ASCO GU Oncology 2009

Robert Dreicer, M.D., M.S., FACP

Chair Dept of Solid Tumor Oncology

Taussig Cancer Institute

Professor of Medicine

Cleveland Clinic Lerner College of Medicine

Inclusion Criteria

• mRCC with component of

clear cell histology

• Measurable or evaluable

disease

Exclusion Criteria

• Prior systemic therapy

• Evidence of CNS

metastases

Stratification:

• Nephrectomy status

• MSKCC risk group

•Primary objective: OS

•Secondary objectives: PFS, ORR, and safety

IFN-/Bevacizumab (n=369)

IFN- 9 MU s.c. 3x/week

Bevacizumab 10 mg/kg IV q2w

IFN- (n=363)

IFN- 9 MU s.c. 3x/week

(n = 732)

R

A

N

D

O

M

I

Z

E

Phase III CALGB 90206 Trial: Study

Design (abstract LBA5019)

Rini et al. J Clin Oncol 2009; 27(suppl):239s

Adverse event

Bevacizumab + IFN

(n=366)

IFN

(n=352)

Any grade 3/4 adverse event 79% 61%

Fatigue/asthenia/malaise 37% 30%

Anorexia 17% 8%

Proteinuria 15% <1%

Hypertension 11% 0%

Hemorrhage 2% <1%

Venous thromboembolism 2% 1%

Gastrointestinal perforation <1% 0%

Arterial ischemia 1% 0%

Frequency of selected grade 3 or 4 AEs

LBA5019

Objective Response

Note: patients with measurable disease only

Bev + IFN (n=325) IFN (n=314)

Overall Response rate 25.5%

[95% CI = 20.9-30.6]

13.1%

[95% CI = 9.5-17.3]

CR 3.7% 1.9%

PR 23.4% 12.7%

p < 0.0001

Duration of response 11.9 months

[95% CI = 8.3 – 14.8]

9.7 months

[95% CI = 7.6 – 19.8]

p = 0.362

LBA5019

Time(months)

Ove

rall

Su

rviv

al (p

rob

ab

ility)

IFN BEV/IFNStratified log-rank p=0.069

Kaplan-Meier Overall Survival Curves by Treatment Arm

0 6 12 18 24 30 36 42 48 54 60

0.0

0.2

0.4

0.6

0.8

1.0

363 286 221 177 148 118 98 64 37 10 1

369 314 242 190 160 139 116 94 42 17 2

IFN

BEV/IFN

Number of Patients at Risk

---- BEV/IFN: Median OS 18.3 months

IFN: Median OS 17.4 months

Kaplan-Meier Overall Survival by Treatment Arm

LBA5019

Median OS (months) according to treatment

arm and subsequent therapy (LBA5019)

Bevacizumab +

Interferon

Interferon Total(unstratified log-rank

p comparing arms)

Stratified HR

Received

2nd-line

therapy

(n=408)

31.4 26.8 28.2(p=0.079)

0.80 (p=0.055)

Did not

receive 2nd-

line therapy

(n=324)

13.1 9.1 10.2(p=0.059)

0.82 (p=0.108)

Total 18.3 17.4 18.1 (p=0.097)

0.86 (p=0.069)

Authors Conclusions LBA5019

Overall survival is greater in patients with metastatic clear cell RCC receiving bevacizumab plus interferon as initial systemic therapy compared to interferon alone, but does not meet pre-defined criteria for significance

Although the favorable effect of bevacizumab plus IFN on OS is preserved regardless of subsequent treatment, the most robust OS is achieved in patients with favorable underlying disease biology who are able to receive subsequent therapy

The combination of bevacizumab and IFN as initial therapy in metastatic RCC patients results in a significantly greater progression-free survival and objective response rate versus IFNA monotherapy

Toxicity is greater in the combination therapy arm, including more fatigue, anorexia, hypertension and proteinuria

Nephrectomized patients

with advanced RCC

Stratification:

Country

MSKCC risk group

•Primary objective: OS

•Secondary objectives: PFS, TTP, TTF, ORR, and safety

•Median follow-up: 22 months

IFN-2a/Bevacizumab (n=327)

IFN- 9 MIU s.c. 3x/week*

Bevacizumab 10 mg/kg IV q2w

until progression

IFN-/placebo (n=322)

IFN- 9 MIU s.c. 3x/week*

placebo 10 mg/kg IV q2w until

progression(n = 649)

R

A

N

D

O

M

I

Z

E

Phase III AVOREN Trial: Study

design

Escudier et al. J Clin Oncol 2009; 27(suppl):239s

(abstract 5020).

