Clinical Edge Journal Scan

Key clinical point: Over half of the patients with childhood-onset hereditary pancreatitis developed exocrine pancreatic insufficiency (EPI). EPI development preceded loss of endocrine function in this rare patient population.

Major finding: Overall, EPI developed in 7 patients at an average age of 12.5±8.4 years, with fecal pancreatic elastase less than 100 mg/g in all patients at disease onset. No evidence of pancreoprive diabetes mellitus (type IIIc) was reported in any patient.

Study details: This retrospective study evaluated 11 patients with childhood-onset (mean age at onset, 7.5±4.2 years) hereditary pancreatitis.

Disclosures: No funding source was identified. The authors declared no conflicts of interest.

Source: Prommer R et al. Wien Klin Wochenschr. 2021 Apr 28. doi: 10.1007/s00508-021-01869-0.

Key clinical point: Over half of the patients with childhood-onset hereditary pancreatitis developed exocrine pancreatic insufficiency (EPI). EPI development preceded loss of endocrine function in this rare patient population.

Major finding: Overall, EPI developed in 7 patients at an average age of 12.5±8.4 years, with fecal pancreatic elastase less than 100 mg/g in all patients at disease onset. No evidence of pancreoprive diabetes mellitus (type IIIc) was reported in any patient.

Study details: This retrospective study evaluated 11 patients with childhood-onset (mean age at onset, 7.5±4.2 years) hereditary pancreatitis.

Disclosures: No funding source was identified. The authors declared no conflicts of interest.

Source: Prommer R et al. Wien Klin Wochenschr. 2021 Apr 28. doi: 10.1007/s00508-021-01869-0.

Key clinical point: Over half of the patients with childhood-onset hereditary pancreatitis developed exocrine pancreatic insufficiency (EPI). EPI development preceded loss of endocrine function in this rare patient population.

Major finding: Overall, EPI developed in 7 patients at an average age of 12.5±8.4 years, with fecal pancreatic elastase less than 100 mg/g in all patients at disease onset. No evidence of pancreoprive diabetes mellitus (type IIIc) was reported in any patient.

Study details: This retrospective study evaluated 11 patients with childhood-onset (mean age at onset, 7.5±4.2 years) hereditary pancreatitis.

Disclosures: No funding source was identified. The authors declared no conflicts of interest.

Source: Prommer R et al. Wien Klin Wochenschr. 2021 Apr 28. doi: 10.1007/s00508-021-01869-0.

Key clinical point: Although locally advanced pancreatic cancer (LAPC) or metastatic pancreatic cancer (MPC) is associated with reduced exocrine function, there is a lack of clear guidelines for the diagnosis and management of exocrine pancreatic insufficiency (EPI) for palliative pancreatic ductal adenocarcinomas.

Major finding: Weight loss and steatorrhea were present in 83.6% and 13.4% of patients, respectively. Median body mass index decreased by 13.3% from preillness state to cancer diagnosis. Despite high rates of referral to dieticians (79.1%), only 24 patients were prescribed pancreatic enzyme replacement therapy. Pancrelipase dose varied from 10,000 to 50,000 units with each meal.

Study details: This retrospective study assessed palliative management in 67 patients with LAPC or MPC.

Disclosures: No specific funding source was identified. The authors declared no conflicts of interest.

Source: Choi CCM et al. ANZ J Surg. 2021 Apr 18. doi: 10.1111/ans.16669.

Key clinical point: Although locally advanced pancreatic cancer (LAPC) or metastatic pancreatic cancer (MPC) is associated with reduced exocrine function, there is a lack of clear guidelines for the diagnosis and management of exocrine pancreatic insufficiency (EPI) for palliative pancreatic ductal adenocarcinomas.

Major finding: Weight loss and steatorrhea were present in 83.6% and 13.4% of patients, respectively. Median body mass index decreased by 13.3% from preillness state to cancer diagnosis. Despite high rates of referral to dieticians (79.1%), only 24 patients were prescribed pancreatic enzyme replacement therapy. Pancrelipase dose varied from 10,000 to 50,000 units with each meal.

Study details: This retrospective study assessed palliative management in 67 patients with LAPC or MPC.

Disclosures: No specific funding source was identified. The authors declared no conflicts of interest.

Source: Choi CCM et al. ANZ J Surg. 2021 Apr 18. doi: 10.1111/ans.16669.

