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Non-Hodgkin’s lymphoma presenting as macroscopic haematuria and acute urinary retention in pregnancy

We present the case of a 30 year old primigravida in her third trimester with visible haematuria secondary to a genital-tract lymphoma. 

 

Authors: Mark Sayles1, Sarah E Gull2, James DD Allan1

1. Department of Urology
West Suffolk Hospital
Hardwick Lane
Bury St Edmunds
Suffolk
IP33 2QZ
2. Department of Obstetrics and Gynaecology
West Suffolk Hospital
Hardwick Lane
Bury St Edmunds
Suffolk
IP33 2QZ

 
Corresponding Author: Mark Sayles, Department of Urology, West Suffolk Hospital, Hardwick Lane, Bury St Edmunds, Suffolk. E-mail: [email protected]

 

Abbreviations
MRI  Magnetic Resonance Imaging
R-CHOP  Rituximab-(Cyclophosphamide, Doxorubicin, Vincristine, Prednisolone)
PCR  Polymerase Chain Reaction
FISH   Flourescent In-Situ Hybridisation
DLBCL   Diffuse Large B-Cell Lymphoma

 

Introduction
 
Non-Hodgkin’s lymphoma of the female genital tract during pregnancy is rare. We present the case of a 30 year old primigravida in her third trimester with visible haematuria secondary to a genital-tract lymphoma. We describe the management of this unusual occurrence and review the relevant literature.

 

Case Report
 
A 30 year old primigravida presented at 29 weeks gestation with macroscopic haematuria and intermittent acute urinary retention associated with blood clots. She had no significant past medical history, and the early pregnancy had been largely unremarkable. Three months earlier she had been treated with oral antibiotics for a presumed urinary tract infection, having presented to her general practitioner with haematuria. She was taking iron supplements because of anaemia noted at a routine antenatal check (haemoglobin 7g/dL).
Ultrasound examination revealed bilateral hydronephrosis and a complex solid mass on the posterior bladder wall. She underwent pelvic MRI, and urgent flexible cystoscopy, vaginal examination, and biopsy under general anaesthesia. MRI showed a 10cm x 8cm irregular soft-tissue mass involving the anterior vaginal wall and fornix, the proximal urethra, and the posterior bladder wall (Figure 1).

 

Figure 1. T2-weighted magnetic resonance images of the abdomen and pelvis in coronal (A) and sagittal (B) section. Note the large mass invading into the bladder, and the proximity of tumour to the gravid uterus.

 

 

The tumour extended into the bladder, and the bilateral hydronephrosis seen on ultrasound imaging was due to involvement of both distal ureters by tumour.
Cystoscopy and examination revealed a partially fixed mass, between the anterior vaginal wall and the bladder, which was invading the trigone. Biopsies were taken from the mass in the bladder and from the portion in the vaginal wall. These were submitted for detailed immunohistochemical analysis.
On microscopy the pathological specimens showed a diffuse infiltrate of large atypical lymphoid cells. Immunostaining demonstrated expression of CD20, BCL2, CD30 and CD5, with a proportion of cells expressing MUM-1. PCR analysis detected clonal IgH and IgΚ rearrangements, while FISH showed no evidence of IgH, BCL2, BCL6, or MYC translocation but detected gain of extra copies of each of these gene loci. In summary, the immunohistochemical analyses were consistent with a diagnosis of diffuse large B cell lymphoma (DLBCL).
After multidisciplinary discussion, it was decided to commence R-CHOP chemotherapy. The fetus was delivered at 35 weeks gestation by classical Caesarian section, between the first and second cycles of chemotherapy. Both mother and fetus tolerated the first cycle of chemotherapy well, and a 2.6 kg boy was born at 35 weeks gestation as planned. The boy spent one week in a special care baby unit because of prematurity, but required no specific isolation measures. The patient’s tumour responded well to chemotherapy, and she remains under long-term follow up.

