scholarly journals Epitheloid myxofibrosarcoma: a rare aggressive variant of myxofibrosarcoma; a study of 5 cases

2021 ◽  
Vol 79 (S1) ◽  
pp. 5-5
Keyword(s):  
Aggressive Variant

scholarly journals Morphologic, Molecular and Clinical Features of Aggressive Variant Prostate Cancer

Cells ◽  
2020 ◽  
Vol 9 (5) ◽  
pp. 1073 ◽  
Author(s):  
Rodolfo Montironi ◽  
Alessia Cimadamore ◽  
Antonio Lopez-Beltran ◽  
Marina Scarpelli ◽  
Gaetano Aurilio ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Androgen Receptor ◽  
Large Cell Carcinoma ◽  
Large Cell ◽  
Final Diagnosis ◽  
Undifferentiated Carcinoma ◽  
Castration Resistant Prostate Cancer ◽  
Platinum Based Chemotherapy ◽  
Intermediate Part ◽  
Aggressive Variant

The term aggressive variant prostate cancer (AVPCa) refers to androgen receptor (AR)-independent anaplastic forms of prostate cancer (PCa), clinically characterized by a rapidly progressive disease course. This involves hormone refractoriness and metastasis in visceral sites. Morphologically, AVPCa is made up of solid sheets of cells devoid of pleomorphism, with round and enlarged nuclei with prominent nucleoli and slightly basophilic cytoplasm. The cells do not show the typical architectural features of prostatic adenocarcinoma and mimic the undifferentiated carcinoma of other organs and locations. The final diagnosis is based on the immunohistochemical expression of markers usually seen in the prostate, such as prostate-specific membrane antigen (PSMA). A subset of AVPCa can also express neuroendocrine (NE) markers such as chromogranin A, synaptophysin and CD56. This letter subset represents an intermediate part of the spectrum of NE tumors which ranges from small cell to large cell carcinoma. All such tumors can develop following potent androgen receptor pathway inhibition. This means that castration-resistant prostate cancer (CRPCa) transdifferentiates and becomes a treatment-related NE PCa in a clonally divergent manner. The tumors that do not show NE differentiation might harbor somatic and/or germline alterations in the DNA repair pathway. The identification of these subtypes has direct clinical relevance with regard to the potential benefit of platinum-based chemotherapy, poly (ADP-ribose) polymerase inhibitors and likely further therapies.

scholarly journals Impact of DNA damage repair defects and aggressive variant features on response to carboplatin‐based chemotherapy in metastatic castration‐resistant prostate cancer

2020 ◽  
Vol 148 (2) ◽  
pp. 385-395
Author(s):  
Peter H. J. Slootbeek ◽  
Marleen L. Duizer ◽  
Maarten J. Doelen ◽  
Iris S. H. Kloots ◽  
Malou C. P. Kuppen ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Dna Damage ◽  
Dna Damage Repair ◽  
Castration Resistant Prostate Cancer ◽  
Castration Resistant ◽  
Damage Repair ◽  
Aggressive Variant

Efficacy of the PD-L1 inhibitor avelumab in neuroendocrine or aggressive variant prostate cancer: Results from a phase II, single-arm study.

2021 ◽  
Vol 39 (6_suppl) ◽  
pp. 89-89
Author(s):  
Landon Carter Brown ◽  
Susan Halabi ◽  
Michael Sandon Humeniuk ◽  
Yuan Wu ◽  
Taofik Oyekunle ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Liver Metastasis ◽  
Adverse Events ◽  
Phase Ii ◽  
Radiographic Progression ◽  
Progression Free Survival ◽  
High Serum ◽  
Small Cell ◽  
Clinical Criteria ◽  
Aggressive Variant