Key clinical point: Although locally advanced pancreatic cancer (LAPC) or metastatic pancreatic cancer (MPC) is associated with reduced exocrine function, there is a lack of clear guidelines for the diagnosis and management of exocrine pancreatic insufficiency (EPI) for palliative pancreatic ductal adenocarcinomas.

Major finding: Weight loss and steatorrhea were present in 83.6% and 13.4% of patients, respectively. Median body mass index decreased by 13.3% from preillness state to cancer diagnosis. Despite high rates of referral to dieticians (79.1%), only 24 patients were prescribed pancreatic enzyme replacement therapy. Pancrelipase dose varied from 10,000 to 50,000 units with each meal.

Study details: This retrospective study assessed palliative management in 67 patients with LAPC or MPC.

Disclosures: No specific funding source was identified. The authors declared no conflicts of interest.

Source: Choi CCM et al. ANZ J Surg. 2021 Apr 18. doi: 10.1111/ans.16669.

Key clinical point: Patients with vs. without exocrine pancreatic insufficiency (EPI) had increased fasting breath hydrogen concentration (FBHC) levels, possibly because of the presence of hydrogen-producing genus Clostridium in the gut. FBHC may have a good potential as a simple test for EPI diagnosis.

Major finding: FBHC levels were significantly higher in the EPI vs. non-EPI (median, 15.70 ppm vs. 2.80 ppm; P less than .001) group and negatively correlated with p-aminobenzoic acid (PABA) excretion rate  (r, −0.523; P less than .001). The occupancy by Clostridia bacteria in intestinal bacterial flora was higher in EPI group (P less than .05).

Study details: This prospective study included 60 inpatients with pancreatic disease who underwent FBHC measurement, N-benzoyl-L-tyrosyl-PABA testing, and microbiome analysis. The PABA excretion rate of 73.4% classified patients into EPI (n=30) and non-EPI (n=30) groups.

Disclosures: No funding was obtained for this study. The authors declared no conflicts of interest.

Source: Uetsuki K et al. BMC Gastroenterol. 2021 May 10. doi: 10.1186/s12876-021-01776-8.

Key clinical point: Patients with vs. without exocrine pancreatic insufficiency (EPI) had increased fasting breath hydrogen concentration (FBHC) levels, possibly because of the presence of hydrogen-producing genus Clostridium in the gut. FBHC may have a good potential as a simple test for EPI diagnosis.

Major finding: FBHC levels were significantly higher in the EPI vs. non-EPI (median, 15.70 ppm vs. 2.80 ppm; P less than .001) group and negatively correlated with p-aminobenzoic acid (PABA) excretion rate  (r, −0.523; P less than .001). The occupancy by Clostridia bacteria in intestinal bacterial flora was higher in EPI group (P less than .05).

Study details: This prospective study included 60 inpatients with pancreatic disease who underwent FBHC measurement, N-benzoyl-L-tyrosyl-PABA testing, and microbiome analysis. The PABA excretion rate of 73.4% classified patients into EPI (n=30) and non-EPI (n=30) groups.

Disclosures: No funding was obtained for this study. The authors declared no conflicts of interest.

Source: Uetsuki K et al. BMC Gastroenterol. 2021 May 10. doi: 10.1186/s12876-021-01776-8.

Key clinical point: Patients with vs. without exocrine pancreatic insufficiency (EPI) had increased fasting breath hydrogen concentration (FBHC) levels, possibly because of the presence of hydrogen-producing genus Clostridium in the gut. FBHC may have a good potential as a simple test for EPI diagnosis.

Major finding: FBHC levels were significantly higher in the EPI vs. non-EPI (median, 15.70 ppm vs. 2.80 ppm; P less than .001) group and negatively correlated with p-aminobenzoic acid (PABA) excretion rate  (r, −0.523; P less than .001). The occupancy by Clostridia bacteria in intestinal bacterial flora was higher in EPI group (P less than .05).

Study details: This prospective study included 60 inpatients with pancreatic disease who underwent FBHC measurement, N-benzoyl-L-tyrosyl-PABA testing, and microbiome analysis. The PABA excretion rate of 73.4% classified patients into EPI (n=30) and non-EPI (n=30) groups.

Disclosures: No funding was obtained for this study. The authors declared no conflicts of interest.

Source: Uetsuki K et al. BMC Gastroenterol. 2021 May 10. doi: 10.1186/s12876-021-01776-8.

