mos in the placebo group (HR for metastasis or death 0.28, 95% CI 0.23-0.35; p<0.001)

Time to symptomatic progression was longer in the apa group.

Question 56

ARAMIS

Answer 56

1509 patients w/ nmCRPC, PSA DT of 10 mos or less, baseline PSA level of 2 ng/mL and an Eastern Cooperative Oncology Group (ECOG) performance status of 0 or 1 were randomized 2:1 to receive darolutamide 600 mg BID vs. placebo while continuing ADT. Median f/u was 17.9 mos. The median MFS was 40.4 mos with darolutamide compared to 18.4 mos w/ placebo (HR 0.41, 95% CI 0.34 to 0.50; p<0.001)

Risk of death was lower and time to pain progression was longer.

Question 57

Treatment strategies for mCRPC (8 categories)

Answer 57

Abiraterone, enazalutamide: mCRPC

Sipuleucel: Asymptomatic/minimal symptoms, no live metastases

Docetaxel, Cabazitazel: mCRPC

Olaparib- DDR mutation following androgen receptor directed therapy

Rucaparib- BCRA 1/1 mutation following AR directed therapy and taxane based chemo

Radium- 223- Symptomatic bone mets

Lu-PSMA-617- PSMA expressing mets. FDA breakthrough therapy designated

Pembrolizumab: Unresectable or metastatic tumor with: 1. High Microsatellite instability or high tumor mutational burden (>/= 10)

Question 58

Definition of castration resistance

Answer 58

serum testosterone level < 50 ng/dl or 1.7 nmol/L + 1 of the following:

Biochemical progression: 3 consecutive rises in PSA at least one week apart, resulting in 25% increases over the nadir, and PSA greater than 2 ng/mL

Radiographic progression: The appearance of new lesions: Either 2 or more new bone lesions on a bone scan and confirmed by other imaging modality (e.g., CT or MRI) if ambiguous or a soft tissue lesion measurable using RECIST criteria

Question 59

Denosumab

Answer 59

human monoclonal antibody against RANK ligand (RANKL), acting to inhibit RANKL, the main driver of osteoclast formation, function and survival

Question 60

What is PSMA

Answer 60

Prostate-specific transmembrane antigen, a transmembrane glutamate carboxypeptidase, is highly expressed on prostate cancer cells, with high expression being an independent biomarker of poor prognosis in both early- and late-stage disease

Question 61

What is Radium-223

Answer 61

an isotope of radium that emits a low level of alpha particle radiation with an affinity for sites of bone metastases. It has a half-life of 11.4 days and works by causing double-stranded DNA breaks.

Question 62

What is Sipuleucel

Answer 62

immunotherapy product that contains patient-specific autologous dendritic cells loaded ex vivo with a recombinant fusion protein consisting of prostatic acid phosphatase (PAP) linked to a granulocyte-macrophage colony stimulating factor (GM-CSF) designed to break immune tolerance to normal tissue antigen PAP.

Question 63

What are PARPi's

Answer 63

Poly(adenosine diphosphate-ribose) polymerases (PARPs) are a large family of 18 proteins which are responsible for facilitating DNA repair caused by either single-strand break or base excision repair pathways. PARP inhibitors cause genomic instability and cell death due to the inability to repair damaged DNA.

Olaparib
Rucaparib

Question 64

MOA and dosing of Cabazitaxel

Answer 64

Cabazitaxel is a second-generation taxane with a broader range of cytotoxicity, high potency that remains cytotoxic for docetaxel-resistant cell lines due to gp-1 overexpression with better blood-brain penetration than docetaxel.

25mg/m2 q21 days + prednisone

Question 65

MOA of Mitoxantrone

Answer 65

anthracycline chemotherapy that acts during multiple phases of the cell cycle to disrupt DNA synthesis and DNA repair.

Currently no role for Mitotoxantrone in treating mCRPC

Question 66

MOA and role of Docetaxel in mCRPC

Answer 66

second-generation taxane chemotherapy that inhibits microtubule assembly into the mitotic spindle, thus arresting the cell cycle during G2/M phase. Docetaxel may also increase apoptosis by downregulation of the BCL2 gene, which tends to be over-expressed in cancer cells.

Tax trial: phase 3 doce plus prednisone vs mitotoxantrone + prednisone

SWOG 9916: Phase 3 doce + estrasmustine vs mitotoxantrone + pred.

Both trial Docetaxel group showed longer median survival compared to control.

Question 67

Tests available to detect cortisol hypersecretion (Cushing Syndrome)

Answer 67

Overnight low-dose (1-mg) dexamethasone suppression test (OST): higher sensitivity for detecting subclinical

Late-night salivary cortisol test (SCT): easiest

24-hour urinary-free cortisol evaluation (UFC): standard test but more time intensive

Question 68

How is a diagnosis of cushing syndrome made after OST

Answer 68

A putative diagnosis of Cushing Syndrome is made if the serum cortisol level is > 5 micrograms/dL following an OST

Question 69

Conn Syndrome

Answer 69

hyperaldosteronism due to a single adrenal nodule

classic syndrome includes hypertension, hypokalemia, and alkalosis, up to 40% of patients with this syndrome are normokalemic

Question 70

How is primary hyperaldosteronism diagnosed

Answer 70

An ARR≥20 along with a concomitant aldosterone concentration above 15 ng/mL suggest the diagnosis of primary hyperaldosteronism

Question 71

Screening Guidelines for hyperaldosternonism (8)

