scholarly journals Radiation dose-response (a Bayesian model) in the radiotherapy of the localized prostatic adenocarcinoma: the reliability of PSA slope changes as a response surrogate endpoint

PeerJ ◽  
2019 ◽  
Vol 7 ◽  
pp. e7172
Author(s):  
Reza Ali Mohammadpour ◽  
Jamshid Yazdani- Charati ◽  
SZahra Faghani ◽  
Ahad Alizadeh ◽  
Mohammadreza Barzegartahamtan
Keyword(s):  
Radiation Dose ◽  
Dose Response ◽  
Specific Antigen ◽  
Surrogate Endpoint ◽  
Assessment System ◽  
T Stage ◽  
Kaplan Meier ◽  
Total Radiation Dose ◽  
Product Limit ◽  
The Relationship

Purpose One of the characteristics of Prostate-Specific Antigen (PSA) is PSA slope. It is the rate of diminishing PSA marker over time after radiotherapy (RT) in prostate cancer (PC) patients. The purpose of this study was to evaluate the relationship between increasing RT doses and PSA slope as a potential surrogate for PC recurrence. Patients and Methods This retrospective study was conducted on PC patients who were treated by radiotherapy in the Cancer Institute of Iran during 2007–2012. By reviewing the records of these patients, the baseline PSA measurement before treatment (iPSA), Gleason score (GS), clinical T stage (T. stage), and periodic PSA measurements after RT and the total radiation dose received were extracted for each patient separately. We used a Bayesian dose-response model, analysis of variance, Kruskal–Wallis test, Kaplan–Meier product-limit method for analysis. Probability values less 0.05 were considered statistically significant. Results Based on the D’Amico risk assessment system, 13.34% of patients were classified as “Low Risk”, 51.79% were “Intermediate Risk”, and 34.87% were “High Risk”. In terms of radiation doses, 12.31% of the patients received fewer than 50 Gy, 15.38% received 50 to 69 Gy, 61.03% received 70 Gy, and 11.28% received more than 70 Gy. The PSA values decreased after RT for all dose levels. The slope of PSA changes was negative for 176 of 195 patients. By increasing the dosage of radiation, the PSA decreased but these changes were not statistically significant (p = 0.701) and PSA slope as a surrogate end point cannot met the Prentice’s criteria for PC recurrence. Conclusion Significant changes in the dose-response relationship were not observed when the PSA slope was considered as the response criterion. Therefore, although the absolute value of the PSA decreased with increasing doses of RT, the relationship between PSA slope changes and increasing doses was not clear and cannot be used as a reliable response surrogate endpoint.

Incidence of lymphoid neoplasms among atomic bomb survivors by histological subtype: 1950-1994

Blood ◽  
2021 ◽  
Author(s):  
Megumu Fujihara ◽  
Ritsu Sakata ◽  
Noriaki Yoshida ◽  
Kotaro Ozasa ◽  
Dale L Preston ◽  
...  
Keyword(s):  
T Cell ◽  
Radiation Dose ◽  
B Cell ◽  
Dose Response ◽  
Atomic Bomb ◽  
Nk Cell ◽  
Precursor Cell ◽  
Atomic Bomb Survivors ◽  
Lymphoid Neoplasms ◽  
The Relationship

Epidemiological data have provided limited and inconsistent evidence on the relationship between radiation exposure and lymphoid neoplasms. We classified 553 lymphoid neoplasm cases diagnosed between 1950 and 1994 in the Life Span Study (LSS) cohort of atomic bomb survivors into WHO subtypes. Mature B-cell neoplasms represented 58%, mature T-cell and NK-cell neoplasms 20%; precursor cell neoplasms, 5%, and Hodgkin lymphoma, 3%; with the remaining 15% classified as non-Hodgkin lymphoid neoplasms or lymphoid neoplasms, not otherwise specified. We used Poisson regression methods to assess the relationship between radiation exposure and the more common subtypes. As in earlier reports, a significant dose response for non-Hodgkin lymphoid neoplasms as a group was seen for males but not females. However, subtype analyses showed that radiation dose was strongly associated with increased precursor cell neoplasms rates, with an estimated excess relative risk per Gy of 16 (95% Confidence interval: 7.0, >533) at age 50. The current data based primarily of tissue-based diagnoses suggest that the association between radiation dose and lymphoid neoplasms as a group is largely driven by the radiation effect on precursor cell neoplasms while presenting no evidence of a radiation dose response for major categories of mature cell neoplasms, either B- or T-/NK-cell, or more specific disease entities (diffuse large B-cell lymphoma, plasma cell myeloma, adult T-cell leukemia/lymphoma) or Hodgkin lymphoma.

Evaluation of clinical phenotype, survival, and circulating tumor cell (CTC) enumeration in men with metastatic castration-resistant prostate cancer (mCRPC).

2013 ◽  
Vol 31 (15_suppl) ◽  
pp. 5031-5031 ◽  
Author(s):  
Rhonda Lynn Bitting ◽  
Patrick Healy ◽  
Susan Halabi ◽  
Daniel J. George ◽  
Jung Hyun Ko ◽  
...  
Keyword(s):  
Prognostic Significance ◽  
Specific Antigen ◽  
Circulating Tumor Cell ◽  
Tumor Burden ◽  
Castration Resistant Prostate Cancer ◽  
Bone Microenvironment ◽  
Castration Resistant ◽  
Kaplan Meier ◽  
Androgen Receptor Activity ◽  
The Relationship

5031 Background: The presence of ≥ 5 CTCs is prognostic for shorter survival in mCRPC men. However, many men have low CTCs despite widespread metastatic disease, suggesting heterogeneity in CTC phenotype or detection. We evaluated the association of baseline CTC enumeration with clinical characteristics and survival in mCRPC men at our institution. Methods: CTCs were enumerated with the standard CellSearch method in mCRPC men in a prospective correlative clinical study. The association between baseline CTC count and prostate-specific antigen (PSA), alkaline phosphatase (AP), lactate dehydrogenase (LDH) was explored using the Spearman correlation (r), and the relationship with Gleason sum, sites of metastasis (mets), and prior docetaxel exposure was explored using summary statistics. The overall survival probability (OS) was estimated by the Kaplan-Meier method. Results: In our cohort, 59/82 men had prior docetaxel exposure, and the median CTC count was 16.5. There were 25 men with visceral mets, 55 with bone-predominant mets, and 2 with lymph node only mets. We found a weak relationship between CTCs and PSA (r=0.20), but a more moderate and significant association with AP (r=0.48) and LDH (r= 0.50). We found no relationship between CTCs and Gleason sum, site of mets, or prior docetaxel. 66 men died, and the median OS was 11.2 months (95% CI: 9.2, 12.7). OS was improved in patients with <5 CTCs at baseline compared to ≥ 5 (8.9 vs. 16.6 months, HR=0.47 (95% CI: 0.27, 0.80)). CTC enumeration may further stratify outcomes in men with mCRPC and either visceral or bone metastasis as shown in the table below. Conclusions: The prognostic significance of CTCs is distinct from other established biomarkers and may reflect a unique biology of metastasis, dissociated in part from androgen receptor activity (as reflected by PSA values) but related in part to bone microenvironment, hypoxia, and tumor burden (as reflected by AP and LDH values). These associations need to be validated in larger trials. [Table: see text]

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