 

Discussion
 
Cancer complicates approximately 1:1000 pregnancies [1]. Lymphoma is the fourth most commonly diagnosed malignancy in pregnancy, complicating approximately 1:6000 deliveries [2]. The majority of lymphomas in women of childbearing age are Hodgkin’s disease, with Non-Hodgkin’s lymphoma (NHL) being much rarer in this age group [2, 3]. When NHL does occur in pregnancy, it tends to be of an aggressive subtype such as DLBCL [4]. In general, primary extranodal disease occurs in 20-30% of lymphoma cases, most frequently involving the gastrointestinal tract or skin [5]. Only 0.5% of extranodal lymphomas originate in the female genital tract [6].
DLBCL is associated with an aggressive natural history; median survival in untreated patients is less than one year [7]. Treatment with a combination chemotherapy regime (Cyclophosphamide, Doxorubicin, Vincristine, and Prednisolone; CHOP) has been standard practice for several decades [8]. The addition of rituximab (a chimeric IgG1κ anti-CD20 monoclonal antibody) to this regime (R-CHOP) significantly reduces the risk of relapse and improves overall survival [9, 10].
Because the diagnosis of cancer during pregnancy is a relatively rare event, experience with the use of chemotherapeutic agents and monoclonal antibodies in pregnancy is limited [1, 2, 11]. Almost all chemotherapeutic agents are known to be teratogenic in animals, and to lead to major malformations or fetal death if administered during the first trimester [12, 13]. Exposure during the second and third trimester is not associated with fetal malformations, but increases the risk of fetal and neonatal death, intrauterine growth retardation, preterm delivery and low birth weight [14]. Clearly, the decision to undergo chemotherapy during pregnancy is complex, and has to balance the risks and benefits to both mother and fetus.
Importantly, there are no preclinical reproductive toxicity data available for rituximab. There are only seven previously documented cases of rituximab being used for lymphoma in pregnancy [15-21]. In the majority of these cases rituximab was administered during the second trimester for an aggressive NHL [15-20]. In one case the patient was taking a maintenance dose of rituximab for relapsing follicular lymphoma during which she conceived unintentionally [21]. The rituximab was stopped and the pregnancy continued to term. Of the seven children exposed to rituximab in utero, three were found to have severely decreased CD19+ B cells as neonates. However, none experienced any significant postnatal infection, and in each case the level of B cells returned to normal within three to six months.

 

Conclusion
 
Rare cancers in pregnancy present diagnostic and therapeutic challenges. The successful outcome in this case required a multidisciplinary approach involving obstetrics and gynaecology, urology, and oncology specialist input. This is the eighth documented case of a fetus being exposed to rituximab, without apparent short term clinically significant effects. However, the long term effects of this exposure are unknown.

 

