High levels of lipoprotein(a) increase the risk for incident cardiovascular disease (CVD) for hypertensive individuals but not for those without hypertension, a new MESA analysis suggests.

There are ways to test for statistical interaction, “in this case, multiplicative interaction between Lp(a) and hypertension, which suggests that Lp(a) is actually modifying the effect between blood pressure and cardiovascular disease. It’s not simply additive,” senior author Michael D. Shapiro, DO, Wake Forest University, Winston-Salem, N.C., told this news organization.

“So that’s new and I don’t think anybody’s looked at that before.”

Although Lp(a) is recognized as an independent cause of atherosclerotic CVD (ASCVD), the significance of Lp(a) in hypertension has been “virtually untapped,” he noted. A recent prospective study reported that elevated CVD risk was present only in individuals with Lp(a) ≥ 30 mg/dL and hypertension but it included only Chinese participants with stable coronary artery disease.

The current analysis, published online in the journal Hypertension, included 6,674 participants in the ongoing Multi-Ethnic Study of Atherosclerosis (MESA), all free of baseline ASCVD, who were recruited from six communities in the United States and had measured baseline Lp(a), blood pressure, and CVD events data over follow-up from 2000 to 2018.

Participants were stratified into four groups based on the presence or absence of hypertension (defined as 140/90 mm Hg or higher or the use of antihypertensive drugs) and an Lp(a) threshold of 50 mg/dL, as recommended by the American College of Cardiology/American Heart Association cholesterol guideline for consideration as an ASCVD risk-enhancing factor.

Slightly more than half of participants were female (52.8%), 38.6% were White, 27.5% were African American, 22.1% were Hispanic, and 11.9% were Chinese American.

According to the researchers, 809 participants had a CVD event over an average follow-up of 13.9 years, including 7.7% of group 1 with Lp(a) < 50 mg/dL and no hypertension, 8.0% of group 2 with Lp(a) ≥ 50 mg/dL and no hypertension, 16.2% of group 3 with Lp(a) < 50 mg/dL and hypertension, and 18.8% of group 4 with Lp(a) ≥ 50 mg/dL and hypertension.

When compared with group 1 in a fully adjusted Cox proportional model, participants with elevated Lp(a) and no hypertension (group 2) did not have an increased risk of CVD events (hazard ratio [HR], 1.09; 95% confidence interval [CI], 0.79-1.50).

CVD risk, however, was significantly higher in group 3 with normal Lp(a) and hypertension (HR, 1.66; 95% CI, 1.39-1.98) and group 4 with elevated Lp(a) and hypertension (HR, 2.07, 95% CI, 1.63-2.62).

Among all participants with hypertension (groups 3 and 4), Lp(a) was associated with a significant increase in CVD risk (HR, 1.24, 95% CI, 1.01-1.53).

“What I think is interesting here is that in the absence of hypertension, we didn’t really see an increased risk despite having an elevated Lp(a),” said Dr. Shapiro. “What it may indicate is that really for Lp(a) to be associated with risk, there may already need to be some kind of arterial damage that allows the Lp(a) to have its atherogenic impact.

“In other words, in individuals who have totally normal arterial walls, potentially, maybe that is protective enough against Lp(a) that in the absence of any other injurious factor, maybe it’s not an issue,” he said. “That’s a big hypothesis-generating [statement], but hypertension is certainly one of those risk factors that’s known to cause endothelial injury and endothelial dysfunction.”

Dr. Shapiro pointed out that when first measured in MESA, Lp(a) was measured in 4,600 participants who were not on statins, which is important because statins can increase Lp(a) levels.

“When you look just at those participants, those 4,600, you actually do see a relationship between Lp(a) and cardiovascular disease,” he said. “When you look at the whole population, including the 17% who are baseline populations, even when you adjust for statin therapy, we fail to see that, at least in the long-term follow up.”

Nevertheless, he cautioned that hypertension is just one of many traditional cardiovascular risk factors that could affect the relationship between Lp(a) and CVD risk. “I don’t want to suggest that we believe there’s something specifically magical about hypertension and Lp(a). If we chose, say, diabetes or smoking or another traditional risk factor, we may or may not have seen kind of similar results.”

When the investigators stratified the analyses by sex and race/ethnicity, they found that Lp(a) was not associated with CVD risk, regardless of hypertension status. In Black participants, however, greater CVD risk was seen when both elevated Lp(a) and hypertension were present (HR, 2.07, 95% CI, 1.34-3.21; P = .001).

Asked whether the results support one-time universal screening for Lp(a), which is almost exclusively genetically determined, Dr. Shapiro said he supports screening but that this was a secondary analysis and its numbers were modest. He added that median Lp(a) level is higher in African Americans than any other racial/ethnic group but the “most recent data has clarified that, per any absolute level of Lp(a), it appears to confer the same absolute risk in any racial or ethnic group.”