Key clinical point: Lumacaftor-ivacaftor treatment for 120 weeks improved exocrine pancreatic insufficiency and pancreatic damage in children as young as 2-5 years of age with cystic fibrosis (CF) homozygous for F508del-CF transmembrane conductance regulator gene.

Major finding: At baseline, 100% of participants had fecal elastase-1 (FE-1) less than 200 µg/g, of which 41 participants had FE-1 less than 15 µg/g. Treatment with lumacaftor-ivacaftor increased FE-1 (mean absolute change [D], 132.6±174.2 µg/g) and decreased immunoreactive trypsinogen (D, −108.5±306.6 ng/mL) from baseline to 120 weeks.

Study details: This phase 3 rollover trial (study 116) included 57 children with CF who completed 24 weeks of lumacaftor-ivacaftor treatment in previous study 115. Patients received weight- and age-based doses of lumacaftor-ivacaftor for additional 96 weeks, totaling 120 weeks of treatment.

Disclosures: This study was funded by Vertex Pharmaceuticals Incorporated (VPI). VPI was funded by CF Foundation for lumacaftor development. Some investigators including the lead author reported ties with VPI and CF Foundation.

Source: Hoppe JE et al. Lancet Respir Med. 2021 May 6. doi: 10.1016/S2213-2600(21)00069-2.

Key clinical point: Lumacaftor-ivacaftor treatment for 120 weeks improved exocrine pancreatic insufficiency and pancreatic damage in children as young as 2-5 years of age with cystic fibrosis (CF) homozygous for F508del-CF transmembrane conductance regulator gene.

Major finding: At baseline, 100% of participants had fecal elastase-1 (FE-1) less than 200 µg/g, of which 41 participants had FE-1 less than 15 µg/g. Treatment with lumacaftor-ivacaftor increased FE-1 (mean absolute change [D], 132.6±174.2 µg/g) and decreased immunoreactive trypsinogen (D, −108.5±306.6 ng/mL) from baseline to 120 weeks.

Study details: This phase 3 rollover trial (study 116) included 57 children with CF who completed 24 weeks of lumacaftor-ivacaftor treatment in previous study 115. Patients received weight- and age-based doses of lumacaftor-ivacaftor for additional 96 weeks, totaling 120 weeks of treatment.

Disclosures: This study was funded by Vertex Pharmaceuticals Incorporated (VPI). VPI was funded by CF Foundation for lumacaftor development. Some investigators including the lead author reported ties with VPI and CF Foundation.

Source: Hoppe JE et al. Lancet Respir Med. 2021 May 6. doi: 10.1016/S2213-2600(21)00069-2.

Key clinical point: Lumacaftor-ivacaftor treatment for 120 weeks improved exocrine pancreatic insufficiency and pancreatic damage in children as young as 2-5 years of age with cystic fibrosis (CF) homozygous for F508del-CF transmembrane conductance regulator gene.

Major finding: At baseline, 100% of participants had fecal elastase-1 (FE-1) less than 200 µg/g, of which 41 participants had FE-1 less than 15 µg/g. Treatment with lumacaftor-ivacaftor increased FE-1 (mean absolute change [D], 132.6±174.2 µg/g) and decreased immunoreactive trypsinogen (D, −108.5±306.6 ng/mL) from baseline to 120 weeks.

Study details: This phase 3 rollover trial (study 116) included 57 children with CF who completed 24 weeks of lumacaftor-ivacaftor treatment in previous study 115. Patients received weight- and age-based doses of lumacaftor-ivacaftor for additional 96 weeks, totaling 120 weeks of treatment.

Disclosures: This study was funded by Vertex Pharmaceuticals Incorporated (VPI). VPI was funded by CF Foundation for lumacaftor development. Some investigators including the lead author reported ties with VPI and CF Foundation.

Source: Hoppe JE et al. Lancet Respir Med. 2021 May 6. doi: 10.1016/S2213-2600(21)00069-2.