References
[1] Pentheroudakis G, Pavlidis N. Cancer and pregnancy: poena magna, not anymore. Eur J Cancer. 2006 Jan: 42:126-40
[2] Pavlidis NA. Coexistence of pregnancy and malignancy. Oncologist. 2002: 7:279-87
[3] Ward FT, Weiss RB. Lymphoma and pregnancy. Semin Oncol. 1989 Oct: 16:397-409
[4] Lishner M, Zemlickis D, Sutcliffe SB, Koren G. Non-Hodgkin’s lymphoma and pregnancy. Leuk Lymphoma. 1994 Aug: 14:411-3
[5] Krol AD, le Cessie S, Snijder S, Kluin-Nelemans JC, Kluin PM, Noordijk EM. Primary extranodal non-Hodgkin’s lymphoma (NHL): the impact of alternative definitions tested in the Comprehensive Cancer Centre West population-based NHL registry. Ann Oncol. 2003 Jan: 14:131-9
[6] Lagoo AS, Robboy SJ. Lymphoma of the female genital tract: current status. Int J Gynecol Pathol. 2006 Jan: 25:1-21
[7] Fisher RI, Miller TP, O’Connor OA. Diffuse aggressive lymphoma. Hematology Am Soc Hematol Educ Program. 2004:221-36
[8] Flowers CR, Sinha R, Vose JM. Improving outcomes for patients with diffuse large B-cell lymphoma. CA Cancer J Clin. 2010 Nov-Dec: 60:393-408
[9] Coiffier B, Lepage E, Briere J, et al. CHOP chemotherapy plus rituximab compared with CHOP alone in elderly patients with diffuse large-B-cell lymphoma. N Engl J Med. 2002 Jan 24: 346:235-42
[10] Pfreundschuh M, Trumper L, Osterborg A, et al. CHOP-like chemotherapy plus rituximab versus CHOP-like chemotherapy alone in young patients with good-prognosis diffuse large-B-cell lymphoma: a randomised controlled trial by the MabThera International Trial (MInT) Group. Lancet Oncol. 2006 May: 7:379-91
[11] Azim HA, Jr., Azim H, Peccatori FA. Treatment of cancer during pregnancy with monoclonal antibodies: a real challenge. Expert Rev Clin Immunol. 2010 Nov: 6:821-6
[12] Cardonick E, Iacobucci A. Use of chemotherapy during human pregnancy. Lancet Oncol. 2004 May: 5:283-91
[13] Leslie KK, Koil C, Rayburn WF. Chemotherapeutic drugs in pregnancy. Obstet Gynecol Clin North Am. 2005 Dec: 32:627-40
[14] Weisz B, Meirow D, Schiff E, Lishner M. Impact and treatment of cancer during pregnancy. Expert Rev Anticancer Ther. 2004 Oct: 4:889-902
[15] Cordeiro A, Machado AI, Borges A, Alves MJ, Frade MJ. Burkitt’s lymphoma related to Epstein-Barr virus infection during pregnancy. Arch Gynecol Obstet. 2009 Aug: 280:297-300
[16] Rey J, Coso D, Roger V, et al. Rituximab combined with chemotherapy for lymphoma during pregnancy. Leuk Res. 2009 Mar: 33:e8-9
[17] Decker M, Rothermundt C, Hollander G, Tichelli A, Rochlitz C. Rituximab plus CHOP for treatment of diffuse large B-cell lymphoma during second trimester of pregnancy. Lancet Oncol. 2006 Aug: 7:693-4
[18] Magloire LK, Pettker CM, Buhimschi CS, Funai EF. Burkitt’s lymphoma of the ovary in pregnancy. Obstet Gynecol. 2006 Sep: 108:743-5
[19] Friedrichs B, Tiemann M, Salwender H, Verpoort K, Wenger MK, Schmitz N. The effects of rituximab treatment during pregnancy on a neonate. Haematologica. 2006 Oct: 91:1426-7
[20] Herold M, Schnohr S, Bittrich H. Efficacy and safety of a combined rituximab chemotherapy during pregnancy. J Clin Oncol. 2001 Jul 15: 19:3439
[21] Kimby E, Sverrisdottir A, Elinder G. Safety of rituximab therapy during the first trimester of pregnancy: a case history. Eur J Haematol. 2004 Apr: 72:292-5

 

Date added to bjui.org: 15/11/2011 


DOI: 10.1002/BJUIw-2011-061-web

 

Basaloid Carcinoma of the Prostate

To our knowledge, we report the only case of BCP treated with combined chemo-radiotherapy based on a regimen used for anal cancers to complete remission.

Authors: Jeffrey, Tuan1; Corbishley, Cathy2 ; Pandha, Hardev3; Khoo, Vincent4

1. National Cancer Centre Singapore, Radiation Oncology
2. St Georges Hospital, Pathology
3. University of Surrey, Faculty of Health and Medical Sciences
4. Royal Marsden Hospital, Radiotherapy

 
Corresponding Author: Jeffrey Tuan,  National Cancer Centre Singapore, Radiation Oncology.  E-mail: [email protected]

 

Abstract
 
Basaloid carcinomas of the prostate (BCP) are rare. Only a few cases are described in detail. Historically, BCP have been treated surgically. A literature review was undertaken to describe the clinical-pathological features and treatment options used which included radical surgery, radiotherapy and/or a combination of both. To our knowledge, we report the only case of BCP treated with combined chemo-radiotherapy based on a regimen used for anal cancers to complete remission. We propose that combination chemo-radiotherapy is an alternative and/or additional treatment option for BCP.
 

