Case report 367
Parotid gland metastasis from prostate cancer: is docetaxel still the best treatment option? Carole Hélisseya, Mathieu Rouannec,d, Francois-Xavier Arnaudb and Sylvestre Le Mouleca Metastases of prostate cancer originating from the parotid gland are rare. However, this presentation raises the question of the management of visceral metastasis in castration-resistant prostate cancer. We report the case of an 87-year-old man who presented with a right painless parotid mass in the context of castration-resistant prostate cancer, indicating progression of the disease. He received medical treatment based on docetaxel. Here, we discuss the impact of new hormonotherapies such as enzalutamide and abiraterone acetate, which may be used for the management of these patients. Anti-Cancer Drugs 26:367–370 Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
Introduction One third of prostate cancer is diagnosed at an advanced stage [1]. The main metastatic site is bone, followed by lymph nodes. Parotid metastasis from prostate carcinoma is uncommon. Only eight cases have been reported in the literature [2–8]. Here, we report the case of a right painless parotid mass, diagnosed in a patient with metastatic castration-resistant prostate cancer (mCRPC). This unusual presentation raises the question about the management of visceral metastases (VMs) in patients with castration-resistant prostate cancer (CRPC).
Anti-Cancer Drugs 2015, 26:367–370 Keywords: castration-resistant prostrate carcinoma, chemotherapy, new hormonotherapies, parotid metastasis Departments of aMedical Oncology, bRadiology, Hôpital d’Instruction des Armées Val de Grâce, cDepartment of Urology, Foch Hospital, Suresnes, Paris and dUFR of Health Sciences, Université Versailles-Saint-Quentin-en-Yvelines, Versailles, France Correspondence to Carole Hélissey, MD, Department of Medical Oncology, Hôpital d’Instruction des Val de Grâce, 74 Boulevard Port-Royal, 75005 Paris, France Tel: + 33 01 40 51 45 54; fax: + 33 01 40 51 45 54; e-mail: [email protected] Received 6 October 2014 Revised form accepted 2 November 2014
Physical examination of the neck indicated a firm, semi fixed, 2 cm in diameter mass located in the parotid area. There were no masses on the right side of the neck and the thyroid was not enlarged. There was no local inflammation and the Stenon’s canal orifice did not show any abnormality. Cranial nerves II through XII were intact. MRI indicated a T1-hypointense and predominantly T2-hyperintense, heterogeneously enhancing mass with lobular contours in the region of the parotid tail, without extension outside the parotid capsule. The margins were well defined. A single
Case presentation
0959-4973 Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
Fig. 1 Parotid metastasis progression bone metastasis
250 200 PSA (ng/ml)
150 100
Bone metastasis
50 0 Au g N -08 ov M -0 ar 8 ch Ju -09 ne Se -09 pt O -09 ct Fe 09 M b-1 ar 0 ch Ju -10 lySe 10 pt N -10 ov -1 Ja 0 nFe 11 M b-1 ar 1 ch -1 1
An 87-year-old man was referred to an otolaryngologist for evaluation of a fast-growing mass in the right upper neck near the angle of the mandible. He did not report on any recent weight loss, trismus, dysphagia, odynophagia, or fever. His medical history was a mCRPC diagnosed 3 years ago. Initial staging indicated undifferentiated adenocarcinoma with a Gleason score 10 (5 + 5) and disseminated bone metastasis. He was followed up in an oncourological clinic with regular monitoring of prostate-specific antigen (PSA) levels. The initial PSA decreased from 42.9 to 9 ng/ml 1 month after introducing hormonal therapy combining gonadotropin-releasing hormone analog with antiandrogen. Twelve months after the initial response, resistance to hormone therapy occurred. The patient was included in a phase II clinical trial evaluating the association of bicalutamide with antiangiogenic therapy. Finally, he received diethylstilbestrol and leuprorelin alone. Figure 1 shows the evolution of PSA over time according to subsequent treatments.
