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Julka et al. J Transl Genet Genom 2020;4:455-63 I http://dx.doi.org/10.20517/jtgg.2020.46 Page 457
tumors. The age at presentation has been reported between 28-78 years (mean age of 50 years) with either
a normal or slightly elevated serum PSA level [13-16] . Due to the slow growing tendency of the ACC of the
prostate, the management of patients with advanced and metastatic disease consists primarily of surgical
resection followed by periodic long-term follow-up. Use of radiotherapy, chemotherapy and targeted
therapies has been reported with inconsistent and varying success [10,15,17,18] . Here, we report a case of ACC of
the prostate with liver metastasis presented with the dilemma of being a urinary bladder cancer.
CASE REPORT
A 79-year-old male patient presented with complaints of three episodes of hematuria over a period of
20 days along with generalized weakness without any significant loss of weight or appetite. The patient
had a past history of coronary artery disease, type 2 diabetes mellitus, hypertension and chronic kidney
disease. The patient had also undergone percutaneous coronary intervention and coronary artery bypass
graft in the past. The general condition of the patient was good with an Eastern Cooperative Oncology
Group performance status of 1. The clinical work-up included PSA and magnetic resonance (MR)
urography. MR urography was suggestive of mass lesion involving the base of the bladder and prostate.
The patient underwent post-transurethral resection of the bladder tumor and prostate. The post-procedure
histopathological report showed morphological features of poorly differentiated adenocarcinoma.
Metastatic work-up was performed (January 2018) using positron emission tomography-computed
tomography (PET-CT) for determination of prostate-specific membrane antigen (PSMA), which showed
slightly increased PSMA uptake in the base of urinary bladder and the adjacent prostate along with a large
PSMA avid (suv max 8.0) hypodense liver lesion in segment VIII, measuring 8.4 cm × 6.2 cm [Figure 1].
Post-transurethral resection of the prostate changes were observed with dila ACC of prostate tion of urethra
and air pocket along the anterior wall of the urinary bladder. Liver biopsy showed the morphological and
IHC features consistent with polymorphic adenoid-basal carcinoma. To understand the histology further,
IHC and biochemical evaluation was conducted for multiple markers. CK7 (keratin 7), CD117 (proto-
oncogene c-Kit) and CKHMW (high-molecular-weight cytokeratin) were found to be positive, but PSA,
CK20 (keratin 20), NK3 Homeobox 1 (NKX3.1), synaptophysin, chromogranin, and alpha-methylacyl-CoA
racemase were negative. Ki-67 proliferation index was 25%-30%. In view of CD 117 positivity, the diagnosis
of ACC was made; however, the origin of prostate or bladder was still not well defined due to negative PSA.
Since, PSA was absent and since the primary bulk of tumor was in the bladder, the possibility of bladder
ACC could not be ruled out, albeit a rare entity and never before reported in the literature. There is one
report of asynchronous ACC of the prostate and transitional cell carcinoma of the urinary bladder in the
[19]
literature; therefore, we kept it as a differential diagnosis .
PSMA avidity can also be present in poorly differentiated carcinomas irrespective of PSA expression
on tumor cells. In view of metastatic disease, we decided to offer chemotherapy to the patient; however,
deciding which chemotherapy to offer was still a matter of debate. Based on the clinical differentials,
the patient could have been offered either the bladder-based chemotherapy on lines of bladder cancer
(gemcitabine + platinum) or docetaxel for prostate origin.
Considering age and co-morbidities, there was only one chance to initiate the appropriate chemotherapy
for the patient. In view of the diagnostic dilemma and rare nature of the disease, we decided to perform
the CANscript test for the patient. CANscript is a novel phenotypic multi-dimensional assay that tests a
patient’s tumor tissue against different drug combinations in an ex vivo implant setting to help a physician
select the most appropriate treatment protocol. CANscript can predict the response to either single-
agent cancer therapeutics or combination therapeutic regimens for the patient under evaluation. This is
accomplished by using fresh tumor tissue from the patient in plates coated with a specific set of tumor
matrix proteins. Further, patient derived autologous ligands are added to the explant platform along with
angiogenic factors and autologous immune cells to maintain the tumor vasculature. In essence, CANscript