*Dose reduction allowed

Phase III AVOREN Trial : Final OS results

Multiple Cox regression analysis for OS:

− HR 0.78 (0.63-0.96); P = .0219

OS not affected by reduction of IFN dose:

− OS 26 months with reduced-dose IFN and 23.3 months

with standard IFNEscudier et al. J Clin Oncol 2009; 27(suppl):239s

(abstract 5020)).

IFN+placebo

(n=322)

IFN+bev

(n=327)HR

Log rank

P Value

Median OS (months)

Unstratified NR NR 0.91 (0.76-1.10) .3360

Stratified 21.3 23.3 0.86 (0.72-1.04) .1291

Median OS after

censoring patients at

time of crossover

(months)

20.8 23.3 0.84 (0.70-1.02) .0766

Phase III AVOREN trial of interferon alpha plus bevacizumab

or placebo in nephrectomized advanced RCC: Final OS results

Subgroup analysis demonstrated similar benefit regardless of age,

Motzer score, baseline VEGF levels, and number of metastatic sites

However, patients without liver metastases demonstrated significant

OS benefit from the addition of bevacizumab (27.5 vs. 21.4 months,

HR 0.76; P = .0155)

Escudier et al. J Clin Oncol 2009;

27(suppl):239s (abstract 5020)

Post-protocol

therapy

N

IFN+plac vs.

IFN+bev

Median OS (months)

HRIFN+placebo IFN+bev

Subsequent TKI 120 vs. 113 33.6 38.6 0.80 (0.56-1.13)

Subsequent

sunitinib92 vs. 83 39.7 43.6 0.88 (0.58-1.35)

Subsequent

sorafenib50 vs. 60 30.7 38.6 0.73 (0.44-1.20)

Phase III study of pazopanib in treatment-naïve or

cytokine-pretreated advanced RCC

Sternberg et al. J Clin Oncol 2009; 27(suppl):240s

(abstract 5021)

Eligibility:

• Locally advanced or

metastatic RCC

• Clear cell histology

• Treatment naive or

failure of 1 prior

cytokine therapy

Stratification:

ECOG PS

Prior nephrectomy

Rx naive (n=233) vs. 1

cytokine failure (n=202)

•Primary objective: PFS

•Secondary objectives: OS, ORR, duration of response, safety, health-related QOL

Pazopanib 800mg qd

Placebo*

(n = 435)

R

A

N

D

O

M

I

Z

E

2:1

(n = 290)

(n = 145)

*Option to crossover via an

open label study at progression

Phase III study of pazopanib in treatment-naïve or

cytokine-pretreated advanced RCC: Efficacy

48% of patients on placebo arm received pazopanib at disease

progressionSternberg et al. J Clin Oncol 2009; 27(suppl):240s

(abstract 5021).

Patient populationplacebo

(n=145)

pazopanib

(n=290)HR P Value

ORR (%)

Overall population 3 30 NR NR

Treatment-naïve* 4 32 NR NR

Cytokine-pretreated† 3 29 NR NR

Median PFS (months)

Overall population 4.2 9.2 0.46 (0.34-0.62) <.0000001

Treatment-naïve* 2.8 11.1 0.40 (0.27-0.60) <.0000001

Cytokine-pretreated† 4.2 7.4 0.54 (0.35-0.84) <.001

Median OS (months) 18.7 21.1 0.73 (0.47-1.12) .02‡

* n = 78 for placebo and 155 for pazopanib; † n = 67 for placebo and 135 for pazopanib

‡ one-sided P value

Phase III study of pazopanib in treatment-naïve or

cytokine-pretreated advanced RCC: Safety

4% of pts in the pazopanib arm and 3% in the placebo arm

experienced grade 5 adverse events

Sternberg et al. J Clin Oncol 2009;

27(suppl):240s (abstract 5021)

Grade 3/4 Adverse Eventsplacebo

(n=145) (%)

pazopanib

(n=290) (%)