L
Phase ll
Dist
L Dist L
Doc
PSA evolution. Doc, docetaxel; Dist, distilben; L, leuprorelin; PSA, prostate-specific antigen.
DOI: 10.1097/CAD.0000000000000188
Copyright © 2014 Wolters Kluwer Health, Inc. Unauthorized reproduction of the article is prohibited.
368
Anti-Cancer Drugs 2015, Vol 26 No 3
Fig. 2
MRI head and neck region. (a) Axial T2. T2-hyperintense in the right parotid area and in the back. Intraparotid ganglions. (b) Coronal T1 with a gadolinium injection and saturation. Heterogeneously enhancing of the lesion, along the muscular structures to the right supraclavicular fossa. Right supraclavicular ganglions.
heterogeneously enhancing ipsilateral level IIA lymph node was identified inferomedial to the mass. There was no contralateral lymph node (Fig. 2a and b). The chest radiograph was normal. A computed abdominal and thoracic tomography showed bone metastasis progression. From a biological standpoint, the PSA level reached 227 ng/ml. A fine-needle aspiration biopsy performed in the clinic showed malignant cells with strong expression of PSA antibody staining related to an intraparotid metastasis of prostatic adenocarcinoma. A docetaxel-based chemotherapy (30 mg/m2/week) was started. The patient received two courses of this drug. Unfortunately, he was admitted to the emergency room with neurological motor deficit after 19 days. MRI of the brain indicated a neoplastic intravascular coagulopathy with multiple cortical and subcortical hyperintensities located in the two lobes. Biological analysis showed diffuse coagulopathy related to disseminated intravascular coagulation [platelets 41 000/mm3, fibrinogen 0.6 g/l (2 < N < 4.5) and D-dimer level more than 20 μg/ml (0 < N < 0.40)]. The patient died 30 days after the initial diagnosis of parotid tumor progression.
Discussion We report a rare and unusual presentation of parotid gland metastasis originating from prostate cancer. To our knowledge, only eight cases have been reported in the literature (Table 1). In fact, visceral disease from CRPC was associated previously with neuroendocrine phenotypes and has rarely been reported [9]. Nowadays, a multitude of new drugs focusing on the treatment of mCRPC have been developed. Over the last few years, the incidence of mCRPC patients with VM has
increased markedly because of the improvement in the management of this disease. In a recent study, Pezaro et al. [10] explored the prevalence of visceral disease among 39 patients treated for a CRPC. The incidence of VM in patients with mCRPC is ranged from 32%. In this study, the delay between resistance to hormonotherapy and the occurrence of VM was ∼ 19 months. In addition, the overall median survival in patients diagnosed with VM was only 7 months. Moreover, the metastatic site was a significant prognostic factor. In fact, the median survival was 10, 14.4, and 19 months, respectively, for patients with liver metastasis, lung metastasis, and bone metastasis [11]. The occurrence of VM and the volume of bone involvement were associated significantly with the overall survival. Indeed, the median survival was 18.2 and 6.1 months for patients with no evident bone disease and with more than six bone lesions, respectively (P = 0.001) [10]. These data suggest that VM developed at a late disease course and were associated with a poor prognosis. Currently, management of patients with VM originating from prostate cancer remains unclear. Pezaro et al. [10] highlighted a significant proportion of patients with VM (14–49%) among the mCRPC population. However, these patients were not eligible for inclusion in clinical trials. Interestingly, new generations of hormonotherapy [i.e. abiraterone acetate (AA) and enzalutamide] significantly prolonged the survival of men with CRPC post-docetaxel and predocetaxel. Therefore, it could be considered in such patients with visceral disease. Interestingly, the COU-AA-301 trial assessed the AA activity in mCRPC patients after docetaxel. AA improved
Copyright © 2014 Wolters Kluwer Health, Inc. Unauthorized reproduction of the article is prohibited.