Answer 71

1. Any patient with sustained blood pressure above 150/100 on three separate measurements taken on different days

2. Hypertension resistant to 3 antihypertensives

3. Hypertension controlled with four or more medications

4. Hypertension and low potassium

5. Hypertension and a newly diagnosed adrenal incidentaloma

6. Hypertension and concomitant sleep apnea

7. Hypertension and a family history of early onset hypertension or stroke before age 40

8. All first-degree relatives of patients with a diagnosis of primary aldosteronism

Question 72

Medications that cause falsely elevated metanephrines

Answer 72

levodopa, monoamine oxidase inhibitors, benzodiazepines, tetracycline, and rapid withdrawal from clonidine

Question 73

How is pheochromocytoma diagnosed

Answer 73

with plasma-free metanephrine and normetanephrine levels or 24-hour total urinary metanephrines and fractionated catecholamines

Caveat: Metanephrines are more sensitive than catecholamines since metabolism is continuous, unlike catecholamine release which occurs episodically.2 The higher sensitivity of metanephrines also means they have a higher false positive rate. However, elevation above designated thresholds (>2x the upper limit of normal) in either study suggests the presence of pheochromocytoma

Question 74

When should sex hormone testing be performed with adrenal masses?

Answer 74

not warranted unless the patient is suspected of having an adrenocortical carcinoma (mass > 4 cm) and/or obvious clinical stigmata of feminization or virilization.

Measure DHEA with 17-Ketosteroids

For women: Get serum testosterone

For men get 17B-estradiol

Question 75

When should sdrenalectomy be performed in nonfunctioning adrenal masses?

Answer 75

If the lesion size increases by ≥ 1 cm or develops functionality, surgery should be considered. However, 75-95% of incidentalomas remain stable in size while 2-8% of previously non-functioning lesions develop functionality, with hypersecretion of cortisol being the most common finding.

Question 76

Associated syndromes with adrenocortical carcinoma

Answer 76

familial syndromes such as Li-Fraumeni, Beckwith-Wiedemann, MEN-1, McCune-Albright, and Carney complex.

Question 77

Main prognostic factors for adrenocortico carcinoma

Answer 77

tumor stage and completeness of surgical resection.

Question 78

Most common sites of adrenal mets

Answer 78

Liver, (48%) lung (45%), LN (29%), bone (13%)

Question 79

Standard treatment for adrenocortical carcinomas

Answer 79

Open adrenalectomy

Question 80

Lymph drainage from the bladder

Answer 80

Level I: internal iliac, obturator, external iliac Level II: comon iliac, presacral Level III: paracaval, para-aortic, and interaortocaval

Question 81

MCC of Granulomatous cystitis

Answer 81

Intravesical BCG

Question 82

Treatment of BCG related granulomatous cystitis

Answer 82

treated with isoniazid (300 mg PO daily) and pyridoxine (vitamin B6, 25 mg PO daily) for 3 months.

Question 83

Causes of bilharzial cystitis

Answer 83

parasitic infection caused by schistosomal species (s. haematobium and S. mansoni).

Question 84

treatment of bladder malakoplakia

Answer 84

transurethral resection/biopsy followed by a prolonged course of antibiotics (1st line = quinolones, 2nd line = rifampin or trimethoprim). Drugs that activate cGMP (bethanechol and vitamin C) may be of benefit.

Question 85

Treatment of Bladder amylodosis

Answer 85

Patients with a high volume of bladder amyloidosis or those recurring frequently with amyloid plaques in the bladder can be treated with intravesical DMSO (50 mL of 50% solution for 30 min every 2 weeks for 3-12 months) to dissolve the unwanted protein. Cystectomy is occasionally required.

Question 86

Inflammatory Myofibroblastic Tumor

Answer 86

presents in patients with irritative LUTS or hematuria.

Question 87

Post operative Spindle cell Nodule

Answer 87

Variant of IMT, occurs after previous surgery. indistinguishable from bladder cancer.

Question 88

Genes associated with Lynch syndrome and Bladder cancer

Answer 88

MSH2, MSH 6, MLH 1, PMS2 seen in colon cancer, 80%) endometrial cancer (80%), gastric, ovrain, and urothelial cancer

Question 89

Genes associated with Peutz Jeghers and Bladder cancer

Answer 89

STK 11 GI hamartomas, Mealonitc macules, intussusception, colon cance, Breast cancer, lung caner, Pancreatic/biliary cancer, sex cord stomal tumors

Question 90

Genes associated with Cowden syndomr and Bladder cancer

Answer 90

PTEN, KLLN Seen in mucocutaneous hamartomas (100%), Breast cancer (80%), Brain tumor, Thyroid cancer, Endometrial cancer, Kidney cancer, Colon cancer, Bladder cancer, melanoma, Macrocephaly

Question 91

Genes associated with Li-Fraumeni and Bladder cancer

Answer 91

P53 & CHEK2 Involved soft tissue sarcoma, breast cancer, bladder cancer, adrenocorticcal carcioma, leujemia

Question 92

Genes associated with neurofibromatosis and Bladder cancer

Answer 92

NF 1 (neurofibromin), NF2 (merlin) Neurofibromas, lish nodules, scoliosis,s cafe au lait spots, acoustic neuromas, schwanomas, meningiomas

Question 93

Recurrence rate of LgTa bladder tumor

Answer 93

15- 70% at one year but low rate of prgoression to higher stage disease with <5% progressing to MIBC

Question 94

Recurrence rate of Hg Ta

Answer 94

13-40% progressing to lamina propria invasion, and 6-25% change of becoming muscle invasion

Question 95

Risk of progression and rcurrence for T1 bladder tumor

Answer 95

50% within 3 years and 80%. cance of recurrence

Question 96

Risk of recurrence of and progression of CIS

Answer 96

82% and 42-83% if not treated with adjuvant intravesical therapy

Question 97

Adjuvant intravesical therapy of intermediate risk NMIBC

Answer 97

intermediate-risk patient a clinician should consider administration of a six-week course of induction intravesical chemotherapy or immunotherapy with BCG.

