tbuckley/cabot-search huggingface dataset:
Updated nomenclature of delirium and acute encephalopathy: statement of ten Societies
Authors: Arjen J. C. Slooter, Wim M. Otte, John W. Devlin, Rakesh C. Arora, Thomas P. Bleck, Jan Claassen, Matthew S. Duprey, E. Wesley Ely, Peter W. Kaplan, Nicola Latronico, Alessandro Morandi, Karin J. Neufeld, Tarek Sharshar, Alasdair M. J. MacLullich, Robert D. Stevens
Journal: Intensive Care Medicine (2020)

Segregation of
Association Between the Use of Antidepressants and the Risk of Type 2 Diabetes: A Large, Population-Based Cohort Study in Japan
Authors: Hiroyuki Miidera, Minori Enomoto, Shingo Kitamura, Hisateru Tachimori, Kazuo Mishima
Journal: Diabetes Care (2020)

This study aimed to reveal the associations between the risk of new-onset type 2 diabetes and the duration of antidepressant use and the antidepressant dose, and between antidepressant use after diabetes onset and clinical outcomes.In this large-scale retrospective cohort study in Japan, new users of antidepressants (exposure group) and nonusers (nonexposure group), aged 20-79 years, were included between 1 April 2006 and 31 May 2015. Patients with a history of diabetes or receipt of antidiabetes treatment were excluded. Covariates were adjusted by using propensity score matching; the associations were analyzed between risk of new-onset type 2 diabetes and the duration of antidepressant use/dose of antidepressant in the exposure and nonexposure groups by using Cox proportional hazards models. Changes in glycated hemoglobin (HbA1c) level were examined in groups with continuous use, discontinuation, or a reduction in the dose of antidepressants.Of 90,530 subjects, 45,265 were in both the exposure and the nonexposure group after propensity score matching; 5,225 patients (5.8%) developed diabetes. Antidepressant use was associated with the risk of diabetes onset in a time- and dose-dependent manner. The adjusted hazard ratio was 1.27 (95% CI 1.16-1.39) for short-term low-dose and 3.95 (95% CI 3.31-4.72) for long-term high-dose antidepressant use. HbA1c levels were lower in patients who discontinued or reduced the dose of antidepressants (F[2,49] = 8.17; P < 0.001).Long-term antidepressant use increased the risk of type 2 diabetes onset in a time- and dose-dependent manner. Glucose tolerance improved when antidepressants were discontinued or the dose was reduced after diabetes onset.
A Locally Transmitted Case of SARS-CoV-2 Infection in Taiwan
Authors: Ying-Chu Liu, Ching-Hui Liao, Chin-Fu Chang, Chu-Chung Chou, Yan-Ren Lin
Journal: New England Journal of Medicine (2020)

A Case of Locally Transmitted SARS-CoV-2 in Taiwan The authors describe transmission of the novel coronavirus from a woman who had been living for several months in Wuhan, China, to her husband, af...
A clinical predictive model of candidaemia by Candida auris in previously colonized critically ill patients
Authors: V. Garcia-Bustos, M. Salavert, A.C. Ruiz-Gaitán, M.D. Cabañero-Navalon, I.A. Sigona-Giangreco, J. Pemán
Journal: Clinical Microbiology and Infection (2020)
化膿性関節炎,壊疽性膿皮症,座瘡および化膿性汗腺炎(PAPASH): PSTPIP1遺伝子の新規変異に関連する新たな自己炎症性症候群
Authors: V Marzano Angelo, Trevisan Valentina, Gattorno Marco, Ceccherini Isabella, DE Simone Clara, Crosti Carlo
Journal: JAMA Dermatology (2013)
Systemic effects of surgery: Quantitative analysis of circulating basic fibroblast growth factor (bFGF), vascular endothelial growth factor (VEGF) and transforming growth factor beta (TGF-β) in patients with breast cancer who underwent limited or extended surgery
Authors: J. Y. Petit, G. Curigliano, F. Bertolini, G. Peruzzotti, S. Gandini, S. Zurrida, S. Martella, R. Ghisini, F. De Braud, A. Goldhirsch
Journal: Journal of Clinical Oncology (2004)