Parotid metastasis in mCRPC Hélissey et al. 369
Table 1
Parotid metastasis from prostate cancer
Age (years)
Histology
Gleason score
77
ADK
UK
72
UK
UK
68
UK
UK
UK
UK
77
ADK
UK
UK
UK
69
ADK
UK
Radiotherapy Diethylstilbestrol
8 months
83
ADK
3+4
UK
UK
73
UK
UK
UK
UK
Cervical mass. Evolutive growth
68
ADK
UK
Hormonotherapy
3 years
Left parotid mass
87
ADK
5+5
Hormonotherapy
3 years
Atrial mass. Evolutive growth
Initial treatment Prostatectomy Bilateral Orchidectomy UK
Date of recurrence
Clinical presentation
4 years
Right parotid mass Movable 2 × 2 cm, otalgia Pain Right parotid mass Evolutive growth FP, ganglion 4 cm right artrial mass Mass 3 cm Eye pain
UK
Parotid histology
Atrial mass Pain Facial hyperesthesia Atrial mass. 9 cm
Treatment
Outcomes
References
ADK low grade differentiated
Chemotherapy Estrogen
Died 2 years after LiVolsi [2] diagnosis
Carcinoma undifferentiated
Parotidectomy
Died 2 months after diagnosis
Carcinoma PSA + Acinous cell
Orchidectomy
Alive 2 years after Gruber et al. diagnosis [4]
ADK Moderate differentiated PSA + ADK undifferentiated PSA +
Leuprolide
Alive 1 year after diagnosis
Moul et al. [5]
Orchidectomy
Died 3 months after diagnosis
Hrebinko et al. [6]
Hormonotherapy Died 6 months after diagnosis Orchidectomy Died 20 months Cyprotérone after diagnosis
Kirkali et al. [7] Simpson and Skálová [8]
Hormonotherapy Died 6 after Chemotherapy Died 1 after
Pouessel et al. [9] This study
ADK, PSA + ADK low grade differentiated PSA + Carcinoma. Acinous cell PSA + ADK, PSA +
months diagnosis month diagnosis
Kucan et al. [3]
ADK, adenocarcinoma; FP, Bell’s palsy; UK, unknown.
the median overall survival similarly in the group with VM (4.6 months) and in the group without VM (4.8 months) [12]. Therefore, AA decreased the risk of death by 21% in the VM group [hazard ratio (HR) = 0.79; 95% confidence interval (CI) = 0.60–1.05]. In this specific subgroup, AA was compared with prednisone alone. The authors found that AA significantly improved the median radiographic progression survival (5.6 vs. 2.8 months, P = 0.0002) and the PSA response rate (28 vs. 7%, P < 0.0001). Recently, the clinical trial COU-AA-302 evaluated AA in patients with chemotherapy-naïve metastatic castration prostate cancer [13]. However, this trial excluded patients with VM. The AFFIRM study evaluated the efficacy of enzalutamide in mCRPC patients. The authors showed that enzalutamide improved the median overall survival to 3.9 months compared with placebo in the VM group [14]. In addition, enzalutamide may be used before chemotherapy in this group. In fact, Beer et al. [15] reported that enzalutamide before chemotherapy improved the median overall survival by 5 months compared with placebo (HR = 0.82, 95% CI = 0.55–1.23). In the present case, we decided to start medical treatment with docetaxel. This patient presented a high tumor burden including more than six bone lesions, a parotid metastasis, and disseminated intravascular coagulation. This treatment was started because of the results of two major trials. First, docetaxel is the treatment option recommended for patients with a poor initial hormone response or severe symptoms such as disseminated intravascular coagulation [16]. The TAX 327
phase III trial assessed docetaxel activity (once a week or once 3 weeks) in mCRPC. Docetaxel improved the median overall survival by 2.4 months compared with mitoxantrone (HR = 0.76, 95% CI = 0.62–0.94, P = 0.009). The response rate was 45% (95% CI = 40–51, P < 0.001) [1]. In addition, the CHARTEED trial, evaluating the combination of androgen deprivation therapy with docetaxel in patients with a high volume of tumor, was reported [17]. The authors report that the median overall survival improved by 17 months with the combination compared with the androgen deprivation therapy alone (32.2–49.2 months, P = 0.0006). Arguably, chemotherapy based on taxanes is the recommended treatment option. However, new hormonotherapies have emerged that may represent alternative options that can be discussed.