Question 98

Adjuvant intravesical therapy of intermediate risk NMIBC

Answer 98

high-risk patient with newly diagnosed CIS, high-grade T1, or high-risk Ta urothelial carcinoma, a clinician should administer a six-week induction course of BCG

Question 99

Induction course. of BCG

Answer 99

The standard induction course is the same for immunotherapy and chemotherapy: the agent is instilled intravesically weekly for a total of 6 doses and then cystoscopy is performed 6 weeks later to assess for response.

Question 100

BCG maintenance schedule

Answer 100

The most common maintenance schedule for BCG is the Lamm/SWOG regimen (triplets of BCG given at 3, 6, 12, 18, 24, 30 and 36 months) which was associated with a 19% improvement in the 5-year recurrence-free survival (41% vs. 60%) and 6%_ improvement in the 5-year worsening-free survival [no progression including pT2 or greater, use of cystectomy, systemic chemotherapy, or radiation therapy; 70% vs. 76%, p=0.04)

Question 101

BCG refractory and next steps

Answer 101

persistent disease after 6 months of BCG therapy or who have progression of disease at 3 months (such as Ta/CIS to T1). Most guidelines recommend assessment at 6 months since

Question 102

BCG relapsing

Answer 102

Describes patients who recur after BCG treatment. This can be early (within 12 months), intermediate (12-24 months), or late (>24 months).

Question 103

BCG intolerance

Answer 103

describes disease persistence secondary to inability to receive adequate BCG due to toxicity/side effects

Question 104

BCG unresponsive and next steps

Answer 104

BCG refractory or those who relapse within 6 months of treatment. There is no additional benefit to more BCG treatment in BCG-unresponsive patients and these are the patients for whom cystectomy is indication or enrollment onto trials of novel therapeutics.

Question 105

Nadoferagene firadenovec

Answer 105

replication incompetent type 5 adenovirus designed to infect the bladder and produce the anticancer cytokine interferon α2b

Question 106

T4 Bladder cancer

Answer 106

Tumor invades any of the following: prostatic stroma, seminal vesicles, uterus, vagina, pelvic wall, abdominal wall

Question 107

T4a Bladder cancer

Answer 107

Tumor invades prostatic stroma, uterus, vagina

Question 108

T4b Bladder cancer

Answer 108

Tumor invades pelvic wall, abdominal wall

Question 109

Distal boundary for LND for MIBC

Answer 109

node of cloquet

Question 110

Proximal boundary for LND for MIBC

Answer 110

Standard: bifurcation of the common iliac Extended: bifurcation of the inferior abdominal Aorta Super extended: Aorta at the origin of the IMA

Question 111

lateral boundary for LND for MIBC

Answer 111

Genitofemoral nerve

Question 112

Inferior boundary for LND for MIBC

Answer 112

Internal iliac LN floor pelvis

Question 113

Posterior boundary for LND for MIBC

Answer 113

Sacrum

Question 114

Overall disease specific survival for organ confined, node negative, UC

Answer 114

60-85% over 5-10 years

Question 115

5 year disease specific survival in patients with extravesical UC disease

Answer 115

50%

Question 116

Absolute contraindication of continent/orthotopic neobladder

Answer 116

A positive invasive urethral margin on frozen section during cystectomy.

Question 117

Relative contraindications for orthotopic urinary diversion (10)

Answer 117

1. Positive intra urethral margin 2. Gross positive margin 3. Pubic bone involvement 4. Neurological dz impairing patients dexterity or continence 5. Severe urethral stricture disease in male pts 6. Chronic renal failure (cr>1.8, GFR <40) 7. Hepatic insufficiency 8. Chronic enteric inflammatory disease 9. Malignant bowel disease 10. Unwillingness/inability to perform self cath.

Question 118

MOA Cisplatin

Answer 118

binds deoxyribonucleic acid (DNA) and produces intra-strand crosslinks and DNA adducts, thus inhibiting DNA replication

Question 119

SE of Cisplatin (3). Which is the dose limiting SE

Answer 119

The dose-limiting toxicity of cisplatin is nephrotoxicity, which peaks at 2 weeks following treatment and is generally reversible. Other potential adverse effects include neurotoxicity (peripheral neuropathy) and ototoxicity (hearing loss)

Question 120

SE of Carboplatin. Which is the dose limiting SE

Answer 120

The principal dose-limiting toxicity of carboplatin is bone marrow suppression, particularly thrombocytopenia. However, carboplatin has not been demonstrated to have equivalent efficacy to cisplatin

Question 121

MOA Paclitaxel

Answer 121

Paclitaxel blocks cell cycle in mitosis by binding to tubulin and interfering with assembly of microtubules

Question 122

Dose limiting SE of Paclitaxel

Answer 122

Its principle dose-limiting toxicity is hypersensitivity, peripheral neuropathy, and myelosuppression.