The authors acknowledge that differential loss to follow-up could have resulted in selection bias in the study and that there were relatively few CVD events in group 2, which may have limited the ability to detect differences in groups without hypertension, particularly in the subgroup analyses. Other limitations are the potential for residual confounding and participants may have developed hypertension during follow-up, resulting in misclassification bias.

Further research is needed to better understand the mechanistic link between Lp(a), hypertension, and CVD, Dr. Shapiro said. Further insights also should be provided by the ongoing phase 3 Lp(a) HORIZON trial evaluating the effect of Lp(a) lowering with the investigational antisense drug, pelacarsen, on cardiovascular events in 8,324 patients with established CVD and elevated Lp(a). The study is expected to be completed in May 2025.

The study was supported by contracts from the National Heart, Lung, and Blood Institute and by grants from the National Center for Advanced Translational Sciences. Dr. Shapiro reports participating in scientific advisory boards with Amgen, Novartis, and Novo Nordisk, and consulting for Regeneron.

A version of this article first appeared on Medscape.com.

High levels of lipoprotein(a) increase the risk for incident cardiovascular disease (CVD) for hypertensive individuals but not for those without hypertension, a new MESA analysis suggests.

There are ways to test for statistical interaction, “in this case, multiplicative interaction between Lp(a) and hypertension, which suggests that Lp(a) is actually modifying the effect between blood pressure and cardiovascular disease. It’s not simply additive,” senior author Michael D. Shapiro, DO, Wake Forest University, Winston-Salem, N.C., told this news organization.

“So that’s new and I don’t think anybody’s looked at that before.”

Although Lp(a) is recognized as an independent cause of atherosclerotic CVD (ASCVD), the significance of Lp(a) in hypertension has been “virtually untapped,” he noted. A recent prospective study reported that elevated CVD risk was present only in individuals with Lp(a) ≥ 30 mg/dL and hypertension but it included only Chinese participants with stable coronary artery disease.

The current analysis, published online in the journal Hypertension, included 6,674 participants in the ongoing Multi-Ethnic Study of Atherosclerosis (MESA), all free of baseline ASCVD, who were recruited from six communities in the United States and had measured baseline Lp(a), blood pressure, and CVD events data over follow-up from 2000 to 2018.

Participants were stratified into four groups based on the presence or absence of hypertension (defined as 140/90 mm Hg or higher or the use of antihypertensive drugs) and an Lp(a) threshold of 50 mg/dL, as recommended by the American College of Cardiology/American Heart Association cholesterol guideline for consideration as an ASCVD risk-enhancing factor.

Slightly more than half of participants were female (52.8%), 38.6% were White, 27.5% were African American, 22.1% were Hispanic, and 11.9% were Chinese American.

According to the researchers, 809 participants had a CVD event over an average follow-up of 13.9 years, including 7.7% of group 1 with Lp(a) < 50 mg/dL and no hypertension, 8.0% of group 2 with Lp(a) ≥ 50 mg/dL and no hypertension, 16.2% of group 3 with Lp(a) < 50 mg/dL and hypertension, and 18.8% of group 4 with Lp(a) ≥ 50 mg/dL and hypertension.

When compared with group 1 in a fully adjusted Cox proportional model, participants with elevated Lp(a) and no hypertension (group 2) did not have an increased risk of CVD events (hazard ratio [HR], 1.09; 95% confidence interval [CI], 0.79-1.50).

CVD risk, however, was significantly higher in group 3 with normal Lp(a) and hypertension (HR, 1.66; 95% CI, 1.39-1.98) and group 4 with elevated Lp(a) and hypertension (HR, 2.07, 95% CI, 1.63-2.62).

Among all participants with hypertension (groups 3 and 4), Lp(a) was associated with a significant increase in CVD risk (HR, 1.24, 95% CI, 1.01-1.53).

“What I think is interesting here is that in the absence of hypertension, we didn’t really see an increased risk despite having an elevated Lp(a),” said Dr. Shapiro. “What it may indicate is that really for Lp(a) to be associated with risk, there may already need to be some kind of arterial damage that allows the Lp(a) to have its atherogenic impact.

“In other words, in individuals who have totally normal arterial walls, potentially, maybe that is protective enough against Lp(a) that in the absence of any other injurious factor, maybe it’s not an issue,” he said. “That’s a big hypothesis-generating [statement], but hypertension is certainly one of those risk factors that’s known to cause endothelial injury and endothelial dysfunction.”

Dr. Shapiro pointed out that when first measured in MESA, Lp(a) was measured in 4,600 participants who were not on statins, which is important because statins can increase Lp(a) levels.

“When you look just at those participants, those 4,600, you actually do see a relationship between Lp(a) and cardiovascular disease,” he said. “When you look at the whole population, including the 17% who are baseline populations, even when you adjust for statin therapy, we fail to see that, at least in the long-term follow up.”