Introduction
Conventional acinar adeno-carcinomas represent the large majority (>90%) of prostate cancers. Variants of conventional prostatic adeno-carcinomas have been described and are important to recognise because the prognosis and treatment may vary substantially. These special variants have a wide histological spectrum and originate from the four types of prostatic epithelium (i.e. secretory epithelium, neuro-endocrine cells, basal cells and transition epithelium). They can occur in a pure form or in association with conventional adeno-carcinomas.
Basal cell carcinoma of the prostate (BCP) is a neoplasm composed of prostatic basal cells. Some tumours resemble its namesake in the skin, comprising large basaloid nests with peripheral palisading and necrosis. Other patterns are similar to florid basal cell hyperplasia or the adenoid basal cell pattern of basal cell hyperplasia (the latter also referred to as adenoid cystic carcinoma). There are only a few publications outlining the diagnosis, treatment, prognosis and outcome for BCP. Traditionally surgery is used but these tumours also respond to concomitant chemo-radiotherapy.
Although most reported BCP are of indolent behaviour (1), there are reports of local recurrence and metastases (2-4). There is a lack of outcome data in BCP reports and their biological behaviour remains uncertain. Due to the limited information on the management and follow-up of BCP, no standard therapeutic approach has been established.
A review of the clinical-pathological features and management options for BCP was undertaken using PubMed, from 1996 to 2009. The keywords used for the search included ‘adenoid cystic’, ‘adenoid cystic-like’, ‘basaloid’ and ‘basal cell carcinoma’ together with ‘treatment’, ‘surgery’, ‘radiotherapy’, ‘radiation’, chemotherapy’ and ‘chemo-radiation’ or ‘chemo-radiotherapy’. Available clinical, histo-pathological, immuno-histochemical, management, outcome and follow-up data were abstracted. The management and follow-up data were reviewed to ascertain the available treatment options for BCP.
Using a BCP case successfully treated with radical chemo-radiotherapy from a regimen used in anal cancers, we propose an alternative management to traditional options of radical surgery and radical radiotherapy. We compared the outcome of our case to that of patients treated with surgery and radiotherapy.

 

Case report
A 78-year-old man presented with lower urinary tract symptoms, nocturia and gross haematuria in November 2002. Examination revealed an enlarged smooth prostate and normal rectum. PSA was 0.8ng/L. An intravenous urogram showed a large prostatic impression into the bladder and significant residual volume post-micturition. Cystoscopy revealed mild trabeculation of the bladder only. Magnetic resonance imaging confirmed numerous cysts within a markedly enlarged prostate (333cc) with atypical T1 and T2 signals. These cysts occupied most of the central gland, compressed the left lateral peripheral zone, extended through the prostatic capsule and invaded the obturator-internus and levator-ani muscles. There was a 2cm lymph node along the left pelvic sidewall. A bone scan was clear of bony metastases.
Histo-pathology revealed BCP with no evidence of conventional prostatic adeno-carcinoma. Malignant sheets of basaloid cells with small islands of keratinising squamous epithelium extensively infiltrated all six biopsy cores. The tumour cells showed mitosis but not necrosis. Immuno-histochemistry focally stained positive for LP34, CAM5.2 and CK 7, but negative for PSA, TTF1, CK20 and chromogranin. There were no histological features of adenoid cystic carcinoma (i.e. cribriform architecture with characteristic basement membrane duplication) and the tumour was morphologically of pure basaloid subtype
 

Figure 1. Extensive infiltration by malignant tumour consisting of sheets of basaloid cells and areas of condensed islands of keratinising squamous epithelium. The tumour cells do not show necrosis but mitoses are seen, and an organoid appearance is noted. 

 

 

This T4N1M0 prostate basaloid carcinoma was discussed in the multidisciplinary meeting. The patient received concurrent chemo-radiotherapy to 65Gy in 35 daily fractions over 7 weeks from December 2002 to February 2003. Chemotherapy comprised of 10 mg/m2 of Mitomycin on Day 1 and 750mg/m2 of 5-Fluro-uracil given as continuous infusion on Day 1 to 4; during the 1st and 5th week of pelvic radiotherapy. He suffered acute urinary retention after his first chemotherapy cycle. This required urinary catheterisation. The urethral catheter was later changed to a supra-pubic catheter. MRI scan done ten months post treatment showed no residual tumour. The patient remained relapse free until 10 June 2005 when he passed away from a ruptured abdominal aneurysm unrelated to his cancer.