Hypertension <1 4

Diarrhea <1 4

Anorexia <1 2

Vomiting 2 3

Fatigue 2 2

Asthenia 0 3

Hemorrhage 0 2

ALT abnormalities 1 12

AST abnormalities <1 8

ALT = alanine transferase; AST = aspartate aminotransferase

RCC Treatment Algorithm: 2009

Setting Patients Therapy

(level 1)

Other Options

(≥ level 2)

Untreated

Good or

Intermediate risk

Sunitinib

Bevacizumab +

IFN

HD IL-2

Sorafenib

Clinical trial

Observation

Poor risk Temsirolimus Sunitinib

Clinical trial

Cytokine-

refractory

Sorafenib

Pazopanib

Sunitinib

Bevacizumab

VEGF-R

refractory

Everolimus

Clinical trial

Sunitinib

Sorafenib

mTOR-refractory Clinical trial Clinical trial

*Adapted from M Atkins, ASCO 2006 & R Bukowski ASCO 2007

Randomized Trial of p53 Targeted

Adjuvant Therapy for Patients with

Organ- Confined Node-Negative

Urothelial Bladder Cancer

Abstract 5017Walter M. Stadler, Seth P. Lerner, Susan Groshen, John P. Stein†, Ellenie Tuazon, David Quinn, Donald G. Skinner, Derek Raghavan, David Esrig, Gary Steinberg, David Wood, Laurence Klotz, Craig Hall, Richard Cote

†Deceased

Years from Cystectomy

Pro

bab

ilit

y o

f N

ot

Recu

rrin

g

p53 negative( n=142)

p53 positive( n=101)

p< 0.001

Esrig, et al NEJM 1994; 1259-64

p53 Status May be Prognostic

STUDY DESIGN

Radical Cystectomy (P1, P2a, P2b, NO, MO)

Registration - Consent to p53 Analysis and

Randomized Trial

IHC, p53 Altered

(>10% nuclear +)

IHC, p53 Wild type

(≤10% nuclear +)

Consent for

Randomization Re-

Confirmed

Consent for

Randomization Not Re-

Confirmed

MVAC x 3

Arm I

Observ.

Arm II

Observ.

Arm IV

Observ.

Arm III

Abstract 5017

Overall Survival: MVAC vs.

Observation (Arm 2)

0.00

0.10

0.20

0.30

0.40

0.50

0.60

0.70

0.80

0.90

1.00

0 12 24 36 48 60 72 84 96 108 120 132

Months Since Randomization

Estim

ate

d

Pro

bab

ility

o

f

Su

rviv

al

MVAC (n=58)

Observed (n=56)

p=0.75

Abstract 5017

Abstract 5017

Authors Conclusions

Unable to confirm prognostic value of p53

Centrally performed IHC may not be analytically valid

Stage migration led to better than expected outcomes

Preliminary data based on too small of a cohort

p53 mutation and pathway analysis pending

Unable to confirm predictive value of p53

See above

Randomization challenges led to underpowered trial

A Multicenter Study of Cisplatin,

Gemcitabine and bevacizumab As First Line

Therapy for Metastatic Urothelial Cancer:

Hoosier Oncology Group Protocol GU04-75

ABSTRACT 5018

N. M. Hahn, W. M. Stadler, R. T. Zon, D. Waterhouse, J. Picus, S. Nattam, C. S. Johnson, S. M. Perkins, M. J. Waddell, C. J. Sweeney

Study Design

Primary Endpoint

Progression Free Survival (PFS)

Secondary Endpoints

Response Rates

Toxicity

Overall Survival (OS)

Abstract 5018

• Maximum of 8 cycles of Cisplatin and Gemcitabine• Maximum 1 year of Bevacizumab therapy*Gemcitabine reduced to 1000 mg/m2 iv d1,8 after first 17 patients due to 7 DVT/PE events

Eligibility Criteria•Metastatic UC (mUC)•ECOG PS 0-1•Cr < 1.5 mg/dl•No prior CTx for mUC•No anticoagulation•No CNS mets

E

N

R

O

L

L

M

E

N

T

Cisplatin 70 mg/m2 iv d1

Gemcitabine* 1250 mg/m2 iv d1,8

Bevacizumab 15 mg/kg iv d1

Cycle length = 21 days

Abstract 5018

STUDY SCHEMA

Median chemotherapy cycles – 6 (2-8)