Question 123

Drugs approved for the primary treatment of metastatic bladder cancer patients who are cisplatin-ineligible and have high PD-L1 expression

Answer 123

Pembro and Atezo

Question 124

Drugs approved for second-line use after progression on platinum-containing chemotherapy metastatic BCa

Answer 124

Pembro, Avelumab, nivolumab

Question 125

FDA approved drug used as maintenance therapy after first line platninum based chemotherapy

Answer 125

Avelumab avelumab maintenance following chemotherapy represents the new standard of care for patients with metastatic or unresectable locally advanced disease

Question 126

Common toxicities observed in patients with immune checkpoint inhibitors

Answer 126

fatigue, pruritis, nausea, diarrhea, asthenia, anemia

Question 127

Rare toxicities observed in patients taking immune checkpoint inhibitors

Answer 127

Endocrinopathies, pneumonitis, colitis, myositis, severe skin rx

Question 128

Erdafitinib

Answer 128

fibroblast growth factor receptor tyrosine kinase inhibitor. It has been granted accelerated FDA-approval for patients with metastatic urothelial carcinoma with FGFR2 or FGFR3 genetic alterations that progressed on platinum-based chemotherap

Question 129

Systemic option for BCG unrepsonsive NMIBC

Answer 129

Pembrolizumab: Blocks the PD-1 receptor and prevents it from interacting with PD-L1 and PD-L2 ligands Dose 200 mg q 3 weeks 400 mg q 6 weeks immuno reactions big concern

Question 130

Indications for radical cystectomy in NMIBC

Answer 130

Small Capacity contract4d bladder or NGB BCG unresponsive HR bladder cancer Very large >10cm bladder tumor Variant histology ( micropapillary, nested, plasmacytoid, neuroendocrine, sarcomatoid), extensive squamous, or glandular differentiation, or presence/absence of LVI.

Question 131

Surveillance of HR NMIBC

Answer 131

cystoscopically at 3 month intervals for the first two years, and then at 6 month intervals for the next 2-3 years, and then annually thereafter

Question 132

Surveillance of LR NMIBC

Answer 132

Low-risk patient whose first surveillance cystoscopy is negative for tumor, a clinician should perform subsequent surveillance cystoscopy six to nine months later, and then annually thereafter

Question 133

management of nested variant UC

Answer 133

radical cystectomy, limited reports of efficacy of NAC

Question 134

management of micropapillary UC

Answer 134

histo is similar to ovarian papillary serous carcinoma. No clear evidence for NAC although there is some pathological downstaging at time of RC

Question 135

management of Plasmacytoid UC

Answer 135

A/w higher rates of positive surgical margins and has propensity to develop peritoneal carcinomatosis. A/w worse CSS outcomes. No consensus of efficacy of NAC, Cystectomy alone or AC. Multimodal approach is common

Question 136

Management of squamous cell carcinoma

Answer 136

radical cystectomy. NAC inconsistent benefit.

Question 137

Management of Adenocarcinoma of the bladder

Answer 137

typically at the dome of the bladder. Mx involves partial cystectomy, or radical cystectomy with PLND NAC not recommended, but AC may have a role similar to UC

Question 138

Management of Neuroendocrine carcinoma of the bladder

Answer 138

includes small cell, large cell, and mixed patterns. Mx includes multimodal therapy starting with upfront Chemo cisplatin/etoposide, etoposide alone, or ifosfamide/doxorubicin.

Question 139

Common sites of bladder metastasis

Answer 139

Obturator nodes (74%) External iliac (65%) Presacral and internal iliac nodes (25%) Perivesical nodes (16%)

Question 140

minimal recommendation for lymph node removal at time of cystectomy

Answer 140

external, internal, obturator lymph nodes (standard)

Question 141

Extended lymph node dissection

Answer 141

external, internal, obturator, aortic bifurcation, or IMA, with pre-sacral nodes.

Question 142

5 year OS for pT2 UC

Answer 142

65%

Question 143

5 year OS for pT3 UC

Answer 143

50%

Question 144

5 year OS for pT4 UC

Answer 144

47%

Question 145

5 year OS for node positive UC

Answer 145

31%

Question 146

Percent improvement in OS and CSS with NAC

Answer 146

5-7% and 9%

Question 147

ddMVAC NAC regimen for bladder cancer

Answer 147

MTX day one Vinblastine day two Doxorubicin day 2 Cisplatin Day two GCSF day 3 Cycle repeats every 14 days.

Question 148

Relative contraindications to performing an orthotopic or continent urinary diversion

Answer 148

* positive intraop urethral margin * gross positive margins * pubic bone involvement * neurologic disease impairing dexterity or continence * Severe urethral stricture dz in men Chronic renal failure (Cr >1.8, GFR <40) Hepatic insufficiency Chronic enteric inflammatory dz Malignant bowel disease Unwillingness/inability to perform self catheterization

Question 149

Metabolic abnormalities with colon or ileum used for urinary diversion

Answer 149

hyperchloremic, hypokalemic, metabolic acidosis

Question 150

Radiosensitizing chemotherapy agents used for trimodal therapy

Answer 150

5-FU, and mitomycin or single agent cisplatin and gemcitabine

Question 151

Dose limiting toxicity of cisplatin

Answer 151

nephrotoxicity (peaks at 2 weeks following tx and is reversible). others: ototoxicity, neurotoxicity (peripheral neuropathy)

Question 152

Dose limiting toxicity of carboplatin

Answer 152

bone marrow suppression. not equivalent in efficacy to cisplatin

Question 153

Dose limiting toxicity of paclitaxel

Answer 153

hypersensitivity, peripheral neuropathy, myelosupression

Question 154

Dose limiting toxicity of gemcitabine

Answer 154

myelosuppression.

Question 155

role of Avelumab maintenance in metastatic bladder cancer

Answer 155

Avelumab maintenance following chemotherapy is the new standard of care for patients with metastatic or unresectable locally advanced disease. FDA approved.