Conclusion
Identification of biomarkers is essential in order to improve the treatment of mCRPC patients and to limit the emergence of resistant clones and reduce. Monitoring the evolution of the disease by carrying out molecular analyses on successive lesions through the natural course of the disease seems to be a promising method in the era of precision cancer medicine. To improve the management of such patients, clinical trials are urgently needed.
Acknowledgements Conflicts of interest
There are no conflicts of interest.
Copyright © 2014 Wolters Kluwer Health, Inc. Unauthorized reproduction of the article is prohibited.
370
Anti-Cancer Drugs 2015, Vol 26 No 3
References Petrylak DP, Tangen CM, Hussain MH, Lara PN Jr, Jones JA, Taplin ME, et al. Docetaxel and estramustine compared with mitoxantrone and prednisone for advanced refractory prostate cancer. N Engl J Med 2004; 351:1513–1520. 2 LiVolsi VA. Prostatic carcinoma presenting as a primary parotid tumor. Oral Surg Oral Med Oral Pathol 1979; 48:447–450. 3 Kucan JO, Frank DH, Robson MC. Tumours metastatic to the parotid gland. Br J Plast Surg 1981; 34:299–301. 4 Gruber B, Moran WJ, Pearle MS, Strauss FF 3rd, Chodak G. Prostate cancer presenting as facial paralysis. Otolaryngol Head Neck Surg 1989; 100:333–338. 5 Moul JW, Paulson DF, Fuller G, Gottfried MR, Floyd WL. Prostate cancer with solitary parotid metastasis correctly diagnosed with immunohistochemical stains. J Urol 1989; 142:1328–1329. 6 Hrebinko R, Taylor SR, Bahnson RR. Carcinoma of prostate metastatic to parotid gland. Urology 1993; 41:272–273. 7 Kirkali Z, Koyuncuoğlu M, Pabuçcuoğlu U, Güneri A, Mungan U. Prostatic carcinoma presenting with painless parotid mass. Urology 1995; 46:406–407. 8 Simpson RH, Skálová A. Metastatic carcinoma of the prostate presenting as parotid tumour. Histopathology 1997; 30:70–74. 9 Pouessel D, Gallet B, Bibeau F, Avancès C, Iborra F, Sénesse P, Culine S. Liver metastases in prostate carcinoma: clinical characteristics and outcome. BJU Int 2007; 99:807–811. 10 Pezaro CJ, Omlin A, Lorente D, Nava Rodrigues D, Ferraldeschi R, Bianchini D, et al. Visceral disease in castration-resistant prostate cancer. Eur Urol 2014; 65:270–273.
11
1
12
13
14
15
16
17
Pond GR, Sonpavde G, de Wit R, Eisenberger MA, Tannock IF, Armstrong AJ. The prognostic importance of metastatic site in men with metastatic castrationresistant prostate cancer. Eur Urol 2014; 65:3–6. Goodman OB Jr, Flaig TW, Molina A, Mulders PF, Fizazi K, Suttmann H, et al. Exploratory analysis of the visceral disease subgroup in a phase III study of abiraterone acetate in metastatic castration-resistant prostate cancer. Prostate Cancer Prostatic Dis 2014; 17:34–39. Ryan CJ, Smith MR, de Bono JS, Molina A, Logothetis CJ, de Souza P, et al. COU-AA-302 Investigators. Abiraterone in metastatic prostate cancer without previous chemotherapy. N Engl J Med 2013; 368:138–148. Scher HI, Fizazi K, Saad F, Taplin ME, Sternberg CN, Miller K, et al. AFFIRM Investigators. Increased survival with enzalutamide in prostate cancer after chemotherapy. N Engl J Med 2012; 367:1187–1197. Beer TM, Armstrong AJ, Rathkopf DE, Loriot Y, Sternberg CN, Higano CS, et al. Enzalutamide in metastatic prostate cancer before chemotherapy. N Engl J Med 2014; 371:424–433. Horwich A, Parker C, de Reijke T, Kataja V. ESMO Guidelines Working Group. Prostate cancer: ESMO Clinical Practice Guidelines for diagnosis, treatment and follow-up. Ann Oncol 2013; 24 (Suppl 6): 106–114. Sweeney C, Chen Y-H, Carducci MA, Liu G, Jarrard DF, Eisenberger MA, et al. Impact on overall survival (OS) with chemohormonal therapy versus hormonal therapy for hormone-sensitive newly metastatic prostate cancer (mPrCa): an ECOG-led phase III randomized trial [Abstract]. J Clin Oncol 2014; 32:LBA2.
