Submit manuscript...
Journal of
eISSN: 2373-633X

Cancer Prevention & Current Research

Case Report Volume 7 Issue 6

A case with primary signet ring cell adenocarcinoma of the prostate and review of the literature

De La Pinta C, Martin M

Department of Radiation Oncology, Hospital Ramon Y Cajal, Spain

Correspondence: De La Pinta C, Department of Radiation Oncology, Hospital Ram›n Y Cajal, Spain

Received: March 20, 2017 | Published: April 18, 2017

Citation: Pinta DLC, Martin M. A case with primary signet ring cell adenocarcinoma of the prostate and review of the literature. J Cancer Prev Curr Res. 2017;7(6):180-182. DOI: 10.15406/jcpcr.2017.07.00258

Download PDF

Keywords

carcinoma, hypertension, pancytopenia, physical examination, duodenoscopy, signet ring cell, adenocarcinoma, prostates

Abbreviations

NA, not applicate; H, hormone; R, radiotherapy; RP, radical prostatectomy; CT, chemotherapy

Case report

Primary signet ring cell carcinoma (SRCC) constitutes approximately 3-4% of the stomach cancers; it is very rare variant of prostate carcinoma. It is estimated to occur in 2.5% of cases of prostate adenocarcinoma.1 Prostate SRCC is diagnosed by eliminating of other organs such as colon and stomach, pancreas, breast, thyroid and bladder. Prognosis is worse than the adenocarcinoma. Only 69 cases have been reported in the English literature since 1979.2 We recently diagnosed a case of primary SRCC of the prostate by this we review previous reports. Based on our case, we present the pathologic, clinical and therapeutic aspects of this rare entity.

In July 2016 an 83-year-old male was referred to our institution for evaluation of a serum prostate antigen (PSA) level of 8, 79 ng/ml. The patient had personal history of hypertension and pancytopenia. He had personal or family history of malignancy. Levels of serum prostatic acid phosphatase (PAP) and carcinoembryonic antigen (CEA) were normal. Physical examination, including digital rectal exam, demonstrated invasion of unilateral seminal vesicles. A prostate needle biopsy was carried out. Histologically, biopsy demonstrated an adenocarcinoma with predominantly of the signet ring cell component, Gleason 8 (4+4) in left prostate lobe (65%). Duodenoscopy and colonoscopy were performed for evaluation of the gastrointestinal and no evidence of tumour was found. Overall, this tumour was regarded as primary SRCC of the prostate. Radionuclide bone scan and computed tomography body were negative for metastatic disease. The patient was diagnosed with primary SRCC of the prostate (T3bN0M0).

In multidisciplinary committee we decided androgen blockade. One month later of blockade, his serum PSA level was reduced to 0.1ng/mL. He was alive with no evidence of disease 8 months after blockade. As in common prostatic adenocarcinoma, the tumor retained hormonal dependency, showing a dramatic response to androgen deprivation therapy.

Discussion

The majority of prostatic cancers are acinar adenocarcinomas. Histological variants of prostatic carcinoma have been variably defined. One approach is to consider two groups of variants. The first group comprises histological variants of acinar adenocarcinoma (atrophic, pseudohyperplastic, foamy, colloid, signet ring, oncocytic and lymphoepithelioma-like carcinomas) and the second group non-acinar carcinoma variants (5-10%).3

The term “signet ring cell” is used to describe cells that have their nuclei displaced by an intracytoplasmic vacuole. These cells are more frequently seen focally within otherwise high-grade prostate cancers and should be considered as part of the Gleason scoring.3 But, Guerin and colleagues1 suggested that SRCC should be classified as a variant of high-grade adenocarcinoma rather than a separate histologic classification. The largest series to date has shown poor survival. Clinically, primary SRCC of the prostate presents with the same classic obstructive and irritative symptoms or asymptomatic as other common adenocarcinomas, the diagnosis of primary prostatic SRCC of the prostate is certainly a histologic diagnosis that can be done using needle biopsy, endoscopic resection specimens or radical prostatectomy. To diagnose primary SRCC of the prostate, tumour should contain more than 25% of these cells. In our patient, the gastrointestinal workup showed no evidence of tumour. Therefore, we assumed that the prostate was the primary source of the tumour. Some series show carcinoembryonic antigen (CEA) positive in 20% of the cases (10) whereas PSA and prostate specific acid phosphatase (PSAP) were positive in 87% of the cases4 and positive staining with periodic acid-schiff stain (PAS) was positive in 60%, with alcian blue 60% and with mucicarmin 50%. Clinically, SRCC of the prostate is usually diagnosed in an advanced stage of disease through elevated PSA levels. However, some cases with SRCC have high carcinoembryonic antigen immunoreactivity, while PSA is negative.