Question 156

FDA approved FGFRi for metastatic UC

Answer 156

erdaftinib in patients with FGFR2 and FGFR3 alterations that progressed on platinum based chemotherapy

Question 157

Clinical manifestations of CHL

Answer 157

retinal angiomas, endolymphatic sac tumors, benign CNS hemangioblastomas, pancreatic cysts, islet tumors, epidiymal cystadenomas, pheochromocytomas

Question 158

Location of mutated VHL tumor suppressor gene

Answer 158

chromosome 3p25-26. codes for E3 ubiquitin ligase complex which regulates degradation of regulatory proteins including hypoxia inducible factor (HIF-1 and HIF-2). Overaccumulation of intracellular HIF --> upregulation of VEGF

Question 159

Characterization of papillary RCC

Answer 159

bilateral and mutifocal Type 1 pap RCC

Question 160

Genetic alteration a/w hereditary papillary RCC

Answer 160

c-met proto oncogene at 7q31

Question 161

Characterization of hereditary leiomyoma RCC

Answer 161

papillary type II RCC with agressive clinical behavior needing early surgical intervention.

Question 162

Clinical manifestation of hereditary leiomyoma RCC

Answer 162

painful cutaneous and uterine leiomyomas

Question 163

Genetic alteration a/w HLRCC

Answer 163

1q42-44, the site of the fumarate hydratase tumor suppressor gene

Question 164

Characterization of birt-hogg-dube syndrome

Answer 164

bilateral multifocal, chromophobe RCC, oncocytomas, hybrid renal tumors

Question 165

Clinical manifestations of birt-hogg-dube syndrome

Answer 165

fibrofoliculomas of the head and neck, pulmonary cysts, spontaneous pneumothorax

Question 166

Genetic alteration a/w BHD

Answer 166

17p11.2 encoding tumor suppressor gene Folliculin

Question 167

Characterization of BAP1 Tumor predisposition syndrome

Answer 167

unifocal ccRCC

Question 168

Clinical manifestations of BAP1 tumor predisposition syndrome

Answer 168

uveal and cutaneous melanomas and mesotheliomas

Question 169

Genetic alteration a/w BAP1

Answer 169

BAP1 gene mapped to 3p2.

Question 170

Characterization of hereditary paraganglimoa-pheochromocytoma syndrome

Answer 170

Unifocal tumor with neoplastic cells

Question 171

Clinical manifestations of Hereditary paraganglioma pheochromocytoma

Answer 171

paragangliomas, pheochromocytomas, GI stromal tumors

Question 172

Genetic alteration a/w HPPS

Answer 172

Succinate dehydrogenase which is a mitochondrial enzyme complex made up of four protein subunits

Question 173

Indications for renal mass biopsy

Answer 173

* When mass is suspected to be hematologic, metastatic, inflammatory, or infectious When RMB will directly influence treatment -election

Question 174

When is RMB not indicated

Answer 174

RMB is not required for young/healthy patients who are not willing to accept the uncertainties associated with RMB or for older/frail patients who will be managed conservatively independent of RMB.

Question 175

Renal mass occuring from PCT

Answer 175

ccRCC - a/w loss of 3p Papillary RCC

Question 176

Renal mass a/w polysomy 7& 17, loss of Y, and MET mutations

Answer 176

Type I papillary RCC

Question 177

Renal mas a/w mutation in fumarate hydratase gene

Answer 177

Type II papillary RCC HLRCC

Question 178

Renal mass arising from the collecting duct

Answer 178

Chromophobe and is histologically similar to oncocytoma Collecting duct carcinoma: rare and aggressive with poor prognosis

Question 179

Rare and most aggressive form of RCC

Answer 179

renal medullary carcinoma. Occurs in young AA adults with sickle cell trait.

Question 180

Neves Zincke Classification of Renal mass tumor thrombus

Answer 180

More useful for surgical approach Level 0: tumor thrombus limited to renal vein Level 1: Extending ,/= above the renal vein Level 2: Extending >2 cm above the renal vein but below the hepatic veins Level 3: At or above the hepatic veins but below the diaphragm Level 4: Extending above the diaphragm

Question 181

Vascular occlusion prior to IVC thrombectomy

Answer 181

Renal artery supplying the affected kidney Infrarenal IVC below thrombus Lumbar veins feeding into the IVC Contralateral renal vein Hepatic blood supply that extends about the hepatic veins. A pringle maneuver performed to decrease the hepatic blood flow by placing a clamp across the hepatic artery and portal vein within the hepatuduodenal ligament. Mainly done for level 3 or higher tumor thrombus Suprarenal IVC above the thrombus.

Question 182

one potentially fatal complication of thrombectomy that should be discussed prior to surgery

Answer 182

1-2% risk for intraoperative embolization of thrombus causing obstruction of pulmonary arteries

Question 183

Keynote-564 adjuvant monotherapy post nephrectomy

Answer 183

KEYNOTE-564:154 Safety and Efficacy Study of Pembrolizumab (MK-3475) as Monotherapy in the Adjuvant Treatment of Renal Cell Carcinoma Post Nephrectomy. Phase III randomization of 950 patients Eligibility criteria: clear cell carcinoma pT2G4; pT3; pT4; pTxN+; M1 resected to NED Pembrolizumab 200mg IV q3 week for 12 months versus placebo pembrolizumab was associated with significantly longer disease-free survival than placebo (DFS at 24 months, 77.3% vs. 68.1%; hazard ratio for recurrence or death, 0.68)

Question 184

when in local treatment of metastatic sites appropriate in patients with metastatic RCC

Answer 184

solitary or oligometastatic RCC that is resectable.