30% patients entered Bevacizumab maintenance portion

60% patients required dose modifications

42% discontinued therapy due to toxicity

21% discontinued Bevacizumab due DVT/PE

Therapy Administration

Abstract 5018

Cisplatin/Gemcitabine + Bevacizumab in

Metastatic Urothelial Cancer: Results

Hahn et al. J Clin Oncol 2009; 27(suppl):239s

(abstract 5018)

Adverse events (n = 43):

− 60% of patients required dose adjustments

• 42% discontinued therapy due to toxicity

• 21% discontinued bevacizumab due to DVT/PE

− DVT/PE incidence

• Gemcitabine 1250 mg/m2 (n = 18) – 39%

• Gemcitabine 1000 mg/m2 (n = 25) – 8%

− 3 treatment-related deaths (all at 1000 mg/m2 dose)

• Cerebral hemorrhage, aortic dissection, sudden cardiac

death

Objective response rate: 25 (58%)

Progression Free SurvivalP

ro

bab

ilit

y o

f n

ot

Pro

gressin

g

Months

Median PFS = 8.2 m (95% CI 6.5 – 10.0)

Median follow-up = 14.6 m (Range 2-37)

12-month PFS = 29%

Abstract 5018

Overall Survival

Median OS = 19.1 m (95% CI 11.5 – 23.4)

Median follow-up = 14.6 m (Range 2-37)

12-month OS = 65%

Abstract 5018

Bevacizumab is associated with significant toxicity in metastatic urothelial carcinoma patients

The PFS of 8.2 months did not meet the designed primary endpoint

The OS of 19.1 months is beyond that expected from cisplatin plus gemcitabine alone

Authors Conclusions

Abstract 5018

Proposed Intergroup Phase III Trial

Antitumor Activity of MDV3100 in a

Phase 1-2 Study of Castration-Resistant

Prostate Cancer

Abstract No: 5011

H. I. Scher, T. Beer, C. Higano, M. Taplin, E. Efstathiou, A. Anand,

D. Hung, M. Hirmand, M. Fleisher, C. SawyersProstate Cancer Clinical Trials Consortium

MDV3100

A Second-Generation Antiandrogen

1. Engineered for activity in prostate cancer cells that

overexpress the androgen receptor (AR).

2. Binds the AR more potently than bicalutamide.

3. Unlike bicalutamide, MDV3100 inhibits nuclear

translocation of the AR and its binding to DNA.

4. Induces apoptosis in prostate cancer cells.

Abstract 5011

Ligand

1. AR Binding Affinity• DHT ~ 5nM

• Bicalutamide ~160 nM

• MDV3100 ~35 nM

2. Nuclear Import• DHT: ++++

• Bicalutamide: ++++

• MDV3100: ++

3. DNA Binding• DHT: ++++

• Bicalutamide: ++

• MDV3100: -

4. Coactivator recruitment• DHT: ++++

• Bicalutamide: ++

• MDV3100: -

The Effects of MDV3100 on the

Androgen Receptor Are Distinct from Bicalutamide

1

2

Chen, Clegg and Scher

3

4

DNA

POL

II

HS

P 9

0

LB

D

HD

DBD

NTD

Phase 1-2 Multicenter Trial in CRPC

Determine safety

Determine pharmacokinetics (PK)

Assess antitumor activity:

Exploratory:

Circulating tumor cells

PET: FDG - 18-fluorodeoxyglucose

PET: FDHT - 18-fluorodihydrotestosterone

Abstract 5011

Key Inclusion Criteria

1. Pathologic confirmation of adenocarcinoma of

prostate

2. Serum testosterone level <50 ng/dL

3. Progressive disease defined as one or more of:

3 rising PSA levels; screening PSA >2 ng/mL

RECIST

Two or more new lesions on bone scan

4. No more than 2 prior chemotherapy regimens,

at least one of which contained docetaxel

Abstract 5011

Trial Design

Single

Dose

6 days

Continuous Dosing

Assess Monthly;

Q3 Month Imaging

Long-Term

Dosing

Indefinite

Cohort 1

Single

Dose

6 days

Continuous Dosing

Assess Monthly;

Q3 Month Imaging

Long-Term

Dosing

Indefinite

Cohort 2

After 28

Day Safety

Subsequent Dose Levels

Cohort expansion at > 60 mg/day12 pre- and 12 post-chemotherapyPost-chemotherapy only at > 480 mg/day Abstract 5011

Demographics/Prior Therapy (N=140)

Med. (range)

AGE (years) 68 (44–93)