 

Discussion
Reports in the literature are confusing, as different investigators have listed BCP under different histological headings. Furthermore there is no consistent management for BCP as the natural history and clinical course can be very variable. The clinical-pathological data available in 61 cases of BCP reported in the literature are shown in Table 1 (2, 5, 6).
The age range of patients with BCP is wide (28–89 years) but BCP is more common in the elderly with a mean and median age of 66 and 68 years respectively. Presenting symptoms are non-specific and may include nocturia, urgency, or acute urinary retention. From Table 1, the main clinical presentation was obstructive urinary symptoms with 42 diagnosed incidentally on trans-urethral resection of prostate (TURP).  On rectal examination, the prostate is usually enlarged and partly indurated. Clinical investigations using serum PSA and preoperative imaging investigations are non-specific; serum PSA can be normal (3) or slightly elevated (2).
BCP is classified in the 2004 World Health Organization (WHO) classification of tumours of the urinary system along with adenoid cystic carcinoma. The WHO classification proposed that malignant basal cell tumours, including adenoid cystic (AC) and basaloid variants, be classified under a single term ‘BCC’. The WHO also issued specific criteria to distinguish benign from malignant basal cell proliferations. Malignant features include an infiltrative pattern, extra-prostatic extension, peri-neural invasion, necrosis and stromal desmoplasia. The primary diagnostic criterion is an infiltrative pattern of desmoplastic stroma. Most of the cases in Table 1 showed a predominantly adenoid cystic pattern, some of mixed pattern and only 6 showed an exclusive basaloid pattern.
Grossly, BCP are white and fleshy, sometimes with micro-cysts, unlike acinar carcinoma, which is usually yellow. These tumours usually show ill-defined, infiltrative edges and involve the transition and peripheral zones. Microscopically, BCP has a broad morphologic spectrum and can be similar to BCC of the skin. The prostate is infiltrated by irregular solid clumps, or trabeculae and larger cellular masses of basaloid cells. The cells have uniform small, round or oval nuclei with scant cytoplasm (7, 8). While there is peripheral pallisading, cribriforming is absent or minimal (7-9).  Occasional glandular, trabecular, and solid areas can be found. The nuclei have basal cell features with angulated nuclear contours, and may be hyper-chromatic or micro-vacuolated. In some cases, sebaceous and squamous differentiation can be seen. Extensive perineural invasion and extra-prostatic extension have been described. Mitoses are absent or only sparsely present. The stroma may show a desmoplastic or myxoid alteration (2).
The pattern of BCP cannot be classified under the Gleason scheme and is not known to correlate with outcome. Therefore Gleason grading is not recommended. According to general consensus, the specific markers for BCP are high molecular weight Keratin and Cytokeratin 14. Usually staining for PSA is negative (10). Other investigators have reported the use of Ki-67 index and Bcl-2 protein for diagnosis of malignancy.
The main differential diagnoses of BCP are benign basal cell hyperplasia and acinar adeno-carcinoma (with a cribriform pattern) [27]. Clinically, the only differentiating factor from conventional adeno-carcinoma is that the PSA is usually normal or only slightly elevated. Although basal cell hyperplasia may have an infiltrating pattern with cellular atypia making diagnosis difficult, this subtype does not extend out of the prostate or into adjacent organs. Other differential diagnoses include metastatic carcinomas and transitional cell carcinoma (TCC). TCC may exhibit a solid growth pattern with peripheral palisading and central necrosis.
Although most reported BCP are of indolent behaviour (1), there are reports of local recurrence and metastases (2-4). Of interest is that metastases often involve liver, lung, and bowel but not bone, as is commonly observed in prostate adeno-carcinoma (2). In one series where outcome is reported, metastasis was documented in 4 of 15 patients (2), following treatment with surgical resection only. From Table 1, local recurrence occurred in 8/62 patients. Metastases developed in 10/62 patients. Median follow-up was 1 year (range 0-19 years) and 27/62 (43.5%) had >1 year follow-up.  Following treatment, there was no evidence of disease recurrence in 38/62 (61.3%). Radiotherapy or chemotherapy may be helpful, but published results are inconsistent (3, 9) (see Table 1).
The diagnosis of BCP requires histo-pathological confirmation. Elevated expression of bcl-2 and high Ki-67 index may aid diagnosis of basal cell proliferative lesions. Furthermore, histo-pathology cannot reliably predict the clinical course.
Due to the presumed indolent nature of BCP and the older age at presentation, most men did not receive definitive therapy beyond the initial diagnostic TURP. Although the biological behaviour is not fully understood, it is now clear that a small subset of BCP have the potential to invade and reoccur locally as well as metastasise. There was local-regional nodal involvement in our patient. We opted for aggressive combined chemo-radiation despite his age. He tolerated treatment well and remained disease-free until death from an unrelated cause 25 months later. Usually surgery is used when disease is confined to the prostate, but where disease extends beyond the prostate, radiotherapy can be considered. With more extensive disease and regional nodal involvement, chemo-radiation is reasonable. To our knowledge, this is the only case of BCP treated with combined chemo-radiotherapy, and treated successfully to complete remission.
Our literature review indicates that BCP is a rare tumour with clinical-pathological features distinct from classical prostate adeno-carcinoma. Whilst surgery has been mainly used, our case showed that combination chemo-radiotherapy is an alternative and/or additional treatment option for BCP.