Question 185

True or False: Cytoreductive nephrectomy should be considered as first line therapy universally in mRCC

Answer 185

False. Especially in intermediate and poor risk dz. two phase III RCT (Surtime and CARMENA) demonstrated CN did not improve 28 week PF recurrence (surtime), and CN w/ post sutent vs sutent alone demonstrated benefit.

Question 186

1st line Agents used for treatment naive Good risk mCCRCC

Answer 186

Sunitinib Pazopanib Pembrolizumab + Axitinib Avelumab + Axitinib Nivolumab + Cabozantinib Pembrolizumab + Lenvatinib Bevacizumab + IFN

Question 187

1st line Agents used for treatment naive intermediate risk mCCRCC

Answer 187

Nivolumab+Ipilimumab Pembrolizumab+Axitinib Avelumab + Axitinib Nivolumab + Cabozantinib Pembrolizumab + Lenvatinib Temsirolimus (poor risk patients)

Question 188

1st line Agents used for previously treated mCCRCC

Answer 188

Preferred: Nivolumab, Cabo Other reqs: Axitinib, lenvatinib +everolimus, Tivozanib

Question 189

Characteristics of NSGCT

Answer 189

Most common GCT Peak incidence 35-40 5% contain syncytiotrophoblasts (resulting in bHCG production) Arise from ITGCN

Question 190

Characteristics of Embryonal Ca

Answer 190

Poorly differentiated, able to differentiate into other NSGCT Peak incidence 25-35y Aggressive tumor with high rate of metastasis

Question 191

Characteristics of Yolk Sac (endodermal sinus tumor)

Answer 191

Pure tumors are rare Most common GCT in children/infants Present in 40% of mixed GCTs Generally produce AFP (never produce bHCG) Schiller-Duval bodies are classic pathologic finding

Question 192

Characteristics of Choriocarcinoma

Answer 192

Less common, very aggressive type of GCT (1% pure, 10% mixed tumors) Peak incidence 20-30 Early hematogenous spread (including brain) High bHCG common, no AFP production

Question 193

Characteristics of Teratoma

Answer 193

Contain well or incompletely differentiated cell layers of endoderm, mesoderm, and/or ectoderm Pure teratomas do not produce AFP or bHCG. Pure teratomas rarely seen in adults (more common in pediatric population) Approximately half of mixed GCT contain teratomatous elements Chemoresistant, radiation-resistant Morbidity related to local growth (“Growing Teratoma Syndrome”) and potential for malignant transformation

Question 194

Only role for testis sparing surgery

Answer 194

should only be considered in a small tumor in a solitary testis, when small bilateral tumors exist, or increased suspicion of a benign tumor.

Question 195

primary drainage of left testicle

Answer 195

para-aortic lymph node

Question 196

primary drainage for right testicle

Answer 196

infrarenal inter-aortocaval lymph nodes, followed by paracaval and para-aortic regions.

Question 197

pT1 testicular tumor

Answer 197

Tumor limited to the testis and epididymis without lymphovascular invasion, may invade tunica albuginea but not tunica vaginalis

Question 198

pT2 testicular tumor

Answer 198

Tumor limited to the testis and epididymis with lymphovascular invasion or tumor involving the tunica vaginalis

Question 199

pT3 testicular tumor

Answer 199

Tumor invades the spermatic cord with or without lymphovascular invasion

Question 200

pT4 Testicular tumor

Answer 200

Tumor invades the scrotum with or without lymphovascular invasion

Question 201

Stage 1 testicular tumor

Answer 201

pT1-4, N0, M0, SX

Question 202

Stage II testicular tumor

Answer 202

Any pT, N0, M0, S1-3

Question 203

Stage III testicular tumor

Answer 203

Any pT, Any N, M1, SX

Question 204

Testicularu serum tumor marker staging

Answer 204

Sx: Tumor markers not available or performed S0: Tumor markers within normal limits S1: LDH <1.5 x normal, hCG<5000 IU/L, AFP <1000 ng/ml S2: LDH 1.5-10 x normal, hCG 5000-50000 IU/L, AFP 1000-10000 ng/ml S3: LDH >10 x normal, hCG>50000 IU/L, AFP >10000 ng/ml

Question 205

Good Prognosis Non-Seminoma

Answer 205

1. Testicular/retroperitoneal primary and 2. No nonpulmonary visceral metastases and 3. Post-orchiectomy STM (all of): — AFP <1000 ng/ml and — hCG <5000 IU/L and — LDH <1.5 x normal

Question 206

Intermediate Prognosis Non-seminoma

Answer 206

1. Testicular/retroperitoneal primary and 2. No non-pulmonary visceral metastases and 3. Post-orchiectomy STM (any of): — AFP 1000-10000 ng/ml and/or — hCG 5000-50000 IU/L and/or — LDH 1.5-10 x normal

Question 207

Poor prognosis Non-seminoma

Answer 207

1. Mediastinal primary 2. Non-pulmonary visceral metastases 3. Post-orchiectomy STM (any of): — AFP >10000 ng/ml and/or — hCG >50000 IU/L and/or — LDH >10 x normal

Question 208

Good Prognosis seminoma

Answer 208

1. Mediastinal primary 2. Non-pulmonary visceral metastases 3. Post-orchiectomy STM (any of): — AFP >10000 ng/ml and/or — hCG >50000 IU/L and/or — LDH >10 x normal

Question 209

Intermediate prognosis seminoma

Answer 209

1. Any primary site and 2. Non-pulmonary visceral metastases and 3. Post-orchiectomy STM: — Normal AFP and — Any hCG and — Any LDH

Question 210

Poor prognosis seminoma

Answer 210

No seminoma patients are poor prognosis

Question 211

Preferred management of Stage 1 seminoma

Answer 211

Surveillance 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

Question 212

Adjuvant option for stage 1 seminoma

Answer 212

1 or 2 cycles of carboplatin (AUC=7 x 1 or 2 cycles)

Question 213

Options for Stage 1 NSGCT

Answer 213

(i) Surveillance, which is the preferred option (ii) RPLND (iii) cisplatin-based chemotherapy.