We reviewed previous English reports and found 69 reported cases of primary SRCC of the prostate. Table 1 shows the results of special treatment of more important cases. Because of its rarity, no recommended treatment has been established. Conventional therapy for prostate cancer has generally been used, involving variable combinations of hormonal therapy, radiation and surgery. Nevertheless, on the basis of the available cases, the effectiveness of hormonal therapy is unpredictable. To date, no definite explanation for this variability has been given however; Lilleby et al.12 reported a case of SRCC treated with Neoadjuvant hormonal therapy and radiotherapy with a favorable response at 12 months of follow-up. Moreover, Kanematsu and Hiura6 reported a case of primary SRCC with an undetectable PSA level 3 years after a radical prostatectomy and preoperative androgen blockade. Akagashi et al.8 further reported a case of an undetectable PSA level 20 months after treatment with complete androgen blockade. No single treatment modality is ideal for treating SRCC, but we consider that more aggressive multimodal treatment should be considered. Androgen deprivation therapy in Yamamoto study was not effective and therefore that systemic chemotherapy (due to possible gastrointestinal tract origin) and irradiation therapy should be recommended.20,21 In our case, treatment response to androgen blockade was good.

 

Stage

Age

PSA/CEA

treatment

Follow up months

Status

Yoshimura et al.5

T3N0M0

65

+/NA

H+R

100

Alive CR

Kanematsu et al.6

T2N0M0

76

237/-

H+RP

36

Alive

Ishizu K7

E-IV ParaAO lymph  nodes

67

46,2/NA

H

2

Alive CR

Akagashi K8

T4N0M0

72

+/NA

H

20

Alive CR

Fujita9

T2aN0M0

75

9,3/-

H+RP

12

Alive

Uemura M10

Local stage

76

28/NA

RP

13

Alive

Derouiche11

T2

85

9,1/-

H

18

Alive

Lilleby 12

T3bN0M0

70

27/-

H+R

12

Alive

Matsuoka Y13

cT4N1M1c

62

364.7/NA

H

15

Died

Warner et al.14

cT1

58

NA

R

Median 30

24

T4M1

82

NA

H

 

5

T4M1

68

NA

H

 

12

T3M1

65

NA

H

 

24

T3a

66

NA

RP

 

108

cT2a

67

1,9

H+R

 

Alive at 48

T3b

79

5,9

CP

 

4

T3b

50

NA

RP+R

 

Alive at 36

T2b

59

4,8

RP+H

 

Alive at 12

Hashimoto Y15

T3N2M2

61

0,19

CT

16

Died

Bonetti LR16

-

70

+

H+R

11

Died

Kwon17

T2bN0M1b

61

14,7

H Progression at 9m docetaxel

11

Died

Celik et al.18

E-IV Bone metastases

66

6658

H+docetaxel

22

Died

Kim et al.19

T3bN0M0

56

0,64

RP+CT Progression

24

Died

Table 1 Results of special treatment of more important cases
NA, not applicate; H, hormone; R, radiotherapy; RP, radical prostatectomy; CT, chemotherapy

Prostate specific antigen values and treatment modalities were not determinants of survival. Many authors reported the poor prognosis of prostate SRCC, with less treatment response and poor prognosis when compared to the classical type of the prostate adenocarcinoma. It is difficult to define an optimum treatment strategy for SRCC of the prostate from the existing data, early diagnosis and local treatment of the prostate when there is no evidence of metastatic disease might improve prognosis. Fujita et al.9 reported that, in primary SRCC of the prostate, the survival rate is about 55% at 3 years and decreases to 12% at 5 years. The same study revealed that prognosis is only related to the stage of the disease at diagnosis and more of these patients present with stage IV.

Conclusion

We conclude that signet-ring-cell carcinoma of the prostate is a variant of poorly differentiated adenocarcinoma of the prostate (high grade).22 Therefore, some authors have hypothesized that prostatic SRCC is not always an aggressive disease.8 The present case of prostatic SRCC responded well to medical therapy, however, tumors can recur after a long period of time. We recommend early, careful assessment for appropriate diagnosis.

Funding

None.

Acknowledgments

None.

Conflict of interest

The authors declare that there is no conflict of interest.