Copyright © 2014 Wolters Kluwer Health, Inc. Unauthorized reproduction of the article is prohibited.
Parotid gland metastasis from prostate cancer: is docetaxel still the best treatment option? Carole Hélisseya, Mathieu Rouannec,d, Francois-Xavier Arnaudb and Sylvestre Le Mouleca Metastases of prostate cancer originating from the parotid gland are rare. However, this presentation raises the question of the management of visceral metastasis in castration-resistant prostate cancer. We report the case of an 87-year-old man who presented with a right painless parotid mass in the context of castration-resistant prostate cancer, indicating progression of the disease. He received medical treatment based on docetaxel. Here, we discuss the impact of new hormonotherapies such as enzalutamide and abiraterone acetate, which may be used for the management of these patients. Anti-Cancer Drugs 26:367–370 Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
Introduction One third of prostate cancer is diagnosed at an advanced stage [1]. The main metastatic site is bone, followed by lymph nodes. Parotid metastasis from prostate carcinoma is uncommon. Only eight cases have been reported in the literature [2–8]. Here, we report the case of a right painless parotid mass, diagnosed in a patient with metastatic castration-resistant prostate cancer (mCRPC). This unusual presentation raises the question about the management of visceral metastases (VMs) in patients with castration-resistant prostate cancer (CRPC).
Anti-Cancer Drugs 2015, 26:367–370 Keywords: castration-resistant prostrate carcinoma, chemotherapy, new hormonotherapies, parotid metastasis Departments of aMedical Oncology, bRadiology, Hôpital d’Instruction des Armées Val de Grâce, cDepartment of Urology, Foch Hospital, Suresnes, Paris and dUFR of Health Sciences, Université Versailles-Saint-Quentin-en-Yvelines, Versailles, France Correspondence to Carole Hélissey, MD, Department of Medical Oncology, Hôpital d’Instruction des Val de Grâce, 74 Boulevard Port-Royal, 75005 Paris, France Tel: + 33 01 40 51 45 54; fax: + 33 01 40 51 45 54; e-mail: [email protected] Received 6 October 2014 Revised form accepted 2 November 2014
Physical examination of the neck indicated a firm, semi fixed, 2 cm in diameter mass located in the parotid area. There were no masses on the right side of the neck and the thyroid was not enlarged. There was no local inflammation and the Stenon’s canal orifice did not show any abnormality. Cranial nerves II through XII were intact. MRI indicated a T1-hypointense and predominantly T2-hyperintense, heterogeneously enhancing mass with lobular contours in the region of the parotid tail, without extension outside the parotid capsule. The margins were well defined. A single
Case presentation
0959-4973 Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
Fig. 1 Parotid metastasis progression bone metastasis
250 200 PSA (ng/ml)
150 100
Bone metastasis
50 0 Au g N -08 ov M -0 ar 8 ch Ju -09 ne Se -09 pt O -09 ct Fe 09 M b-1 ar 0 ch Ju -10 lySe 10 pt N -10 ov -1 Ja 0 nFe 11 M b-1 ar 1 ch -1 1
An 87-year-old man was referred to an otolaryngologist for evaluation of a fast-growing mass in the right upper neck near the angle of the mandible. He did not report on any recent weight loss, trismus, dysphagia, odynophagia, or fever. His medical history was a mCRPC diagnosed 3 years ago. Initial staging indicated undifferentiated adenocarcinoma with a Gleason score 10 (5 + 5) and disseminated bone metastasis. He was followed up in an oncourological clinic with regular monitoring of prostate-specific antigen (PSA) levels. The initial PSA decreased from 42.9 to 9 ng/ml 1 month after introducing hormonal therapy combining gonadotropin-releasing hormone analog with antiandrogen. Twelve months after the initial response, resistance to hormone therapy occurred. The patient was included in a phase II clinical trial evaluating the association of bicalutamide with antiangiogenic therapy. Finally, he received diethylstilbestrol and leuprorelin alone. Figure 1 shows the evolution of PSA over time according to subsequent treatments.