Due to the heterogeneity of outcomes and study designs, consensus on definitive prostate cancer risk assessment has been somewhat elusive. Differences in outcomes based on ethnicity and race have been observed, but much data on risk has originally been obtained in populations with lower ethnic and racial diversity, complicating extrapolation to larger populations. Huynh-Le et al developed an updated polygenic hazard score (PHS₂) based on a single nucleotide polymorphism (SNP) panel (46 total SNPs) for prostate cancer patients with multiple ethnicities (African, Asian, and European ancestries). This updated PHS₂ score stratified men into higher and lower risks for any, aggressive, and fatal prostate cancers in a statistically significant way. Camargo et al took a different approach and evaluated whether 2 SNPs were prognostic in prostate cancer: rs1834306 corresponding to microRNA 100 (miR 100) and rs2910164 from miR 146a. There were no differences in miR 100 or miR 156a between patients with local prostate cancer or a control group of men without prostate cancer. In addition, there were no differences in the chance of particular genotypes between the 2 groups. There was an association between lower presence of rs1834306 (miR 100) and patients with PSA > 10 mg/mL and between a higher amount of the polymorphic allele for rs2910164 (miR 146A).

The 3 studies summarized here demonstrate the ongoing challenges in how to identify nuances that will affect clinical decision-making in PSA screening and to identify prognostic features that associate with particular outcomes. The study by Bergengren confirmed the current state of PSA screening in that balancing diagnosis and potential overtreatment with modest survival outcomes is challenging. While the studies by Huynh-Le  et al and Camargo et al have interesting findings, the use of SNPs and miR in prostate cancer prognosis is still not ready for routine clinical use in prostate cancer management.

Due to the heterogeneity of outcomes and study designs, consensus on definitive prostate cancer risk assessment has been somewhat elusive. Differences in outcomes based on ethnicity and race have been observed, but much data on risk has originally been obtained in populations with lower ethnic and racial diversity, complicating extrapolation to larger populations. Huynh-Le et al developed an updated polygenic hazard score (PHS₂) based on a single nucleotide polymorphism (SNP) panel (46 total SNPs) for prostate cancer patients with multiple ethnicities (African, Asian, and European ancestries). This updated PHS₂ score stratified men into higher and lower risks for any, aggressive, and fatal prostate cancers in a statistically significant way. Camargo et al took a different approach and evaluated whether 2 SNPs were prognostic in prostate cancer: rs1834306 corresponding to microRNA 100 (miR 100) and rs2910164 from miR 146a. There were no differences in miR 100 or miR 156a between patients with local prostate cancer or a control group of men without prostate cancer. In addition, there were no differences in the chance of particular genotypes between the 2 groups. There was an association between lower presence of rs1834306 (miR 100) and patients with PSA > 10 mg/mL and between a higher amount of the polymorphic allele for rs2910164 (miR 146A).

The 3 studies summarized here demonstrate the ongoing challenges in how to identify nuances that will affect clinical decision-making in PSA screening and to identify prognostic features that associate with particular outcomes. The study by Bergengren confirmed the current state of PSA screening in that balancing diagnosis and potential overtreatment with modest survival outcomes is challenging. While the studies by Huynh-Le  et al and Camargo et al have interesting findings, the use of SNPs and miR in prostate cancer prognosis is still not ready for routine clinical use in prostate cancer management.

Due to the heterogeneity of outcomes and study designs, consensus on definitive prostate cancer risk assessment has been somewhat elusive. Differences in outcomes based on ethnicity and race have been observed, but much data on risk has originally been obtained in populations with lower ethnic and racial diversity, complicating extrapolation to larger populations. Huynh-Le et al developed an updated polygenic hazard score (PHS₂) based on a single nucleotide polymorphism (SNP) panel (46 total SNPs) for prostate cancer patients with multiple ethnicities (African, Asian, and European ancestries). This updated PHS₂ score stratified men into higher and lower risks for any, aggressive, and fatal prostate cancers in a statistically significant way. Camargo et al took a different approach and evaluated whether 2 SNPs were prognostic in prostate cancer: rs1834306 corresponding to microRNA 100 (miR 100) and rs2910164 from miR 146a. There were no differences in miR 100 or miR 156a between patients with local prostate cancer or a control group of men without prostate cancer. In addition, there were no differences in the chance of particular genotypes between the 2 groups. There was an association between lower presence of rs1834306 (miR 100) and patients with PSA > 10 mg/mL and between a higher amount of the polymorphic allele for rs2910164 (miR 146A).

The 3 studies summarized here demonstrate the ongoing challenges in how to identify nuances that will affect clinical decision-making in PSA screening and to identify prognostic features that associate with particular outcomes. The study by Bergengren confirmed the current state of PSA screening in that balancing diagnosis and potential overtreatment with modest survival outcomes is challenging. While the studies by Huynh-Le  et al and Camargo et al have interesting findings, the use of SNPs and miR in prostate cancer prognosis is still not ready for routine clinical use in prostate cancer management.