Question 214

Option for patients with stage 1 NSGCT who do not accept surveillance or primary RPLND

Answer 214

1 cycle Bleomycin, Etoposide, Cisplatin

Question 215

Stage 1 NSGCT N1 treatment recommendation

Answer 215

surveillance based on low risk of recurrence (~10 - 20%)

Question 216

Stage 1 NSGCT N2-3 treatment recommendation

Answer 216

Chemotherapy preferred based on higher recurrence rate (~50-70). Following grossly complete resection, with normal post-RPLND STM, recommended regimens include either EP or BEP for 2 cycles for pN1 or pN2 disease; or 4 cycles of EP or 3 cycles of BEP for pN3 disease.

Question 217

Mainstay treatment for Stage IIA pure seminoma

Answer 217

RT

Question 218

Mainstay treatment for stage IIB pure seminoma

Answer 218

Chemotherapy

Question 219

Preferred treatment for management of Stage II seminoma with bulky lymphadenopathy

Answer 219

bulky lymphadenopathy (> 3 cm), chemotherapy is preferred to RT, with both the NCCN and EAU guidelines recommending 4 courses of EP or 3 cycles of BEP

Question 220

Standard treat,emt pf Stage IIC seminoma

Answer 220

The standard treatment for IIC seminoma patients is chemotherapy with 3 cycles of BEP or 4 cycles of EP

Question 221

management of advanced seminoma after 1st line therapy with persistent mass

Answer 221

The NCCN guidelines recommend surveillance of masses ≤ 3 cm, while masses > 3 cm can either be observed or be further evaluated with a 2-18fluoro-deoxy-2-D-glucose positron emission tomography (PET) scan performed at least 6 weeks after completion of chemotherapy. For FDG-avid masses, resection or biopsy is recommended. If the final pathology demonstrates viable tumor, patients should receive 2 additional cycles of chemotherapy. In the case of incomplete resection of viable tumor, then 4 cycles of second-line chemotherapy is recommended.

Question 222

Management of Stage IIA NSGCT pN1

Answer 222

if an adequate complete RPLND was performed and no concerns of surgical compromise exist, surveillance is preferred for pN1.

Question 223

Management of Stage IIA NSGCT pN2

Answer 223

chemotherapy is preferred with EP or BEP for 2 cycles due to the ~50% risk of relapse

Question 224

Management of Stage IIA NSGCT pN3

Answer 224

Chemotherapy with 4 cycles of EP or 3 cycles of BEP is recommended for pN3 disease given the nearly 100% relapse rate

Question 225

Management of Stage IIB NSGCT

Answer 225

Primary chemotherapy with 4 cycles of EP or 3 cycles of BEP may be used for IIB disease. Following chemotherapy, post-chemotherapy RPLND (PC-RPLND) is recommended for any residual masses > 1cm on subsequent imaging in the setting of negative STM

Question 226

Low risk UTUC

Answer 226

Unifocal disease Tumor size <2cm Low-grade cytology Low-grade URS biopsy No invasive aspect on CTU

Question 227

High-risk UTUC

Answer 227

Hydronephrosis Tumor size >2cm High-grade cytology High-grade URS biopsy Multifocal disease Previous radical cystectomy for bladder cancer Variant histology

Question 228

T/F: Intraluminal BCG is not recommended for the management of UTUC

Answer 228

True

Question 229

UTUC POUT Trial

Answer 229

demonstrated that adjuvant chemotherapy consisting of 4 cycles of gemcitabine-cisplatin (gemcitabine-carboplatin if GFR 30–49 ml/min) resulted in improved progression-free survival compared with surveillance

Question 230

UTUC CheckMate 274

Answer 230

evaluated adjuvant nivolumab in a similar setting. This study, which was double-blinded and placebo-controlled, demonstrated that nivolumab improved the proportion of patients disease-free at 6 months from 60.3% to 74.9%, improving median disease-free survival from 10.8 to 20.8 months

Question 231

Indication for Radical nephroureterectomy in UTUC

Answer 231

High-grade UTUC and low-grade UTUC, where nephron-sparing options are not feasible or oncologically appropriate

Question 232

Cellular lining of the male anterior penile urethra

Answer 232

SSE-Stratified Squamous Epithelium --> SCU-Stratified Columnar Epithelium, --> PSCU-Pseudostratified Columnar Urothelium

Question 233

Blood supply to anterior male urethra

Answer 233

internal iliac--> internal pudendal--> common penile artery--> 3 branches: (1) bulbuourethral artery, (2) Cavernosal Artery, (3) dorsal artery