L
Phase ll
Dist
L Dist L
Doc
PSA evolution. Doc, docetaxel; Dist, distilben; L, leuprorelin; PSA, prostate-specific antigen.
DOI: 10.1097/CAD.0000000000000188
Copyright © 2014 Wolters Kluwer Health, Inc. Unauthorized reproduction of the article is prohibited.
368
Anti-Cancer Drugs 2015, Vol 26 No 3
Fig. 2
MRI head and neck region. (a) Axial T2. T2-hyperintense in the right parotid area and in the back. Intraparotid ganglions. (b) Coronal T1 with a gadolinium injection and saturation. Heterogeneously enhancing of the lesion, along the muscular structures to the right supraclavicular fossa. Right supraclavicular ganglions.
heterogeneously enhancing ipsilateral level IIA lymph node was identified inferomedial to the mass. There was no contralateral lymph node (Fig. 2a and b). The chest radiograph was normal. A computed abdominal and thoracic tomography showed bone metastasis progression. From a biological standpoint, the PSA level reached 227 ng/ml. A fine-needle aspiration biopsy performed in the clinic showed malignant cells with strong expression of PSA antibody staining related to an intraparotid metastasis of prostatic adenocarcinoma. A docetaxel-based chemotherapy (30 mg/m2/week) was started. The patient received two courses of this drug. Unfortunately, he was admitted to the emergency room with neurological motor deficit after 19 days. MRI of the brain indicated a neoplastic intravascular coagulopathy with multiple cortical and subcortical hyperintensities located in the two lobes. Biological analysis showed diffuse coagulopathy related to disseminated intravascular coagulation [platelets 41 000/mm3, fibrinogen 0.6 g/l (2 < N < 4.5) and D-dimer level more than 20 μg/ml (0 < N < 0.40)]. The patient died 30 days after the initial diagnosis of parotid tumor progression.
Discussion We report a rare and unusual presentation of parotid gland metastasis originating from prostate cancer. To our knowledge, only eight cases have been reported in the literature (Table 1). In fact, visceral disease from CRPC was associated previously with neuroendocrine phenotypes and has rarely been reported [9]. Nowadays, a multitude of new drugs focusing on the treatment of mCRPC have been developed. Over the last few years, the incidence of mCRPC patients with VM has
increased markedly because of the improvement in the management of this disease. In a recent study, Pezaro et al. [10] explored the prevalence of visceral disease among 39 patients treated for a CRPC. The incidence of VM in patients with mCRPC is ranged from 32%. In this study, the delay between resistance to hormonotherapy and the occurrence of VM was ∼ 19 months. In addition, the overall median survival in patients diagnosed with VM was only 7 months. Moreover, the metastatic site was a significant prognostic factor. In fact, the median survival was 10, 14.4, and 19 months, respectively, for patients with liver metastasis, lung metastasis, and bone metastasis [11]. The occurrence of VM and the volume of bone involvement were associated significantly with the overall survival. Indeed, the median survival was 18.2 and 6.1 months for patients with no evident bone disease and with more than six bone lesions, respectively (P = 0.001) [10]. These data suggest that VM developed at a late disease course and were associated with a poor prognosis. Currently, management of patients with VM originating from prostate cancer remains unclear. Pezaro et al. [10] highlighted a significant proportion of patients with VM (14–49%) among the mCRPC population. However, these patients were not eligible for inclusion in clinical trials. Interestingly, new generations of hormonotherapy [i.e. abiraterone acetate (AA) and enzalutamide] significantly prolonged the survival of men with CRPC post-docetaxel and predocetaxel. Therefore, it could be considered in such patients with visceral disease. Interestingly, the COU-AA-301 trial assessed the AA activity in mCRPC patients after docetaxel. AA improved
Copyright © 2014 Wolters Kluwer Health, Inc. Unauthorized reproduction of the article is prohibited.
