Purpose: While multi-parametric magnetic resonance imaging (MRI) shows great promise in assisting with prostate cancer diagnosis and localization, subtle differences in appearance between cancer and normal tissue lead to many false positive and false negative interpretations by radiologists. We sought to automatically detect aggressive cancer (Gleason pattern 4) and indolent cancer (Gleason pattern 3) on a per-pixel basis on MRI to facilitate the targeting of aggressive cancer during biopsy.
Methods: We created the Stanford Prostate Cancer Network (SPCNet), a convolutional neural network model, trained to distinguish between aggressive cancer, indolent cancer, and normal tissue on MRI. Ground truth cancer labels were obtained by registering MRI with whole-mount digital histopathology images from patients who underwent radical prostatectomy. Before registration, these histopathology images were automatically annotated to show Gleason patterns on a per-pixel basis. The model was trained on data from 78 patients who underwent radical prostatectomy and 24 patients without prostate cancer. The model was evaluated on a pixel and lesion level in 322 patients, including six patients with normal MRI and no cancer, 23 patients who underwent radical prostatectomy, and 293 patients who underwent biopsy. Moreover, we assessed the ability of our model to detect clinically significant cancer (lesions with an aggressive component) and compared it to the performance of radiologists.
Results: Our model detected clinically significant lesions with an area under the receiver operator characteristics curve of 0.75 for radical prostatectomy patients and 0.80 for biopsy patients. Moreover, the model detected up to 18% of lesions missed by radiologists, and overall had a sensitivity and specificity that approached that of radiologists in detecting clinically significant cancer.
Conclusions: Our SPCNet model accurately detected aggressive prostate cancer. Its performance approached that of radiologists, and it helped identify lesions otherwise missed by radiologists. Our model has the potential to assist physicians in specifically targeting the aggressive component of prostate cancers during biopsy or focal treatment.
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http://dx.doi.org/10.1002/mp.14855 | DOI Listing |
Cureus
December 2024
Department of Internal Medicine, Division of Hematology and Oncology, University of Texas Southwestern Medical Center, Dallas, USA.
Disseminated intravascular coagulation (DIC) is a hematological disorder characterized by the abnormal activation of the coagulation system, which leads to widespread clotting and subsequent consumption coagulopathy. DIC is often associated with the progression of prostate cancer and can be a life-threatening condition. In this case report, we present a patient with recurrent DIC in the setting of advanced prostate cancer.
View Article and Find Full Text PDFClin Hematol Int
January 2025
Service d'Hématologie Clinique et Thérapie Cellulaire Hôpital Saint-Antoine.
Individuals with chronic lymphocytic leukemia (CLL) or small lymphocytic lymphoma (SLL) have a high risk of developing other malignancies (OMs). The development of OMs may be associated with the advanced age of CLL/SLL patients, presence of a tumor-promoting microenvironment, immune alterations inherent to CLL/SLL, or chemotherapy. Importantly, the occurrence of OMs following frontline fludarabine, cyclophosphamide and rituximab (FCR) treatment is associated with a reduction in the overall survival (OS).
View Article and Find Full Text PDFProstate cancer (PC) progresses from benign epithelium through pre-malignant lesions, localized tumors, metastatic dissemination, and castration-resistant stages, with some cases exhibiting phenotype plasticity under therapeutic pressure. However, high-resolution insights into how cell phenotypes evolve across successive stages of PC remain limited. Here, we present the Prostate Cancer Cell Atlas (PCCAT) by integrating ∼710,000 single cells from 197 human samples covering a spectrum of tumor stages.
View Article and Find Full Text PDFUnlabelled: Inadequate response to androgen deprivation therapy (ADT) frequently arises in prostate cancer, driven by cellular mechanisms that remain poorly understood. Here, we integrated single-cell RNA sequencing, single-cell multiomics, and spatial transcriptomics to define the transcriptional, epigenetic, and spatial basis of cell identity and castration response in the mouse prostate. Leveraging these data along with a meta-analysis of human prostates and prostate cancer, we identified cellular orthologs and key determinants of ADT response and resistance.
View Article and Find Full Text PDFFront Immunol
December 2024
Yi-Huan Genitourinary Cancer Group, The First Affiliated Hospital of Ningbo University, Ningbo, China.
Primary small cell neuroendocrine carcinoma of the prostate is extremely rare, highly aggressive, and has a very poor prognosis, with an overall survival typically not exceeding one year. Standard treatment is generally based on the regimen for small cell lung cancer (SCLC), with guidelines recommending etoposide combined with cisplatin (EP regimen) as the first-line treatment. However, their therapeutic effects are limited.
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