672 Background: Tumor growth is angiogenesis dependent. Perioperative increases of proangiogenic factors may have a cell mitogen effect on residual cancer cell. Methods: We collected peripheral vein blood samples from 84 consecutive breast cancer patients who underwent various types of surgery, classified according to the magnitude of tissue injury: minimal (quadrantectomy), moderate (mastectomy without reconstruction), and heavy [mastectomy followed by reconstruction with TRAM]. Samples were collected one day before surgical resection (D-1), at the end of surgery (D 0), and on 1st (D+1), 2nd (D+2) and 5th (D+5) day after surgery. VEGF, bFGF and TGFβ levels were measured in serum samples. Results: On average, a continuous decrease was observed for all growth factors from the day before operation to the 5th day after operation. The changes from the operation were found statistically significant for TGF-β for all time points. The reduction from operation was found significant also for VEGF at 24–48 hours after. A different trend for type of operation was observed at five days for all growth factors: an increase was observed for patients who underwent extended respect to moderate surgery. These differences were found statistically significant for bFGF and VEGF (p=0.05 and p=0.025 respectively). A statistically different trend for type of surgery was observed also for TGF-β at 24–48 hours: a minor reduction, compared to time of operation, was observed for minimal surgery, an intermediate reduction for moderate surgery and a higher decrease for extended surgery. Conclusions: "Trapping" of angiogenic cytokines in the surgical wound milieu should be considered for a risk of perioperative stimulation of residual cancer cells. A better understanding of the time interval during which the sequelae of events in wound healing occur in relation to prognosis may be the basis for defining new therapeutic strategies that can interfere with tumor outgrowth potentially related to wound healing processes. No significant financial relationships to disclose.
GLP-1 receptor agonists synergize with DYRK1A inhibitors to potentiate functional human β cell regeneration
Authors: Courtney Ackeifi, Peng Wang, Esra Karakose, Jocelyn E. Manning Fox, Bryan J. González, Hongtao Liu, Jessica Wilson, Ethan Swartz, Cecilia Berrouet, Yansui Li, Kunal Kumar, Patrick E. MacDonald, Roberto Sanchez, Bernard Thorens, Robert DeVita, Dirk Homann, Dieter Egli, Donald K. Scott, Adolfo Garcia-Ocaña, Andrew F. Stewart
Journal: Science Translational Medicine (2020)