Key clinical point: Single nucleotide polymorphisms (SNP) can serve as prognostic factors for prostate cancer

Major finding: In patients with prostate cancer, SNP rs2910164 of miR146a was more common in patients with a Gleason score of 7 or higher than those with a Gleason score of less than 7 (P=0.043); in addition, SNP rs1834306 of miR100 was overexpressed in those with pT3 staging compared to pT2 (P = 0.004).

Study details: The data come from a review of 100 patients with clinically localized prostate cancer who underwent radical prostatectomy and 68 controls without prostate cancer.

Disclosures: The study was supported in part by a grant from the Sao Paulo Research Foundation. The researchers had no financial conflicts to disclose.

Source: Camargo JA et al. Int J Biol Markers. 2021 May 25. doi: 10.1177/172460082199746.

Key clinical point: Single nucleotide polymorphisms (SNP) can serve as prognostic factors for prostate cancer

Major finding: In patients with prostate cancer, SNP rs2910164 of miR146a was more common in patients with a Gleason score of 7 or higher than those with a Gleason score of less than 7 (P=0.043); in addition, SNP rs1834306 of miR100 was overexpressed in those with pT3 staging compared to pT2 (P = 0.004).

Study details: The data come from a review of 100 patients with clinically localized prostate cancer who underwent radical prostatectomy and 68 controls without prostate cancer.

Disclosures: The study was supported in part by a grant from the Sao Paulo Research Foundation. The researchers had no financial conflicts to disclose.

Source: Camargo JA et al. Int J Biol Markers. 2021 May 25. doi: 10.1177/172460082199746.

Key clinical point: Single nucleotide polymorphisms (SNP) can serve as prognostic factors for prostate cancer

Major finding: In patients with prostate cancer, SNP rs2910164 of miR146a was more common in patients with a Gleason score of 7 or higher than those with a Gleason score of less than 7 (P=0.043); in addition, SNP rs1834306 of miR100 was overexpressed in those with pT3 staging compared to pT2 (P = 0.004).

Study details: The data come from a review of 100 patients with clinically localized prostate cancer who underwent radical prostatectomy and 68 controls without prostate cancer.

Disclosures: The study was supported in part by a grant from the Sao Paulo Research Foundation. The researchers had no financial conflicts to disclose.

Source: Camargo JA et al. Int J Biol Markers. 2021 May 25. doi: 10.1177/172460082199746.

Key clinical point: Increased bone involvement was negatively correlated with overall survival after radioligand therapy for prostate cancer.

Major finding: The median overall survival for prostate cancer patients with less than 6 bone lesions, 6-20 lesions, more than 20 lesions, and diffuse lesions was 18 months, 13 months, 11 months, and 8 months, respectively.

Study details: The data come from 319 men with progressive metastatic castration-resistant prostate cancer who underwent radioligand therapy with lutetium prostate-specific membrane antigen (Lu-PSMA-617).

Disclosures: The study received no outside funding. The researchers had no financial conflicts to disclose.

Source: Ahmadzadehfar H et al. Eur J Nucl Med Mol Imaging. 2021 May 25. doi: 10.1007/s00259-021-05383-3.

Key clinical point: Increased bone involvement was negatively correlated with overall survival after radioligand therapy for prostate cancer.

Major finding: The median overall survival for prostate cancer patients with less than 6 bone lesions, 6-20 lesions, more than 20 lesions, and diffuse lesions was 18 months, 13 months, 11 months, and 8 months, respectively.

Study details: The data come from 319 men with progressive metastatic castration-resistant prostate cancer who underwent radioligand therapy with lutetium prostate-specific membrane antigen (Lu-PSMA-617).

Disclosures: The study received no outside funding. The researchers had no financial conflicts to disclose.

Source: Ahmadzadehfar H et al. Eur J Nucl Med Mol Imaging. 2021 May 25. doi: 10.1007/s00259-021-05383-3.

Key clinical point: Increased bone involvement was negatively correlated with overall survival after radioligand therapy for prostate cancer.

Major finding: The median overall survival for prostate cancer patients with less than 6 bone lesions, 6-20 lesions, more than 20 lesions, and diffuse lesions was 18 months, 13 months, 11 months, and 8 months, respectively.

Study details: The data come from 319 men with progressive metastatic castration-resistant prostate cancer who underwent radioligand therapy with lutetium prostate-specific membrane antigen (Lu-PSMA-617).

