ACTIVE SURVEILLANCE OF MEN WITH HGPIN BY EMPIRIC DELAYED INTERVAL BIOPSIES DEMONSTRATES A SIGNIFICANT LONG-TERM RISK OF CANCER PROGRESSION

2008 ◽  
Vol 179 (4S) ◽  
pp. 712-712
Author(s):  
Guilherme Godoy ◽  
George Huang ◽  
Basir Tareen ◽  
Herbert Lepor ◽  
Samir S Taneja
2020 ◽  
Vol 19 ◽  
pp. e1922-e1923
Author(s):  
A. Brassetti ◽  
F. Proietti ◽  
G. Napodano ◽  
R. Sanseverino ◽  
F. Badenchini ◽  
...  

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Moeko Tanaka ◽  
Sachi Yamaguchi ◽  
Yoh Iwasa

Abstract Cancer is caused by the lifetime accumulation of multiple somatic deformations of the genome and epigenome. At a very low rate, mistakes occur during genomic replication (e.g., mutations or modified epigenetic marks). Long-lived species, such as elephants, are suggested to have evolved mechanisms to slow down the cancer progression. Recently, the life span of companion dogs has increased considerably than before, owing to the improvement of their environment, which has led to an increase in the fraction of companion dogs developing cancer. These findings suggest that short-term responses of cancer risk to longevity differ from long-term responses. In this study, to clarify the situation, we used a simple multi-step model for cancer. The rates of events leading to malignant cancer are assumed to be proportional to those of genomic replication error. Perfect removal of replication error requires a large cost, resulting in the evolution of a positive rate of genomic replication error. The analysis of the model revealed: that, when the environment suddenly becomes benign, the relative importance of cancer enhances, although the age-dependent cancer risk remains unchanged. However, in the long run, the genomic error rate evolves to become smaller and mitigates the cancer risk.


2019 ◽  
Vol 39 (5) ◽  
pp. 499-508
Author(s):  
Anirudh Tomer ◽  
Dimitris Rizopoulos ◽  
Daan Nieboer ◽  
Frank-Jan Drost ◽  
Monique J. Roobol ◽  
...  

Background. Low-risk prostate cancer patients enrolled in active surveillance programs commonly undergo biopsies for examination of cancer progression. Biopsies are conducted as per a fixed and frequent schedule (e.g., annual biopsies). Since biopsies are burdensome, patients do not always comply with the schedule, which increases the risk of delayed detection of cancer progression. Objective. Our aim is to better balance the number of biopsies (burden) and the delay in detection of cancer progression (less is beneficial) by personalizing the decision of conducting biopsies. Data Sources. We used patient data of the world’s largest active surveillance program (Prostate Cancer Research International Active Surveillance; PRIAS). It enrolled 5270 patients, had 866 cancer progressions, and an average of 9 prostate-specific antigen (PSA) and 5 digital rectal examination (DRE) measurements per patient. Methods. Using joint models for time-to-event and longitudinal data, we model the historical DRE and PSA measurements and biopsy results of a patient at each follow-up visit. This results in a visit and patient-specific cumulative risk of cancer progression. If this risk is above a certain threshold, we schedule a biopsy. We compare this personalized approach with the currently practiced biopsy schedules via an extensive and realistic simulation study, based on a replica of the patients from the PRIAS program. Results. The personalized approach saved a median of 6 biopsies (median: 4, interquartile range [IQR]: 2–5) compared with the annual schedule (median: 10, IQR: 3–10). However, the delay in detection of progression (years) is similar for the personalized (median: 0.7, IQR: 0.3–1.0) and the annual schedule (median: 0.5, IQR: 0.3–0.8). Conclusions. We conclude that personalized schedules provide substantially better balance in the number of biopsies per detected progression for men with low-risk prostate cancer.


2019 ◽  
Vol 109 (4) ◽  
pp. 1133-1144 ◽  
Author(s):  
Maria H Traka ◽  
Antonietta Melchini ◽  
Jack Coode-Bate ◽  
Omar Al Kadhi ◽  
Shikha Saha ◽  
...  

ABSTRACT Background Epidemiological evidence suggests that consumption of cruciferous vegetables is associated with reduced risk of prostate cancer progression, largely attributed to the biological activity of glucosinolate degradation products, such as sulforaphane derived from glucoraphanin. Because there are few therapeutic interventions for men on active surveillance for prostate cancer to reduce the risk of cancer progression, dietary approaches are an appealing option for patients. Objective We evaluated whether consumption of a glucoraphanin-rich broccoli soup for 1 y leads to changes in gene expression in prostate tissue of men with localized prostate cancer. Methods Forty-nine men on active surveillance completed a 3-arm parallel randomized double-blinded intervention study for 12 mo and underwent transperineal template biopsy procedures and dietary assessment at the start and end of the study. Patients received a weekly 300 mL portion of soup made from a standard broccoli (control) or from 1 of 2 experimental broccoli genotypes with enhanced concentrations of glucoraphanin, delivering 3 and 7 times that of the control, respectively. Gene expression in tissues from each patient obtained before and after the dietary intervention was quantified by RNA sequencing followed by gene set enrichment analyses. Results In the control arm, there were several hundred changes in gene expression in nonneoplastic tissue during the 12 mo. These were associated with an increase in expression of potentially oncogenic pathways including inflammation processes and epithelial–mesenchymal transition. Changes in gene expression and associated oncogenic pathways were attenuated in men on the glucoraphanin-rich broccoli soup in a dose-dependent manner. Although the study was not powered to assess clinical progression, an inverse association between consumption of cruciferous vegetables and cancer progression was observed. Conclusion Consuming glucoraphanin-rich broccoli soup affected gene expression in the prostate of men on active surveillance, consistent with a reduction in the risk of cancer progression. This trial was registered at clinicaltrials.gov as NCT01950143.