Glucagon-like peptide-1 receptor (GLP1R) agonists and dipeptidyl peptidase 4 inhibitors are widely prescribed diabetes drugs due to their ability to stimulate insulin secretion from remaining β cells and to reduce caloric intake. Unfortunately, they fail to increase human β cell proliferation. Small-molecule inhibitors of dual-specificity tyrosine-regulated kinase 1A (DYRK1A) are able to induce adult human β cell proliferation, but rates are modest (~2%), and their specificity to β cells is limited. Here, we provide evidence that combining any member of the GLP1R agonist class with any member of the DYRK1A inhibitor class induces a synergistic increase in human β cell replication (5 to 6%) accompanied by an actual increase in numbers of human β cells. GLP1R agonist-DYRK1A inhibitor synergy required combined inhibition of DYRK1A and an increase in cAMP and did not lead to β cell dedifferentiation. These beneficial effects on proliferation were seen in both normal human β cells and β cells derived from individuals with type 2 diabetes. The ability of the GLP1R agonist-DYRK1A inhibitor combination to enhance human β cell proliferation, human insulin secretion, and blood glucose control extended in vivo to studies of human islets transplanted into euglycemic and streptozotocin-diabetic immunodeficient mice. No adverse events were observed in the mouse studies during a 1-week period. Because of the relative β cell specificity of GLP1R agonists, the combination provides an improved, although not complete, degree of human β cell specificity.
Imaging mass cytometry and multiplatform genomics define the phenogenomic landscape of breast cancer
Authors: H. Raza Ali, Hartland W. Jackson, Vito R. T. Zanotelli, Esther Danenberg, Jana R. Fischer, Helen Bardwell, Elena Provenzano, H. Raza Ali, M. Al Sa’d, S. Alon, Samuel Aparicio, G. Battistoni, S. Balasubramanian, R. Becker, Bernd Bodenmiller, E. S. Boyden, D. Bressan, A. Bruna, B. Marcel, Carlos Caldas, M. Callari, I. G. Cannell, H. Casbolt, N. Chornay, Y. Cui, A. Dariush, K. Dinh, A. Emenari, Y. Eyal-Lubling, J. Fan, E. Fisher, E. A. González-Solares, C. González-Fernández, D. Goodwin, W. Greenwood, F. Grimaldi, G. J. Hannon, O. Harris, S. Harris, C. Jauset, J. A. Joyce, E. D. Karagiannis, T. Kovačević, L. Kuett, R. Kunes, A. Küpcü Yoldaş, D. Lai, E. Laks, H. Lee, M. Lee, G. Lerda, Y. Li, A. McPherson, N. Millar, C. M. Mulvey, F. Nugent, C. H. O’Flanagan, M. Paez-Ribes, I. Pearsall, F. Qosaj, A. J. Roth, Oscar M. Rueda, T. Ruiz, K. Sawicka, L. A. Sepúlveda, S. P. Shah, A. Shea, A. Sinha, A. Smith, S. Tavaré, S. Tietscher, I. Vázquez-García, S. L. Vogl, N. A. Walton, A. T. Wassie, S. S. Watson, S. A. Wild, E. Williams, J. Windhager, C. Xia, P. Zheng, X. Zhuang, Oscar M. Rueda, Suet-Feung Chin, Samuel Aparicio, Carlos Caldas, Bernd Bodenmiller
Journal: Nature Cancer (2020)
Long-Term Exposure to Fine Particulate Matter and Cardiovascular Disease in China
Authors: Fengchao Liang, Fangchao Liu, Keyong Huang, Xueli Yang, Jianxin Li, Qingyang Xiao, Jichun Chen, Xiaoqing Liu, Jie Cao, Chong Shen, Ling Yu, Fanghong Lu, Xianping Wu, Xigui Wu, Ying Li, Dongsheng Hu, Jianfeng Huang, Yang Liu, Xiangfeng Lu, Dongfeng Gu
Journal: Journal of the American College of Cardiology (2020)
Auger radiopharmaceutical therapy targeting prostate-specific membrane antigen in a micrometastatic model of prostate cancer
Authors: Colette J. Shen, Il Minn, Robert F. Hobbs, Ying Chen, Anders Josefsson, Mary Brummet, Sangeeta R. Banerjee, Cory F. Brayton, Ronnie C. Mease, Martin G. Pomper, Ana P. Kiess
Journal: Theranostics (2020)

Auger radiopharmaceutical therapy is a promising strategy for micrometastatic disease given high linear energy transfer and short range in tissues, potentially limiting normal tissue toxicities. We previously demonstrated anti-tumor efficacy of a small-molecule Auger electron emitter targeting the prostate-specific membrane antigen (PSMA), 2-[3-[1-carboxy-5-(4-[125I]iodo-benzoylamino)-pentyl]-ureido]-pentanedioic acid), or 125I-DCIBzL, in a mouse xenograft model. Here, we investigated the therapeutic efficacy, long-term toxicity, and biodistribution of 125I-DCIBzL in a micrometastatic model of prostate cancer (PC). Methods: To test the therapeutic efficacy of 125I-DCIBzL in micrometastatic PC, we used a murine model of human metastatic PC in which PSMA+ PC3-ML cells expressing firefly luciferase were injected intravenously in NSG mice to form micrometastatic deposits. One week later, 0, 0.37, 1.85, 3.7, 18.5, 37, or 111 MBq of 125I-DCIBzL was administered (intravenously). Metastatic tumor burden was assessed using bioluminescence imaging (BLI). Long-term toxicity was evaluated via serial weights and urinalysis of non-tumor-bearing mice over a 12-month period, as well as final necropsy. Results: In the micrometastatic PC model, activities of 18.5 MBq 125I-DCIBzL and above significantly delayed development of detectable metastatic disease by BLI and prolonged survival in mice. Gross metastases were detectable in control mice and those treated with 0.37-3.7 MBq 125I-DCIBzL at a median of 2 weeks post-treatment, versus 4 weeks for those treated with 18.5-111 MBq 125I-DCIBzL (P<0.0001 by log-rank test). Similarly, treatment with ≥18.5 MBq 125I-DCIBzL yielded a median survival of 11 weeks, compared with 6 weeks for control mice (P<0.0001). At 12 months, there was no appreciable toxicity via weight, urinalysis, or necropsy evaluation in mice treated with any activity of 125I-DCIBzL, which represents markedly less toxicity than the analogous PSMA-targeted α-particle emitter. Macro-to-microscale dosimetry modeling demonstrated lower absorbed dose in renal cell nuclei versus tumor cell nuclei due to lower levels of drug uptake and cellular internalization in combination with the short range of Auger emissions. Conclusion: PSMA-targeted radiopharmaceutical therapy with the Auger emitter 125I-DCIBzL significantly delayed development of detectable metastatic disease and improved survival in a micrometastatic model of PC, with no long-term toxicities noted at 12 months, suggesting a favorable therapeutic ratio for treatment of micrometastatic PC.
Solitary Lip Extranodal Natural Killer/T-Cell Lymphoma on FDG PET/CT
Authors: Jianhua Zhang, Shusheng Li, Yan Fan, Qian Li, Lin Nong
Journal: Clinical Nuclear Medicine (2020)