89 Background: Men with metastatic neuroendocrine/small cell and aggressive variant prostate cancer (NEPC/AVPC) have poor outcomes despite platinum and taxane chemotherapy. These tumors share common features with small cell lung cancer, including higher tumor mutational burden and genomic alterations, and thus may be responsive to immunotherapy. Methods: We conducted a single arm, 2-stage phase II investigator-sponsored trial, (PICK-NEPC, NCT03179410) with the PD-L1 inhibitor avelumab in patients with NEPC/AVPC. NEPC/AVPC was defined either by histologic criteria (neuroendocrine or small cell features) by central pathology review or by aggressive variant clinical criteria (prior progression on abiraterone or enzalutamide with liver metastasis, bulky radiographic progression and low PSA, or high serum LDH). Prior chemotherapy or hormonal therapy was allowed. Avelumab 10 mg/kg IV every 2 weeks was administered until progression or unacceptable toxicity with ongoing ADT. The primary endpoint was overall response rate (ORR) defined by modified PCWG3 and iRECIST criteria. Results: We consented 19 men with AVPC/NEPC, and 15 initiated treatment with avelumab. The median age was 71 (range 51-85), and 27% had neuroendocrine or small cell histology, while 73% met AVPC clinical criteria with adenocarcinoma histology. Men had received a median of two prior systemic therapies (range 1-3) including carboplatin (27%), docetaxel (73%), enzalutamide (67%), and abiraterone (47%). Median PSA was 54 ng/mL (range 0-393) and 73% had liver metastasis. The ORR by iRECIST was 6.7% (95% CI 0-32%) with 1 CR, 0 PRs, 3 (20%) with stable disease, and 11 (73%) with progressive disease. The patient with a CR had NEPC with a CNS metastasis that was found to be MSI-high/TMB-high due to a somatic MSH2 alteration; he finished 12 months of avelumab and maintains a durable CR and undetectable PSA 6 months after completing all therapy including ADT. Median radiographic progression free survival was 1.8 months (95% CI 1.6-2.0 mo) and median time on therapy was 56 days (range 28-356). Median overall survival was 7.4 mo (85% CI 2.8-12.5 mo). Two grade 3 adverse events (abdominal pain due to hepatic disease progression versus immune hepatitis and pericarditis), and one grade 4 (immune hepatitis) adverse event were attributed to avelumab with no grade 5 adverse events. Grade 1 or 2 infusion-related reactions were experienced by 9 (60%). Conclusions: PD-L1 inhibition with avelumab demonstrated limited clinical efficacy in men with metastatic NEPC/AVPC other than in those with MSI-high disease. Further research is needed into mechanisms of immune evasion in NEPC/AVPC to develop novel immunotherapies. Clinical trial information: NCT03179410.

scholarly journals EMT, stemness and tumor plasticity in aggressive variant neuroendocrine prostate cancers

2018 ◽  
Vol 1870 (2) ◽  
pp. 229-238 ◽  
Author(s):  
Rama Soundararajan ◽  
Anurag N. Paranjape ◽  
Sankar Maity ◽  
Ana Aparicio ◽  
Sendurai A. Mani
Keyword(s):  
Tumor Plasticity ◽  
Prostate Cancers ◽  
Aggressive Variant

scholarly journals Clinicopathologic Diagnostic Approach to Aggressive Variant Prostate Cancer

2019 ◽  
Vol 144 (1) ◽  
pp. 18-23 ◽  
Author(s):  
Varsha Manucha ◽  
John Henegan
Keyword(s):  
Prostate Cancer ◽  
English Language ◽  
Treatment Strategies ◽  
Castration Resistant Prostate Cancer ◽  
Ongoing Research ◽  
Castration Resistant ◽  
Current Review ◽  
Pathologic Features ◽  
Neuroendocrine Carcinomas ◽  
Aggressive Variant

Context.— Aggressive variant prostate cancer (AVPCa) develops in a subset of patients with metastatic castration-resistant prostate cancer. The clinical and histologic overlap of AVPCa with other neuroendocrine carcinomas of the prostate has resulted in a lack of consensus on its terminology and treatment. Objective.— To review AVPCa to familiarize pathologists with this entity so they can actively participate in the detection, ongoing research, and evolving management of AVPCa. Data Sources.— The English language literature was reviewed. Conclusions.— The current review summarizes the pathologic features of AVPCa, describes how it has been defined clinically, and discusses how biomarkers may inform treatment strategies in the future.

scholarly journals Aggressive variant of splenic marginal zone lymphoma characterized using a cancer panel test and treated with rituximab-containing chemotherapy

Medicine ◽  
2020 ◽  
Vol 99 (35) ◽  
pp. e21938
Author(s):  
Kazuya Ishiguro ◽  
Yasushi Sasaki ◽  
Yoshitake Takagi ◽  
Takeshi Niinuma ◽  
Hiromu Suzuki ◽  
...  
Keyword(s):  
Marginal Zone ◽  
Marginal Zone Lymphoma ◽  
Splenic Marginal Zone Lymphoma ◽  
Panel Test ◽  
Aggressive Variant ◽  
Cancer Panel
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