Disclosures: The study received no outside funding. The researchers had no financial conflicts to disclose.

Source: Ahmadzadehfar H et al. Eur J Nucl Med Mol Imaging. 2021 May 25. doi: 10.1007/s00259-021-05383-3.

Key clinical point: The Polygenic Hazard Score (PHS2) was effective for risk-stratifying men for prostate cancer in a large, multiethnic data set.

Major finding: The Polygenic Hazard Score (PHS2) indicated hazard ratios for prostate cancer, aggressive cancer, and prostate cancer-specific death of 5.32, 5.88, and 5.68, respectively, when researchers compared the 80^th and 20^th PHS2 percentiles.

Study details: The data come from 80,491 men enrolled in the OncoArray genetic project; researchers tested the polygenic hazard score (PHS2, adapted for OncoArray) for association with age at diagnosis of any and aggressive prostate cancer.

Disclosures: The study was supported in part by the National Institutes of Health/National Institute of Biomedical Imaging and Bioengineering, the United States Department of Defense, the University of California, the Research Council of Norway, K.G. Jebsen Stiftelsen, and South East Norway Health Authority. Lead author Dr. Huynh-Le had no financial conflicts to disclose.

Source: Huynh-Le M-P et al. Nat Commun. 2021 Feb 23. doi: 10.1038/s41467-021-21287-0.

Key clinical point: The Polygenic Hazard Score (PHS2) was effective for risk-stratifying men for prostate cancer in a large, multiethnic data set.

Major finding: The Polygenic Hazard Score (PHS2) indicated hazard ratios for prostate cancer, aggressive cancer, and prostate cancer-specific death of 5.32, 5.88, and 5.68, respectively, when researchers compared the 80^th and 20^th PHS2 percentiles.

Study details: The data come from 80,491 men enrolled in the OncoArray genetic project; researchers tested the polygenic hazard score (PHS2, adapted for OncoArray) for association with age at diagnosis of any and aggressive prostate cancer.

Disclosures: The study was supported in part by the National Institutes of Health/National Institute of Biomedical Imaging and Bioengineering, the United States Department of Defense, the University of California, the Research Council of Norway, K.G. Jebsen Stiftelsen, and South East Norway Health Authority. Lead author Dr. Huynh-Le had no financial conflicts to disclose.

Source: Huynh-Le M-P et al. Nat Commun. 2021 Feb 23. doi: 10.1038/s41467-021-21287-0.

Key clinical point: The Polygenic Hazard Score (PHS2) was effective for risk-stratifying men for prostate cancer in a large, multiethnic data set.

Major finding: The Polygenic Hazard Score (PHS2) indicated hazard ratios for prostate cancer, aggressive cancer, and prostate cancer-specific death of 5.32, 5.88, and 5.68, respectively, when researchers compared the 80^th and 20^th PHS2 percentiles.

Study details: The data come from 80,491 men enrolled in the OncoArray genetic project; researchers tested the polygenic hazard score (PHS2, adapted for OncoArray) for association with age at diagnosis of any and aggressive prostate cancer.

Disclosures: The study was supported in part by the National Institutes of Health/National Institute of Biomedical Imaging and Bioengineering, the United States Department of Defense, the University of California, the Research Council of Norway, K.G. Jebsen Stiftelsen, and South East Norway Health Authority. Lead author Dr. Huynh-Le had no financial conflicts to disclose.

Source: Huynh-Le M-P et al. Nat Commun. 2021 Feb 23. doi: 10.1038/s41467-021-21287-0.

Key clinical point: Increased use of PSA testing and diagnostic activity increased the number of men diagnosed with low and intermediate-risk prostate cancer.

Major finding: The number of men diagnosed with prostate cancer increased by 48% in the high diagnostic activity model compared to the low diagnostic activity model (423 cases per 100,000 me per year vs. 286 cases per 100,000 men per year). 

Study details: The data come from a cohort study of 188,884 men aged 64-77 years diagnosed with prostate cancer between 1996 and 2016 in Sweden. The researchers used a simulation model to compare scenarios of high and low diagnostic activity for prostate cancer.

Disclosures: The study was funded by the Swedish Cancer Society. The researchers had no financial conflicts to disclose.

Source: Bergengren O et al. JAMA Netw Open. 2021 May 17. doi: 10.1001/jamanetworkopen.2021.9444.