PSA (ng/mL) 50 (2–2,159)

N (%)

PRIOR HORMONE THERAPY 140 (100%)

1 line 32 (23%)

2 lines 42 (30%)

>3 lines 66 (47%)

CHEMOTHERAPY 75 (54%)

Abstract 5011

MDV3100 Was Generally Well-Tolerated

Adverse Event All Doses

(N = 140)

240 mg/day

(N = 60)

G2 G3 G2 G3

Fatigue

Nausea

Anorexia

Seizure

29 (21%)

11 ( 8%)

4 ( 3%)

12 (9%)

3 (2%)

8 (13%)

2 ( 3%)

3 (5%)

1. Only one subject discontinued treatment due to fatigue which coincided with

disease progression

2. Two witnessed seizures (one each at 600 and 360 mg/day) and a possible

unwitnessed seizure (at 480 mg/day) were reported

Both patients with witnessed seizures were taking concomitant medications

that can cause seizure

3. MTD determined to be 240 mg/day; patients at higher doses were lowered to

240 mg/day

Possibly Related Grade 2/3 Adverse Events in >2 Patients

Abstract 5011

Waterfall Plot of Best Percent PSA Change

from BaselineChemotherapy-Naïve (N=65) Post-Chemotherapy (N=75)

62% (40/65)

>50% Decline

51% (38/75)

>50% Decline

Authors Conclusions

MDV3100 is a second-generation antiandrogen

engineered for activity in cells that overexpress AR,

unique from bicalutamide

The drug active in CRPC both before and following

chemotherapy as demonstrated by declines in PSA,

imaging, CTC conversion rates, and PET

MDV3100 is generally well-tolerated

Phase III trial will open this year

Abstract 5011

Southwest Oncology Group S9921:

Prolonged Event Free Survival in High

Risk Prostate Cancer (PC) Patients

Receiving Adjuvant Androgen Deprivation

Abstract 5009

L. Michael Glode, Cathy M. Tangen, Maha H.A. Hussain, David P. Wood, Jr. , Gregory P. Swanson, David I. Quinn, Nancy Dawson, Naomi Balzer-Haas, E. David Crawford, Benjamin Ely, Ian M. Thompson

Background

Study conceived 1997-98

Mitoxantrone approved 1996 by FDA for

palliative treatment of HRPC

Canadian Palliation trial (JCO 14:1756)

CALGB 9182 (JCO 17:2506)

Improved QOL compared to hydrocortisone alone

Improved time to treatment failure

No difference in survival

Abstract 5009

SWOG 9921

Intergroup Participants: CALGB, ECOG

Eligibility

Prostatectomy ≤ 120 days prior to registration and one or

more of the following:

Path Gleason sum > 8

pT3b (seminal vesicle) or pT4 or N1

Path Gleason’s sum 7 and positive margin

Preop PSA >15ng/ml, or biopsy Gleason >7, or PSA

>10ng/ml with biopsy Gleason > 6

Abstract 5009

PSA>20,T3b, T4 or N1 or

Gleason > 8,or T3a, + margin,

and Gleason 7

RA

ND

OM

IZE

CAB X 24 months

Mitoxantrone 12 mg/m2 d1+ Prednisone 5 mg BID d1-21

Q 3 Weeks X 6 andCAB x 24 months

983496

487

Trial Design

Abstract 5009

Causes of Death (17 total)

Prostate Cancer – 7

Other Cancers – 4

Cardiovascular Disease – 1

Other Causes – 5

Abstract 5009

Testosterone (T) Recovery (> 50ng/ml)

• Per protocol, T measured every 6 month intervals until > ILLN.

• Patients included in analysis: ≥1 T measurement within the first 12

months after completing CAB

Median

T Recovery

Time*

(95% CI)

6 Month*

Overall

T Recovery

(95% CI)

12 Month*

Overall

T Recovery

(95% CI)

18 Month*

Overall

T Recovery

(95% CI)

9.5 Months

(8.7, 10.5)

27.8%

(5.6, 71.4)

75.3%

(50.8, 90.0)

89.5%

(69.8,96.9)

* Recovery time measured from completion of CAB

Abstract 5009

Authors Conclusions

S9921 shows better than predicted DF-survival in high risk prostate cancer patients who received 2 years of CAB Potential causes: stage migration, patient selection,

lead time bias, effects of CAB itself. Comparable survival data are seen in selected

contemporary studies

75% of patients have testosterone recovery to above castrate level within one year of stopping CAB