Parotid metastasis in mCRPC Hélissey et al. 369
Table 1
Parotid metastasis from prostate cancer
Age (years)
Histology
Gleason score
77
ADK
UK
72
UK
UK
68
UK
UK
UK
UK
77
ADK
UK
UK
UK
69
ADK
UK
Radiotherapy Diethylstilbestrol
8 months
83
ADK
3+4
UK
UK
73
UK
UK
UK
UK
Cervical mass. Evolutive growth
68
ADK
UK
Hormonotherapy
3 years
Left parotid mass
87
ADK
5+5
Hormonotherapy
3 years
Atrial mass. Evolutive growth
Initial treatment Prostatectomy Bilateral Orchidectomy UK
Date of recurrence
Clinical presentation
4 years
Right parotid mass Movable 2 × 2 cm, otalgia Pain Right parotid mass Evolutive growth FP, ganglion 4 cm right artrial mass Mass 3 cm Eye pain
UK
Parotid histology
Atrial mass Pain Facial hyperesthesia Atrial mass. 9 cm
Treatment
Outcomes
References
ADK low grade differentiated
Chemotherapy Estrogen
Died 2 years after LiVolsi [2] diagnosis
Carcinoma undifferentiated
Parotidectomy
Died 2 months after diagnosis
Carcinoma PSA + Acinous cell
Orchidectomy
Alive 2 years after Gruber et al. diagnosis [4]
ADK Moderate differentiated PSA + ADK undifferentiated PSA +
Leuprolide
Alive 1 year after diagnosis
Moul et al. [5]
Orchidectomy
Died 3 months after diagnosis
Hrebinko et al. [6]
Hormonotherapy Died 6 months after diagnosis Orchidectomy Died 20 months Cyprotérone after diagnosis
Kirkali et al. [7] Simpson and Skálová [8]
Hormonotherapy Died 6 after Chemotherapy Died 1 after
Pouessel et al. [9] This study
ADK, PSA + ADK low grade differentiated PSA + Carcinoma. Acinous cell PSA + ADK, PSA +
months diagnosis month diagnosis
Kucan et al. [3]
ADK, adenocarcinoma; FP, Bell’s palsy; UK, unknown.