Abstract A 54-year-old man presented with a history of upper lip pain for 4 weeks. Biopsy of the lip lesion revealed extranodal natural killer/T-cell lymphoma. 18 F-FDG PET/CT scan showed the solely high uptake in the right upper lip without any other nodal or extranodal involvements.
Abstract P4-14-06: Express model of hereditary multigene mutation analysis in breast cancer patients
Authors: Albert Grinshpun, Einat Carmon, Luna Kaduri, Aviad Zick, Shiri Shkedi, Edna Shalom, Avital Granit, Liza Monas, Tamar Shaldovsky, Tamar Hamburger, Vardiella Meiner, Tamar Peretz
Journal: Cancer Research (2020)

Abstract Introduction Traditionally, women with family history of breast and ovarian cancer, or young age at presentation, are referred to BRCA1\2 mutation testing. The growing information regarding other genes involved in predisposition to breast cancer (regardless of specific family history) and the potential impact of germline alterations on surgical and oncologic management led us to establish a model to perform a quick multigene mutation evaluation among breast cancer patients at our cancer institute. Methods All breast cancer patients that required genetic counselling (according to treating oncologist/surgeon’s judgement) were referred, after thorough explanation and signing informed-consent forms, to a 'genetic coordinator' and 'genetic nurse'. They provided each patient with a second pre-test explanation and ordered wide hereditary cancer gene panel (83-genes, Invitae). Results were given within 2-4 weeks. All patients\results were registered centrally at our center and discussed at routine Onco-genetic Multidisciplinary Board (OMB). A referral for formal genetic counselling is offered to all patients, and rapid track is arranged for patients with positive results. Results During a 12-months pilot period, 130 breast cancer patients were examined via the model, and 109 results were received; 44 patients (41%) had no abnormal findings, 50 patients (45%) had variants of uncertain clinical significance, and 15 patients (14%) were found carriers of pathogenic variants (ATM n=2, BRCA1 n=1, BRCA2 n=2, CHEK2 n=3, MUTYH n=1, PALB2 n=2, RAD50 n=1, RECQL4 n=1, TP53 n=2). Among this group, 3 patients (20%) had immediate panel-driven treatment decisions: Mastectomy to avoid radiotherapy (RAD50 carrier), oophorectomy during lumpectomy (BRCA2 carrier), and bilateral risk-reducing mastectomy instead of lumpectomy (TP53 carrier). Conclusions The creation of an Express-model for broad germline analysis allows to obtain rapid and meaningful results with impact on treatment. We believe that the Express-model should be considered as an integral tool of multimodal care of breast cancer patients. Citation Format: Albert Grinshpun, Einat Carmon, Luna Kaduri, Aviad Zick, Shiri Shkedi, Edna Shalom, Avital Granit, Liza Monas, Tamar Shaldovsky, Tamar Hamburger, Vardiella Meiner, Tamar Peretz. Express model of hereditary multigene mutation analysis in breast cancer patients [abstract]. In: Proceedings of the 2019 San Antonio Breast Cancer Symposium; 2019 Dec 10-14; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2020;80(4 Suppl):Abstract nr P4-14-06.
Abstract P2-10-17: Tissue prevalence and cellular heterogeneity of 9p24.1 amplification in TNBC in African American women
Authors: Karen S. Anderson, Tammey Naab, Lori K Koslosky, Megan Anderson, Michael Lewis, Yasmine Kanaan, Ali Afsari, Luisel Ricks-Santi, Barbara A. Pockaj, Michael T Barrett
Journal: Cancer Research (2020)