Much longer follow-up of S9921 will be required to observe any differences in survival due to mitoxantrone

Abstract 5009

Phase II Trials of Abiraterone Acetate in Castration

Resistant Prostate Cancer

1Ryan et al. J Clin Oncol 2009; 27(suppl):245s (abstract

5046)2Reid et al. J Clin Oncol 2009; 27(suppl):246s (abstract 5047)

3Danila et al. J Clin Oncol 2009; 27(suppl):246s (abstract

5048)

Patient population NPSA decline ≥

50%

Tumor

response

(RECIST)

ECOG PS

Improvement

(at least one level)

CRPC: Chemotherapy

naïve1 33 24 (73%)PR: 9 (27%)

SD: 19 (58%)8 (61.5%)

CRPC: Prior docetaxel247 24 (51%)

PR: 6 (13%)

SD: 25 (53%)11 (35%)

CRPC: Prior docetaxel3

No prior ketoconazole

Prior ketoconazole

31

27

16 (52%)

8 (30%)

(n = 18)

PR: 3 (17%)

SD: 11 (61%)

16 (48%)

Phase II Trials of Abiraterone Acetate in Castration Resistant

Prostate Cancer: Grade 3/4 Adverse Events

1Ryan et al. J Clin Oncol 2009; 27(suppl):245s (abstract 5046)2Reid et al. J Clin Oncol 2009; 27(suppl):246s (abstract 5047)

3Danila et al. J Clin Oncol 2009; 27(suppl):246s (abstract 5048)

Ryan (n = 33) Reid (n = 47)* Danila (n = 58)*

Hematological

Lymphopenia NR 2 (4%) 5 (9%)

Anemia NR 3 (6%) NR

Nonhematologic

Peripheral edema 1 (3%) 0 NR

Fatigue 0 4 (8.5%) NR

Nausea NR 3 (6%) NR

Vomiting NR 3 (6%) NR

•Common toxicities (all grades) in at least two trials: peripheral

edema, fatigue, hypokalemia, arthralgia

*Experienced by ≥ 2 patients

Fleisher H, et al. abstract 5049

Circulating tumor cells (CTC) in patients with metastatic castration-

resistant prostate cancer (CRPC) receiving abiraterone acetate (AA) after

failure of docetaxel –based chemotherapy

Preliminary findings suggest correlation with

CTC decline and PSA decline

Prospectively built into phase III abiraterone

program

IMPACT Overall Survival: Primary Endpoint

Intent-to-Treat Population

0 6 12 18 24 30 36 42 48 54 60 660

25

50

75

100

Perc

ent

Surv

ival

Survival (Months)

P = 0.032 (Cox model)

HR = 0.775 [95% CI: 0.614, 0.979]

Median Survival Benefit = 4.1 Mos.

Sipuleucel-T (n = 341)

Median Survival: 25.8 Mos.

Placebo (n = 171)

Median Survival: 21.7 Mos.

PF Schellhammer, et al. LBA 9 AUA 2009

LocallyAdvancedDisease

Rising PSAHormone

Naive

Rising PSACastrate

MetastasesCastrate

Asymptomatic

MetastasesCastrate

Symptomatic

OrganConfined

Metastatic Disease

(De novo)

Clinical States In Prostate Cancer

MetastasesCastrate

SymptomaticPost Docetaxel

Modified from Scher H, et al.

Conclusions: Renal Cancer

Lots of active agents, need to sort out optimal

sequence taking into account efficacy, cost,

toxicity

New generations of TKI’s may be equally

effective but perhaps less toxic- cant

emphasize how important that may be

Combination therapy is going to be difficult,

toxicity remains significant impediment to

further development

Conclusions: Urothelial Cancer

Progress remains painfully slow

Gemcitabine/cisplatin/bevacizumab of

interest, but toxicity remains SIGNIFICANT

CONCERN

Phase III will have real time toxicity

monitoring by CALGB

Conclusions: Prostate Cancer

Near term future for advanced prostate

cancer therapeutics, is much brighter—BUT

WILL BE VERY EXPENSIVE

Androgen receptor targeting therapy IS

HERE- STOP USING TERM HORMONE

REFRACTORY/ANDROGEN

INDEPENDENT

CASTRATE RESISTANT