References

  1. Guerin D, Hasan N, Keen CE. Signet ring cell differentiation in adenocarcinoma of the prostate: a study of five cases. Histopathology. 1993;22(4):367–371.
  2. Uyama T, Moriwaki S. Papillary and mucus–forming adenocarcinomas of prostate. Urology. 1979;13(4): =432–444.
  3. Humphrey PA. Histological variants of prostatic carcinoma and their significance. Histopathology. 2012;60(4):59–74.
  4. Randolph TL, Amin MB, Ro JY, et al. Histologic variants of adenocarcinoma and other carcinomas of prostate: pathologic criteria and clinical significance. Mod Pathol. 1997;10(6):612–629.
  5. Yoshimura K, Fukui I, Ishikawa Y, et al. Locally–confined signet–ring cell carcinoma of the prostate: a case report of a long–term survivor. Int J Urol. 1996;3(5):406–407.
  6. Kanematsu A, Hiura M. Primary signet ring cell adenocarcinoma of the prostate treated by radical prostatectomy after preoperative androgen deprivation. Int J Urol. 1997;4(5):522–523.
  7. Ishizu K, Hirata H, Naito K, et al. Signet ring cell carcinoma of the prostate successfully treated with endocrine therapy: a case report). Hinyokika Kiyo. 2003;49(5):281–283.
  8. Akagashi K, Tanda H, Kato S, et al. Signet–ring cell carcinoma of the prostate effectively treated with maximal androgen blockade. Int J Urol. 2003;10(8):456–458.
  9. Fujita K, Sugao H, Gotoh T, et al. Primary signet ring cell carcinoma of the prostate: report and review of 42 cases. Int J Urol. 2004;11(3):178–881.
  10. Uemura M, Nakagawa M, Kanno N, et al. Signet ring–cell carcinoma of the prostate: a case report. Hinyokika Kiyo. 2004;50(9):645–647.
  11. Derouiche A, Ouni A, Kourda N, et al. A new case of signet ring cell carcinoma of the prostate. Clin Genitourin Cancer. 2007;5(7):455–456.
  12. Lilleby W, Axcrona K, Alfsen CG, et al. Diagnosis and treatment of primary signet–ring cell carcinoma of the prostate. Acta Oncol (Madr). 2007;46(8):1195–1197.
  13. Matsuoka Y, Arai G, Ishimaru H, et al. Primary signet–ring cell carcinoma of the prostate. Can J Urol. 2007;14(6):3764–3766.
  14. Warner JN, Nakamura LY, Pacelli A, et al. Primary Signet Ring Cell Carcinoma of the Prostate. Mayo Clin Proc. 2007;85(12): 1130–1136.
  15. Hashimoto Y, Imanishi K, Okamoto A, et al. An Aggressive Signet Ring Cell Carcinoma of the Prostate in a Japanese Man. Case Rep Oncol. 2011;4(3): 517–520.
  16. Bonetti LR, Lupi M, Stauder E, et al. An unusual case of signet ring cell adenocarcinoma of the prostate. Pathologica. 2011;103(2): 40–42.
  17. Kwon WA, Oh TH, Ahn SH, et al. Primary signet ring cell carcinoma of the prostate. Can Urol Assoc J. 2013;7(11–12):768–771.
  18. Celik O, Budak S, Ekin G, et al. A case with primary signet ring cell adenocarcinoma of the prostate and review of the literature. Arch Ital di Urol e Androl. 2014;86(2):148.
  19. Kim SW, Kim W, Cho YH, et al. Primary signet ring cell carcinoma of the prostate treated by radical cystoprostatectomy and chemoradiotherapy. Can. Urol. Assoc. J. 2016;10(5–6): E204–E206.
  20. Roldán AM, Núñez NF, Grande E, et al. A Primary Signet Ring Cell Carcinoma of the Prostate With Bone Metastasis With Impressive Response to FOLFOX and Cetuximab. Clin Genitourin Cancer. 2012;10(3):199–201.
  21. Yamamoto S, Ito T, Akiyama A, et al. M1 prostate cancer with a serum level of prostate–specific antigen less than 10 ng/mL. Int J Urol. 2001;8(7):374–379.
  22. Ro JY, Naggar EA, Ayala AG, et al. Signet–ring–cell carcinoma of the prostate. Electron–microscopic and immunohistochemical studies of eight cases. Am J Surg Pathol. 1988;129(6):453–460.
Creative Commons Attribution License

©2017 Pinta, et al. This is an open access article distributed under the terms of the, which permits unrestricted use, distribution, and build upon your work non-commercially.