scholarly journals First case of ductal adenocarcinoma of the prostate with MAP3K1 homozygous deletion

2021 ◽  
Author(s):  
Kazunori Shojo ◽  
Takeo Kosaka ◽  
Kohei Nakamura ◽  
Hiroshi Hongo ◽  
Hiroaki Kobayashi ◽  
...  
2020 ◽  
Author(s):  
Kazunori Shojo ◽  
Takeo Kosaka ◽  
Kohei Nakamura ◽  
Hiroshi Hongo ◽  
Shuji Mikami ◽  
...  

Abstract Background: Ductal adenocarcinoma of the prostate is a rare prostate cancer variant and associated with higher stage and greater risk of recurrence and mortality. Optimal systemic therapy for metastatic ductal adenocarcinoma is not known. Many case reports are needed for further understanding of clinical and molecular features about it. Herein we report the first case of a man who was diagnosed with ductal adenocarcinoma of the prostate with mitogen-activated protein kinase 1 (MAP3K1, MEKK1) homozygous deletion.Case Presentation: A 67-year-old man presented with ductal adenocarcinoma of the prostate accompanied by multiple lung metastases and advanced bone metastases. We performed channel transurethral resection of the prostate and confirmed the diagnosis of ductal adenocarcinoma of the prostate. DNA sequencing identified a TP53 somatic point mutation (p.Gly245Ser) as the pathogenic variant. Furthermore, a homozygous deletion was observed in MAP3K1 (MEKK1). The patient received enzalutamide but deceased five months after presenting to our institution.Conclusion: To our knowledge, this is the first report of ductal adenocarcinoma of the prostate with a MAP3K1 homozygous deletion. Accumulation of whole-exome sequencing data is expected to inform future advances in therapy development.


2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Hiroaki Kobayashi ◽  
Takeo Kosaka ◽  
Kohei Nakamura ◽  
Kazunori Shojo ◽  
Hiroshi Hongo ◽  
...  

Abstract Background Ductal adenocarcinoma and neuroendocrine cancer are rare subtypes of prostate cancer with poor prognosis and limited therapeutic options. We present the first case of ductal adenocarcinoma having a neuroendocrine phenotype. Case presentation A 63-year-old man presented with gross hematuria and urinary retention, and his serum prostate-specific antigen level was 4.58 ng/mL. We performed transurethral resection of the prostate, and the diagnosis was ductal adenocarcinoma with a Gleason score of 5 + 4 for acinar adenocarcinoma. Magnetic resonance imaging showed local invasion of left lobe of the prostate and bone metastasis of the left trochanteric section of the femur. Multidisciplinary treatments such as androgen deprivation therapy, chemoradiation therapy, and surgery for metastatic lesions have led to long-term survival. Since next-generation sequencing revealed PTEN and RB1 co-loss and TP53 mutations, we re-evaluated the immunohistochemistry and he was found to be positive for synaptophysin. Conclusions This is the first Japanese case of ductal adenocarcinoma with a neuroendocrine phenotype. Genetic analysis may help not only guide the therapeutic strategies, but also sometimes with the diagnosis.


2014 ◽  
Vol 2014 ◽  
pp. 1-4
Author(s):  
Edgar Linden-Castro ◽  
Marcela Pelayo-Nieto ◽  
Alejandro Alias-Melgar ◽  
Daniel Espinosa-Perezgrovas ◽  
Ivan Ramirez-Galindo ◽  
...  

Ductal adenocarcinoma of the prostate is a rare histological variant that only represents<1% of prostate tumors. This histological variant has several important clinical implications with respect to their evolution, clinical prognosis, and treatment. We report the case of a 64-year-old patient with ductal adenocarcinoma of the prostate, which progresses to castration-resistant prostate cancer, that was treated with abiraterone acetate with good clinical response, to our knowledge, the first case of ductal adenocarcinoma of the prostate in treatment with abiraterone acetate.