Abstract Introduction: Amplification of chromosome 9p24.1 encoding PDL1, PDL2, and JAK2 (the PDJ amplicon) has been detected in 5-25% of triplenegative breast cancers (TNBC), and is associated with poor outcome and activation of the JAK/STAT pathway. Here, we have developed a robust multiplexed fluorescence in situ hybridization (FISH) assay for detection of 9p24.1 amplification, and assessed the frequency and cellular distribution of the PDJ amplicon in a cohort of African American (AA) women with TNBC. Methods: The FISH assay combines three chromosome 9 probes to simultaneously target JAK2 and PD-L1 (9p24.1, PDJ), chromosome 9q22, and the 9q34.1 regions. This enables discrimination of PDJ amplicons from whole chromosome 9p arm gains and from chromosome 9 ploidies that occur in the background of genomic instability in aneuploid cancer genomes. Fifty cells were scored for each probe and the average copy number was obtained. We defined PDJ amplification as PDJ&amp;gt;4, PDJ/9q22 ratio≥2, and/or PDJ/9q34.1 ratio≥2. The assay was benchmarked to array CGH of flow sorted TNBC tissue from Mayo Clinic Arizona (n=14). Tissue microarrays from TNBC PDX tumors (n=20) and from African American women with TNBC (n=87) were assessed. Results: Using selected TNBC tissue with known CGH data, the FISH assay tightly correlated with PDJ copy number in 13/14 cases. The discordant case was negative by CGH on a biopsy with low tumor content, but FISH positive on tissue section (PDJ &amp;gt;7.5 and a PDJ/9q22 ratio=4). Of 20 TNBC PDX tumors, 5 were amplified by FISH. Twelve of 87 (14%) of tumors had PDJ amplification by FISH, of which ten were from breast tissue and two were from lymph node. Of these 12, PDJ&amp;gt;4 (n=0), PDJ/9q22 ratio≥2 (n=6), and PDJ/9q34.1 ratio≥2 (n=10). Significant intratumoral variation was observed with the presence of single cells with &amp;gt;10 PDJ copies in 8/17 (47%) amplified and 0/90 non-amplified total cases. Conclusion: 9p24.1 (PDJ) amplification encoding JAK2, PD-L1, and PD-L2 is detected by three-color FISH in 14% of TNBC from African American women. Individual cells with ≥10 copies of PDJ was seen exclusively in 8/17 amplified cases. We identified 5 PDX tumors which may provide valuable preclinical models for the amplicon. The association of this biomarker with clinical outcome will be presented. Citation Format: Karen S. Anderson, Tammey Naab, Lori K Koslosky, Megan Anderson, Michael Lewis, Yasmine Kanaan, Ali Afsari, Luisel Ricks-Santi, Barbara A. Pockaj, Michael T Barrett. Tissue prevalence and cellular heterogeneity of 9p24.1 amplification in TNBC in African American women [abstract]. In: Proceedings of the 2019 San Antonio Breast Cancer Symposium; 2019 Dec 10-14; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2020;80(4 Suppl):Abstract nr P2-10-17.
Hippocampal Avoidance During Whole-Brain Radiotherapy Plus Memantine for Patients With Brain Metastases: Phase III Trial NRG Oncology CC001
Authors: Paul D. Brown, Vinai Gondi, Stephanie Pugh, Wolfgang A. Tome, Jeffrey S. Wefel, Terri S. Armstrong, Joseph A. Bovi, Cliff Robinson, Andre Konski, Deepak Khuntia, David Grosshans, Tammie L. S. Benzinger, Deborah Bruner, Mark R. Gilbert, David Roberge, Vijayananda Kundapur, Kiran Devisetty, Sunjay Shah, Kenneth Usuki, Bethany Marie Anderson, Baldassarre Stea, Harold Yoon, Jing Li, Nadia N. Laack, Tim J. Kruser, Steven J. Chmura, Wenyin Shi, Snehal Deshmukh, Minesh P. Mehta, Lisa A. Kachnic
Journal: Journal of Clinical Oncology (2020)