 

Table 1. Clinico- pathologic Correlation of Morphology with Reported Outcome

 

 
No. Age Predominant Pattern Specimen Necrosis RP findings Treatment Prognosis FU years
1 69 AC-P, Basaloid TUR No NED 3
2 66 AC-P TUR No RT NED 1
3 60 AC-P TUR No Unknown No FU
4 76 AC-P TUR NA NED <1
5(3) 60 AC-P/Basaloid TUR No RP NED 6
6(3) 68 AC-P TUR No RT NED <1
7 NA Basaloid NBx NA Unknown No FU
8(9) 38 AC-P NBx No RP, RT Unknown No FU
9(2) 28 Basaloid TUR No RT, Chemo NED 2
10(6) 44 AC-P NBx No RP, RT LR 7
11 43 AC-P/Basaloid NBx NA RP, RT Unknown No FU
12(7) 65 Basaloid Nbx RP Lung, bone mets 1
13(1) 69 AC-P TUR NED 2
14(1) 49 AC-P NBx Extenteration Lung, para-vertebral mets. DOD 3
15(1) NA AC-P TUR Liver mets No FU
16(1) 81 Basaloid NBx RP Lung corpus cavernosum mets No FU
17(1) 68 AC-P TUR Alive with tumour 6
18(1) 43 AC-P. squamous TUR RP NED 5
19(1) 46 AC-P NBx Extenteration Liver colon, DOD 2
20(1) 70 AC-P NBx Alive with tumour 2
21(1) 83 AC-P TUR RT NED 2
22(1) 53 AC-P TUR NED 1
23(1) 60 Basaloid, squamous TUR Unknown No FU
24(1) 77 AC-P TUR NED <1
25(1) 87 Basaloid, squamous TUR NED <1
26(1) 82 Basaloid, squamous TUR NED <1
27(1) 55 AC-P NBx RP, RT Alive with tumour 11
28(1) 74 Basaloid TUR Unknown No FU
29(1) 63 Basaloid TUR RP NED 5
30(1) 64 AC-P NBx RP NED 2
31(1) 81 Basaloid TUR NED <1
32(4) 63 Big solid nests TUR Yes RT and Chemo Penile mets, LR 1
33(4) 51 Big solid nests NBx + TUR Yes RT Bone, liver, lung mets 1
34(4) 86 Big solid nests TUR Yes Lung, LR 2
35(4) 69 Big solid nests RP Yes EPE; MAR+ RP, RT and Chemo Lung and liver, LR <1
36(4) 56 Big solid nests TUR + RP Yes EPE; SV+ RP NED 1
37(4) 53 Big solid nests TUR + RP No EPE; MAR+ RP NED 1
38(4) 83 Big solid nests TUR No NA No FU
39(4) 73 Big solid nests NBx No NED 9
40(4) 87 Small solid nests TUR No NED 10
41(4) 65 Small solid nests NBx No NED 9
42(4) 66 Small solid nests TUR No NED 6
43(4) 51 Small solid nests TUR No NED <1
44(4) 77 Small solid nests TUR No Unknown No FU
45(4) 62 Small solid nests TUR No NED 1
46(4) 76 Small solid nests TUR No NED 1
47(4) 65 Small solid nests NBx No NED <1
48(4) 89 Small solid nests TUR No Unknown No FU
49(4) 82 Small solid nests NBx No NED 2
50(4) 73 Small solid nests TUR No NED <1
51(4) 66 AC-P TUR + RP No No Tumour Pre-RP RT + RP NED 19
52(4) 74 AC-P TUR No NED 6
53(4) 76 AC-P TUR No NED 1
54(4) 70 AC-P Nbx No OC RP NED 5
55(4) 66 AC-P TUR No EPE RP NED 4
56(4) 78 BCH TUR No Unknown No FU
57(4) 76 BCH TUR No NED <1
58(4) 69 BCH TUR No Unknown No FU
59(4) 42 BCH TUR No EPE RP NED 8
60(4) 71 BCH with nodules Enuc + TURs No NED 11
61(5) 68 Big solid nests RP Yes EPE RP and Chemo Lung, liver mets. LR, DOD <1
62 78 Small solid nests NBx No RT and Chemo NED 3
 