Question 234

Blood supply to posterior male urethra

Answer 234

inferior vesical and middle rectal

Question 235

Lymphatic drainage of the anterior male urethra

Answer 235

superficial and deep inguinal lymph nodes

Question 236

Lymphatic drainage of posterior male urethra

Answer 236

pelvic lymph nodes

Question 237

Cellular lining of the distal female urethra

Answer 237

Non-keratinized stratified squamous cells

Question 238

Blood supply of the female distal urethra

Answer 238

Vaginal artery

Question 239

Blood Supply of the female proximal urethra

Answer 239

Internal pudendal artery

Question 240

Lymphatic drainage of the female distal urethra

Answer 240

Superficial and deep inguinal nodes

Question 241

Lymphatic drainage of the proximal female urethra

Answer 241

External iliac, internal iliac and obturator nodes

Question 242

Most common location of urethral carcinoma in men

Answer 242

proximal urethra (urothelial)

Question 243

Tis Urethral carcinoma

Answer 243

-Carcinoma in situ -Prostatic urethra or periurethral or prostatic ducts without stromal invasion

Question 244

pTa urethral carcinoma

Answer 244

Non Invasive papillary carcinoma or verrucous carcinoma

Question 245

pT1 urethral carcinoma

Answer 245

Invades lamina propria

Question 246

pT2 urethral carcinoma

Answer 246

Invades corpus spongiosum or periurethral muscle. - Invades prostatic stroma (either by ducts or direct extension)

Question 247

PT3 Urethral carcinoma

Answer 247

invades corpus cavernosum or anterior vagina invades peri-prostatic fat

Question 248

pT4 urethral carcinoma

Answer 248

invades adjacent organs (bladder, rectum, uterus)

Question 249

Recommended image modality for staging urethral carcinoma

Answer 249

MRI

Question 250

Treatment of choice for small non invasvie tumors of the distal urethra

Answer 250

TUR, consider prostatic biopsioes prostatic biopsies since tumor recurrences can involve the prostatic urethra in up to 40% of cases

Question 251

Surgical management of pT3 urethral carcinoma

Answer 251

Tumors invading the corpora cavernosa (T3) require penectomy. For tumors of the distal penile urethra, partial penectomy may be possible

Question 252

T/F men s/p radical cystectomy require urethrectomy if evidence of prostatic urethral recurrence is present

Answer 252

False 25% of radical cystectomy specimens performed for urothelial carcinoma will have some degree of prostatic involvement. However, most patients do not require urethrectomy (distal to the prostate) and only those with clear clinical evidence of urethral cancer distal to the prostatic urethra should undergo urethrectomy at the time of cystectomy.

Question 253

pTa penile cancer

Answer 253

Noninvasive localized squamous cell carcinoma

Question 254

pT1 penile cancer

Answer 254

Glans: Tumor invades lamina propria Foreskin: Tumor invades dermis, lamina propria, or dartos fascia Shaft: Tumor invades connective tissue between epidermis and corpora regardless of location All sites with or without lymphovascular invasion or perineural invasion and is or is not high grade

Question 255

pT1a penile cancer

Answer 255

Tumor is without lymphovascular invasion or perineural invasion and is not high grade (i.e., grade 3 or sarcomatoid)

Question 256

pT1b penile cancer

Answer 256

Tumor exhibits lymphovascular invasion and/or perineural invasion or is high grade (i.e., grade 3 or sarcomatoid)

Question 257

pT2 penile cancer

Answer 257

Tumor invades into corpus spongiosum (either glans or ventral shaft) with or without urethral invasion

Question 258

pT3 penile cancer

Answer 258

Tumor invades into corpora cavemosum (including tunica albuginea) with or without urethral invasion

Question 259

pT4 penile cancer

Answer 259

Tumor invades into adjacent structures (i.e., scrotum, prostate, pubic bone)

Question 260

cN1 penile cancer

Answer 260

Palpable mobile unilateral inguinal lymph node

Question 261

cN2 penile cancer

Answer 261

Palpable mobile ≥ 2 unilateral inguinal nodes or bilateral inguinal lymph nodes

Question 262

cN3 penile cancer

Answer 262

Palpable fixed inguinal nodal mass or pelvic lymphadenopathy unilateral or bilatera

Question 263

pN1 penile cancer

Answer 263

≤2 unilateral inguinal metastasis without extranodal extension

Question 264

pN2 penile cancer

Answer 264

≥3 unilateral inguinal metastases or bilateral metastases

Question 265

pN3 penile cancer

Answer 265

extranodal extension of lymph node metastases or pelvic lymph node metastases

Question 266

Management of Tis and Ta penile tumors

Answer 266

topical therapy using 5% imiquimod or 5-fluorouracil as well as wide local excision encompassing circumcision for penile tumors situated on the penile foreskin are the preferred primary treatment approaches

Question 267

Management of low grade cT1 penile cancer

Answer 267

preferably offered penile preserving surgery consisting of a wide local excision +/- thick split thickness (STSG) or full thickness (FTSG) skin graft, with alternative options being laser ablative therapy or radiotherapy.

Question 268

Management of nonpalpable lymph nodes in penile cancer

Answer 268

T1 or higher high grade proceed with bilateral superficial ILND with deep ILND if any positive LN. Have to get at least 15 nodes

Question 269

Management of palpable (non-bulky) nodes

Answer 269

LN divided into NB ILN (<4 cm) and those with Bulky ILN Patients should undergo dx FNA or go straight to ILND if clinical suspcious for mets If FNA is negative or non -dx then proceed wto wife erxcisional LN biopsy If negative--surveillance IF positive- ILND

Question 270

Management of palpable (bulky lymph nodes) in penile cancer

Answer 270

first step is get tissue diagnosis upfront ILND for highly symptomatic patients ipsilateral PLND in pts with 2+ positive ILN on superficial or deep

Question 271

Indication for Radical nephroureterectomy in UTUC

Answer 271

High-grade UTUC and low-grade UTUC, where nephron-sparing options are not feasible or oncologically appropriate