PURPOSE Radiation dose to the neuroregenerative zone of the hippocampus has been found to be associated with cognitive toxicity. Hippocampal avoidance (HA) using intensity-modulated radiotherapy during whole-brain radiotherapy (WBRT) is hypothesized to preserve cognition. METHODS This phase III trial enrolled adult patients with brain metastases to HA-WBRT plus memantine or WBRT plus memantine. The primary end point was time to cognitive function failure, defined as decline using the reliable change index on at least one of the cognitive tests. Secondary end points included overall survival (OS), intracranial progression-free survival (PFS), toxicity, and patient-reported symptom burden. RESULTS Between July 2015 and March 2018, 518 patients were randomly assigned. Median follow-up for alive patients was 7.9 months. Risk of cognitive failure was significantly lower after HA-WBRT plus memantine versus WBRT plus memantine (adjusted hazard ratio, 0.74; 95% CI, 0.58 to 0.95; P = .02). This difference was attributable to less deterioration in executive function at 4 months (23.3% v 40.4%; P = .01) and learning and memory at 6 months (11.5% v 24.7% [ P = .049] and 16.4% v 33.3% [ P = .02], respectively). Treatment arms did not differ significantly in OS, intracranial PFS, or toxicity. At 6 months, using all data, patients who received HA-WBRT plus memantine reported less fatigue ( P = .04), less difficulty with remembering things ( P = .01), and less difficulty with speaking ( P = .049) and using imputed data, less interference of neurologic symptoms in daily activities ( P = .008) and fewer cognitive symptoms ( P = .01). CONCLUSION HA-WBRT plus memantine better preserves cognitive function and patient-reported symptoms, with no difference in intracranial PFS and OS, and should be considered a standard of care for patients with good performance status who plan to receive WBRT for brain metastases with no metastases in the HA region.
Comparative prognostic implication of treatment response assessments in mCRPC: PERCIST 1.0, RECIST 1.1, and PSA response criteria
Authors: Erik M. Velez, Bhushan Desai, Lingyun Ji, David I. Quinn, Patrick M. Colletti, Hossein Jadvar
Journal: Theranostics (2020)

Accurate appraisal of treatment response in metastatic castrate-resistant prostate cancer (mCRPC) is challenging in view of remarkable tumor heterogeneity and the available choices among many established and novel therapeutic approaches. The purpose of this single-center prospective study was to evaluate the comparative prognostic utility of PERCIST 1.0 in predicting overall survival (OS) in patients with mCRPC compared to RECIST 1.1 and prostate-specific antigen (PSA)-based treatment response assessments. Methods: Patients with mCRPC were prospectively enrolled if they were beginning systemic medical therapy or transitioning to new systemic therapy after not responding to a prior treatment. All patients underwent a baseline 18F-fluorodeoxyglucose (FDG) positron emission tomography/ computed tomography (PET/CT) prior to the initiation of treatment and again 4 months after the start of therapy. Patients' responses to treatment at 4 months compared to baseline were evaluated with RECIST 1.1, PERCIST 1.0 and PSA response criteria. The associations between patients' response categories and OS were evaluated. OS was defined as the duration in time between the date of baseline PET/CT to death from any cause. Patients with different response status were compared with logrank tests. Survival probabilities were calculated using the Kaplan-Meier method. Results: Patients with progressive disease by PSA response criteria at 4 months demonstrated significantly shorter OS (24-month OS probability: 18% ± 11%) compared to patients with stable disease, SD, (44% ± 19%, p=0.03) and complete response, CR, or partial response, PR, (53% ± 11%, p=0.03). RECIST 1.1 response criteria demonstrated a similar trend in OS, however no statistically significant differences were noted between patients with PD (25% ± 15%) compared to SD/non-CR, non-PD (54% ± 13%) and CR/PR (54% ± 14%) (p=0.13). PERCIST 1.0 criteria demonstrated significant differences in OS between responders, CMR/PMR (56% ± 12%), compared to SMD (38% ± 17%, p=0.03) and PMD (21% ± 10%, p=0.01). Patients with progressive disease by both PERICST 1.0 and PSA response criteria demonstrated significantly worse OS (24-month OS: 0%, 12-month OS: 31% ± 14%) compared to patients with progressive disease by either response criteria. Conclusion: PERCIST 1.0 may provide significant prognostic information for patients with mCRPC undergoing systemic chemotherapy, particularly when incorporated with PSA treatment response criteria.