Note: AC-P indicates adenoid-cystic pattern; BCH, basal cell hyperplasia pattern; Chemo, chemotherapy; Enuc, enucleation; FU, follow-up; Loc, local recurrence; EPE, extra-prostatic extension; LR, local recurrence; MAR, margins; Mets, metastases; NA, not assessable; Nbx, needle biopsy; NED, no evidence of disease; OC, organ confined; RP, radical prostatectomy; RT, radiation; squamous, squamous metaplasia; SV, seminal vesicles; TUR, trans-urethal resection; DOD, died of disease.
 

 

References
1. Randolph TL, Amin MB, Ro JY, Ayala AG. Histologic variants of adenocarcinoma and other carcinomas of prostate: pathologic criteria and clinical significance. Mod Pathol. 1997;10(6):612-29.
2. Iczkowski KA, Ferguson KL, Grier DD, Hossain D, Banerjee SS, McNeal JE et al. Adenoid cystic/basal cell carcinoma of the prostate: clinicopathologic findings in 19 cases. Am J Surg Pathol. 2003;27(12):1523-9.
3. Schmid HP, Semjonow A, Eltze E, Wortler K, Hertle L. Late recurrence of adenoid cystic carcinoma of the prostate. Scand J Urol Nephrol. 2002;36(2):158-9.
4. Young RH, Frierson HF, Jr., Mills SE, Kaiser JS, Talbot WH, Bhan AK. Adenoid cystic-like tumor of the prostate gland. A report of two cases and review of the literature on “adenoid cystic carcinoma” of the prostate. Am J Clin Pathol. 1988;89(1):49-56.
5. Ali TZ, Epstein JI. Basal cell carcinoma of the prostate: a clinicopathologic study of 29 cases. Am J Surg Pathol. 2007;31(5):697-705.
6. Hudson E, Rashid M, Carter AC, Lester JF. Basaloid carcinoma of the prostate: a case report and review of the literature. Eur J Cancer Care (Engl). 2008;17(5):509-11.
7. Denholm SW, Webb JN, Howard GC, Chisholm GD. Basaloid carcinoma of the prostate gland: histogenesis and review of the literature. Histopathology. 1992;20(2):151-5.
8. Mastropasqua MG, Pruneri G, Renne G, De Cobelli O, Viale G. Basaloid cell carcinoma of the prostate. Virchows Arch. 2003;443(6):787-91.
9. McKenney JK, Amin MB, Srigley JR, Jimenez RE, Ro JY, Grignon DJ et al. Basal cell proliferations of the prostate other than usual basal cell hyperplasia: a clinicopathologic study of 23 cases, including four carcinomas, with a proposed classification. Am J Surg Pathol. 2004;28(10):1289-98.
10. Ahn SK, Kim K, Choi IJ, Lee JM. Adenoid cystic carcinoma of the prostate gland–pathological review with a case report. Yonsei Med J. 1991;32(1):74-8.

 
Date added to bjui.org: 02/08/2011 


DOI: 10.1002/BJUIw-2011-025-web

 

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