2019 ◽  
Vol 9 (2) ◽  
pp. 28
Author(s):  
Rayan El Hassan ◽  
John Corr ◽  
Rajiv Pillai

A 65 year old gentleman was referred with symptoms of haematuria and haematospermia in association with an elevated prostate specific antigen (PSA). He was investigated with a flexible cystoscopy, Ultrasound scan and a computed tomography (CT) of his abdomen and pelvis. These failed to reveal any abnormality. Magnetic resonance imaging (MRI) revealed a Prostate Imaging Reporting and Data System PIRADS 2 lesion in the left peripheral gland and PIRADS 3 lesion on the right side posterolaterally at the level of mid gland of the prostate. He went on to have Transrectal ultrasound biopsies of his prostate (TRUS Bx) that excluded any pathology. On follow up visits his PSA continued to rise and he underwent Template biopsies of the prostate. The histological features had no evidence of any Prostatic intraepithelial carcinoma (PIN) or other malignancies. Flexible cystoscopy was repeated due to his persistent haematospermia. This showed prominent papillary lesions over his verumontanum and prostatic urethra. Biopsies from these areas revealed Ductal Adenocarcinoma of the Prostate (DACP). A subsequent staging MRI revealed unchanged appearance of the PIRADS2 nodule. There was however some low signal extending into the right seminal vesicle which is more pronounced than on the previous scan reported as PIRADS3. Subsequent mapping Template biopsies and Transurethral biopsies revealed a Gleason 4+4 DCAP. A staging CT and bone scan excluded any metastasis. He went on to receive an open radical prostatectomy and pelvic lymph node dissection as a curative treatment for his locally advanced disease.


Gut ◽  
2018 ◽  
Vol 68 (7) ◽  
pp. 1245-1258 ◽  
Author(s):  
Wenjia Wang ◽  
Scott C Friedland ◽  
Bing Guo ◽  
Michael R O’Dell ◽  
William B Alexander ◽  
...  

ObjectiveHere, we evaluate the contribution of AT-rich interaction domain-containing protein 1A (ARID1A), the most frequently mutated member of the SWItch/sucrose non-fermentable (SWI/SNF) complex, in pancreatic homeostasis and pancreatic ductal adenocarcinoma (PDAC) pathogenesis using mouse models.DesignMice with a targeted deletion of Arid1a in the pancreas by itself and in the context of two common genetic alterations in PDAC, Kras and p53, were followed longitudinally. Pancreases were examined and analysed for proliferation, response to injury and tumourigenesis. Cancer cell lines derived from these models were analysed for clonogenic, migratory, invasive and transcriptomic changes.ResultsArid1a deletion in the pancreas results in progressive acinar-to-ductal metaplasia (ADM), loss of acinar mass, diminished acinar regeneration in response to injury and ductal cell expansion. Mutant Kras cooperates with homozygous deletion of Arid1a, leading to intraductal papillary mucinous neoplasm (IPMN). Arid1a loss in the context of mutant Kras and p53 leads to shorter tumour latency, with the resulting tumours being poorly differentiated. Cancer cell lines derived from Arid1a-mutant tumours are more mesenchymal, migratory, invasive and capable of anchorage-independent growth; gene expression analysis showed activation of epithelial-mesenchymal transition (EMT) and stem cell identity pathways that are partially dependent on Arid1a loss for dysregulation.ConclusionsARID1A plays a key role in pancreatic acinar homeostasis and response to injury. Furthermore, ARID1A restrains oncogenic KRAS-driven formation of premalignant proliferative IPMN. Arid1a-deficient PDACs are poorly differentiated and have mesenchymal features conferring migratory/invasive and stem-like properties.


2019 ◽  
Vol 18 (1) ◽  
pp. e471
Author(s):  
K. Chow ◽  
L-M. Wong ◽  
J. Bedo ◽  
A.T. Papenfuss ◽  
J.S. Peters ◽  
...  

2011 ◽  
Vol 42 (4) ◽  
pp. 606-607
Author(s):  
Hemamali Samaratunga ◽  
John Yaxley ◽  
Brett Delahunt

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