2018 ◽  
Vol 64 (2) ◽  
pp. 228-233
Author(s):  
Vladimir Lubyanskiy ◽  
Vasiliy Seroshtanov ◽  
Ye. Semenova

The aim: To analyze results of surgical treatment of patients with chronic pancreatitis (CP) and to assess the causes of pancreatic cancer after surgical treatment. Materials and methods: 137 patients had duodenum-preserving resections of the pancreas. Results: In the histological examination of the pancreas it was established that the growth of fibrous tissue was registered in patients with CP., which in 19 (13.8%) almost completely replaced the acinar tissue. In the long term after the operation from 6 months to 2 years in 8 patients (5.8%) pancreatic cancer was detected. Possible causes of tumor origin were analyzed, the value of preservation of ductal hypertension, which affects the state of the duct’s epithelium, was established. The most commonly used for treatment of chronic pancreatitis the Frey surgery removed pancreatic hypertension but in two patients during the operation an insufficient volume of the pancreatic head was reconstructed. In the case of the abandonment of a large array of fibrous tissue, local hypertension was retained in the region of the ductal structures of the head, which led to the transformation of the duct epithelium. An essential factor in the problem of the preservation of pancreatic hypertension were the stenosis of pancreatic intestinal anastomoses, they arose in the long term in 4 operated patients. With stenosis of anastomosis after duodenum-preserving resection both the hypertension factor and the regeneration factor could be realized, which under certain circumstances might be significant. Conclusion: After resection of the pancreas for CP cancer was diagnosed in 5.8% of patients. The main method of preventing the risk of cancer was performing the Frey surgery for CP eliminating pancreatic hypertension in the head region of the pancreas. Diagnosis of stenosis in the late period after resection of the pancreas was an important element in the prevention of recurrence of cancer since a timely reconstructive operation could improve the drainage of duct structures.


2021 ◽  
Author(s):  
Yuta Yamashita ◽  
Yasuhiko Yamano ◽  
Yoshinao Muro ◽  
Haruka Koizumi ◽  
Takuya Takeichi ◽  
...  

Cancers ◽  
2021 ◽  
Vol 13 (13) ◽  
pp. 3368
Author(s):  
Dafina Petrova ◽  
Andrés Catena ◽  
Miguel Rodríguez-Barranco ◽  
Daniel Redondo-Sánchez ◽  
Eloísa Bayo-Lozano ◽  
...  

Many adult cancer patients present one or more physical comorbidities. Besides interfering with treatment and prognosis, physical comorbidities could also increase the already heightened psychological risk of cancer patients. To test this possibility, we investigated the relationship between physical comorbidities with depression symptoms in a sample of 2073 adult cancer survivors drawn from the nationally representative National Health and Nutrition Examination Survey (NHANES) (2007–2018) in the U.S. Based on information regarding 16 chronic conditions, the number of comorbidities diagnosed before and after the cancer diagnosis was calculated. The number of comorbidities present at the moment of cancer diagnosis was significantly related to depression risk in recent but not in long-term survivors. Recent survivors who suffered multimorbidity had 3.48 (95% CI 1.26–9.55) times the odds of reporting significant depressive symptoms up to 5 years after the cancer diagnosis. The effect of comorbidities was strongest among survivors of breast cancer. The comorbidities with strongest influence on depression risk were stroke, kidney disease, hypertension, obesity, asthma, and arthritis. Information about comorbidities is usually readily available and could be useful in streamlining depression screening or targeting prevention efforts in cancer patients and survivors. A multidimensional model of the interaction between cancer and other physical comorbidities on mental health is proposed.


Cancers ◽  
2021 ◽  
Vol 13 (14) ◽  
pp. 3617
Author(s):  
Fabrizio Fabrizi ◽  
Roberta Cerutti ◽  
Carlo M. Alfieri ◽  
Ezequiel Ridruejo

Chronic kidney disease is a major public health issue globally and the risk of cancer (including HCC) is greater in patients on long-term dialysis and kidney transplant compared with the general population. According to an international study on 831,804 patients on long-term dialysis, the standardized incidence ratio for liver cancer was 1.2 (95% CI, 1.0–1.4) and 1.5 (95% CI, 1.3–1.7) in European and USA cohorts, respectively. It appears that important predictors of HCC in dialysis population are hepatotropic viruses (HBV and HCV) and cirrhosis. 1-, 3-, and 5-year survival rates are lower in HCC patients on long-term dialysis than those with HCC and intact kidneys. NAFLD is a metabolic disease with increasing prevalence worldwide and recent evidence shows that it is an important cause of liver-related and extra liver-related diseases (including HCC and CKD, respectively). Some longitudinal studies have shown that patients with chronic hepatitis B are aging and the frequency of comorbidities (such as HCC and CKD) is increasing over time in these patients; it has been suggested to connect these patients to an appropriate care earlier. Antiviral therapy of HBV and HCV plays a pivotal role in the management of HCC in CKD and some combinations of DAAs (elbasvir/grazoprevir, glecaprevir/pibrentasvir, sofosbuvir-based regimens) are now available for HCV positive patients and advanced chronic kidney disease. The interventional management of HCC includes liver resection. Some ablative techniques have been suggested for HCC in CKD patients who are not appropriate candidates to surgery. Transcatheter arterial chemoembolization has been proposed for HCC in patients who are not candidates to liver surgery due to comorbidities. The gold standard for early-stage HCC in patients with chronic liver disease and/or cirrhosis is still liver transplant.


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