Key clinical point: Increased use of PSA testing and diagnostic activity increased the number of men diagnosed with low and intermediate-risk prostate cancer.

Major finding: The number of men diagnosed with prostate cancer increased by 48% in the high diagnostic activity model compared to the low diagnostic activity model (423 cases per 100,000 me per year vs. 286 cases per 100,000 men per year). 

Study details: The data come from a cohort study of 188,884 men aged 64-77 years diagnosed with prostate cancer between 1996 and 2016 in Sweden. The researchers used a simulation model to compare scenarios of high and low diagnostic activity for prostate cancer.

Disclosures: The study was funded by the Swedish Cancer Society. The researchers had no financial conflicts to disclose.

Source: Bergengren O et al. JAMA Netw Open. 2021 May 17. doi: 10.1001/jamanetworkopen.2021.9444.

Key clinical point: Increased use of PSA testing and diagnostic activity increased the number of men diagnosed with low and intermediate-risk prostate cancer.

Major finding: The number of men diagnosed with prostate cancer increased by 48% in the high diagnostic activity model compared to the low diagnostic activity model (423 cases per 100,000 me per year vs. 286 cases per 100,000 men per year). 

Study details: The data come from a cohort study of 188,884 men aged 64-77 years diagnosed with prostate cancer between 1996 and 2016 in Sweden. The researchers used a simulation model to compare scenarios of high and low diagnostic activity for prostate cancer.

Disclosures: The study was funded by the Swedish Cancer Society. The researchers had no financial conflicts to disclose.

Source: Bergengren O et al. JAMA Netw Open. 2021 May 17. doi: 10.1001/jamanetworkopen.2021.9444.

Key clinical point: Treatment with lutetium prostate-specific membrane antigen (Lu-PSMA) therapy at 6.0 GBq and 7.4 GBq yielded similar PSA response rates and overall survival for patients with progressive metastatic castrate resistant prostate cancer.

Major finding: The primary endpoint of PSA response of at least a 50% reduction from baseline after 2 treatment cycles was met in 28% of the whole cohort, and 46% and 19%, respectively, for treatment regimens of 6.0 GBq and 7.4 GBq.

Study details: The data come from a prospective, phase II trial of 71 men with progressive, metastatic castrate resistant prostate cancer. The patients were randomized to Lu-PSMA therapy at doses of either 6.0 vs 7.4 GBq.

Disclosures: The original study was supported by Endocyte. The researchers had no financial conflicts to disclose.  

Source: Calais J. et al. J Nucl Med. 2021 May 20. doi: 10.2967/jnumed.121.261982.

Key clinical point: Treatment with lutetium prostate-specific membrane antigen (Lu-PSMA) therapy at 6.0 GBq and 7.4 GBq yielded similar PSA response rates and overall survival for patients with progressive metastatic castrate resistant prostate cancer.

Major finding: The primary endpoint of PSA response of at least a 50% reduction from baseline after 2 treatment cycles was met in 28% of the whole cohort, and 46% and 19%, respectively, for treatment regimens of 6.0 GBq and 7.4 GBq.

Study details: The data come from a prospective, phase II trial of 71 men with progressive, metastatic castrate resistant prostate cancer. The patients were randomized to Lu-PSMA therapy at doses of either 6.0 vs 7.4 GBq.

Disclosures: The original study was supported by Endocyte. The researchers had no financial conflicts to disclose.  

Source: Calais J. et al. J Nucl Med. 2021 May 20. doi: 10.2967/jnumed.121.261982.

Key clinical point: Treatment with lutetium prostate-specific membrane antigen (Lu-PSMA) therapy at 6.0 GBq and 7.4 GBq yielded similar PSA response rates and overall survival for patients with progressive metastatic castrate resistant prostate cancer.

Major finding: The primary endpoint of PSA response of at least a 50% reduction from baseline after 2 treatment cycles was met in 28% of the whole cohort, and 46% and 19%, respectively, for treatment regimens of 6.0 GBq and 7.4 GBq.

Study details: The data come from a prospective, phase II trial of 71 men with progressive, metastatic castrate resistant prostate cancer. The patients were randomized to Lu-PSMA therapy at doses of either 6.0 vs 7.4 GBq.

Disclosures: The original study was supported by Endocyte. The researchers had no financial conflicts to disclose.  

Source: Calais J. et al. J Nucl Med. 2021 May 20. doi: 10.2967/jnumed.121.261982.