the median overall survival similarly in the group with VM (4.6 months) and in the group without VM (4.8 months) [12]. Therefore, AA decreased the risk of death by 21% in the VM group [hazard ratio (HR) = 0.79; 95% confidence interval (CI) = 0.60–1.05]. In this specific subgroup, AA was compared with prednisone alone. The authors found that AA significantly improved the median radiographic progression survival (5.6 vs. 2.8 months, P = 0.0002) and the PSA response rate (28 vs. 7%, P < 0.0001). Recently, the clinical trial COU-AA-302 evaluated AA in patients with chemotherapy-naïve metastatic castration prostate cancer [13]. However, this trial excluded patients with VM. The AFFIRM study evaluated the efficacy of enzalutamide in mCRPC patients. The authors showed that enzalutamide improved the median overall survival to 3.9 months compared with placebo in the VM group [14]. In addition, enzalutamide may be used before chemotherapy in this group. In fact, Beer et al. [15] reported that enzalutamide before chemotherapy improved the median overall survival by 5 months compared with placebo (HR = 0.82, 95% CI = 0.55–1.23). In the present case, we decided to start medical treatment with docetaxel. This patient presented a high tumor burden including more than six bone lesions, a parotid metastasis, and disseminated intravascular coagulation. This treatment was started because of the results of two major trials. First, docetaxel is the treatment option recommended for patients with a poor initial hormone response or severe symptoms such as disseminated intravascular coagulation [16]. The TAX 327
phase III trial assessed docetaxel activity (once a week or once 3 weeks) in mCRPC. Docetaxel improved the median overall survival by 2.4 months compared with mitoxantrone (HR = 0.76, 95% CI = 0.62–0.94, P = 0.009). The response rate was 45% (95% CI = 40–51, P < 0.001) [1]. In addition, the CHARTEED trial, evaluating the combination of androgen deprivation therapy with docetaxel in patients with a high volume of tumor, was reported [17]. The authors report that the median overall survival improved by 17 months with the combination compared with the androgen deprivation therapy alone (32.2–49.2 months, P = 0.0006). Arguably, chemotherapy based on taxanes is the recommended treatment option. However, new hormonotherapies have emerged that may represent alternative options that can be discussed.
Conclusion
Identification of biomarkers is essential in order to improve the treatment of mCRPC patients and to limit the emergence of resistant clones and reduce. Monitoring the evolution of the disease by carrying out molecular analyses on successive lesions through the natural course of the disease seems to be a promising method in the era of precision cancer medicine. To improve the management of such patients, clinical trials are urgently needed.
Acknowledgements Conflicts of interest
There are no conflicts of interest.
Copyright © 2014 Wolters Kluwer Health, Inc. Unauthorized reproduction of the article is prohibited.
370
Anti-Cancer Drugs 2015, Vol 26 No 3
References Petrylak DP, Tangen CM, Hussain MH, Lara PN Jr, Jones JA, Taplin ME, et al. Docetaxel and estramustine compared with mitoxantrone and prednisone for advanced refractory prostate cancer. N Engl J Med 2004; 351:1513–1520. 2 LiVolsi VA. Prostatic carcinoma presenting as a primary parotid tumor. Oral Surg Oral Med Oral Pathol 1979; 48:447–450. 3 Kucan JO, Frank DH, Robson MC. Tumours metastatic to the parotid gland. Br J Plast Surg 1981; 34:299–301. 4 Gruber B, Moran WJ, Pearle MS, Strauss FF 3rd, Chodak G. Prostate cancer presenting as facial paralysis. Otolaryngol Head Neck Surg 1989; 100:333–338. 5 Moul JW, Paulson DF, Fuller G, Gottfried MR, Floyd WL. Prostate cancer with solitary parotid metastasis correctly diagnosed with immunohistochemical stains. J Urol 1989; 142:1328–1329. 6 Hrebinko R, Taylor SR, Bahnson RR. Carcinoma of prostate metastatic to parotid gland. Urology 1993; 41:272–273. 7 Kirkali Z, Koyuncuoğlu M, Pabuçcuoğlu U, Güneri A, Mungan U. Prostatic carcinoma presenting with painless parotid mass. Urology 1995; 46:406–407. 8 Simpson RH, Skálová A. Metastatic carcinoma of the prostate presenting as parotid tumour. Histopathology 1997; 30:70–74. 9 Pouessel D, Gallet B, Bibeau F, Avancès C, Iborra F, Sénesse P, Culine S. Liver metastases in prostate carcinoma: clinical characteristics and outcome. BJU Int 2007; 99:807–811. 10 Pezaro CJ, Omlin A, Lorente D, Nava Rodrigues D, Ferraldeschi R, Bianchini D, et al. Visceral disease in castration-resistant prostate cancer. Eur Urol 2014; 65:270–273.
11
1
12
13
14
15
16
17
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