Nevertheless, he cautioned that hypertension is just one of many traditional cardiovascular risk factors that could affect the relationship between Lp(a) and CVD risk. “I don’t want to suggest that we believe there’s something specifically magical about hypertension and Lp(a). If we chose, say, diabetes or smoking or another traditional risk factor, we may or may not have seen kind of similar results.”

When the investigators stratified the analyses by sex and race/ethnicity, they found that Lp(a) was not associated with CVD risk, regardless of hypertension status. In Black participants, however, greater CVD risk was seen when both elevated Lp(a) and hypertension were present (HR, 2.07, 95% CI, 1.34-3.21; P = .001).

Asked whether the results support one-time universal screening for Lp(a), which is almost exclusively genetically determined, Dr. Shapiro said he supports screening but that this was a secondary analysis and its numbers were modest. He added that median Lp(a) level is higher in African Americans than any other racial/ethnic group but the “most recent data has clarified that, per any absolute level of Lp(a), it appears to confer the same absolute risk in any racial or ethnic group.”

The authors acknowledge that differential loss to follow-up could have resulted in selection bias in the study and that there were relatively few CVD events in group 2, which may have limited the ability to detect differences in groups without hypertension, particularly in the subgroup analyses. Other limitations are the potential for residual confounding and participants may have developed hypertension during follow-up, resulting in misclassification bias.

Further research is needed to better understand the mechanistic link between Lp(a), hypertension, and CVD, Dr. Shapiro said. Further insights also should be provided by the ongoing phase 3 Lp(a) HORIZON trial evaluating the effect of Lp(a) lowering with the investigational antisense drug, pelacarsen, on cardiovascular events in 8,324 patients with established CVD and elevated Lp(a). The study is expected to be completed in May 2025.

The study was supported by contracts from the National Heart, Lung, and Blood Institute and by grants from the National Center for Advanced Translational Sciences. Dr. Shapiro reports participating in scientific advisory boards with Amgen, Novartis, and Novo Nordisk, and consulting for Regeneron.

A version of this article first appeared on Medscape.com.

High levels of lipoprotein(a) increase the risk for incident cardiovascular disease (CVD) for hypertensive individuals but not for those without hypertension, a new MESA analysis suggests.

There are ways to test for statistical interaction, “in this case, multiplicative interaction between Lp(a) and hypertension, which suggests that Lp(a) is actually modifying the effect between blood pressure and cardiovascular disease. It’s not simply additive,” senior author Michael D. Shapiro, DO, Wake Forest University, Winston-Salem, N.C., told this news organization.

“So that’s new and I don’t think anybody’s looked at that before.”

Although Lp(a) is recognized as an independent cause of atherosclerotic CVD (ASCVD), the significance of Lp(a) in hypertension has been “virtually untapped,” he noted. A recent prospective study reported that elevated CVD risk was present only in individuals with Lp(a) ≥ 30 mg/dL and hypertension but it included only Chinese participants with stable coronary artery disease.

The current analysis, published online in the journal Hypertension, included 6,674 participants in the ongoing Multi-Ethnic Study of Atherosclerosis (MESA), all free of baseline ASCVD, who were recruited from six communities in the United States and had measured baseline Lp(a), blood pressure, and CVD events data over follow-up from 2000 to 2018.

Participants were stratified into four groups based on the presence or absence of hypertension (defined as 140/90 mm Hg or higher or the use of antihypertensive drugs) and an Lp(a) threshold of 50 mg/dL, as recommended by the American College of Cardiology/American Heart Association cholesterol guideline for consideration as an ASCVD risk-enhancing factor.

Slightly more than half of participants were female (52.8%), 38.6% were White, 27.5% were African American, 22.1% were Hispanic, and 11.9% were Chinese American.

According to the researchers, 809 participants had a CVD event over an average follow-up of 13.9 years, including 7.7% of group 1 with Lp(a) < 50 mg/dL and no hypertension, 8.0% of group 2 with Lp(a) ≥ 50 mg/dL and no hypertension, 16.2% of group 3 with Lp(a) < 50 mg/dL and hypertension, and 18.8% of group 4 with Lp(a) ≥ 50 mg/dL and hypertension.

When compared with group 1 in a fully adjusted Cox proportional model, participants with elevated Lp(a) and no hypertension (group 2) did not have an increased risk of CVD events (hazard ratio [HR], 1.09; 95% confidence interval [CI], 0.79-1.50).

CVD risk, however, was significantly higher in group 3 with normal Lp(a) and hypertension (HR, 1.66; 95% CI, 1.39-1.98) and group 4 with elevated Lp(a) and hypertension (HR, 2.07, 95% CI, 1.63-2.62).

Among all participants with hypertension (groups 3 and 4), Lp(a) was associated with a significant increase in CVD risk (HR, 1.24, 95% CI, 1.01-1.53).

“What I think is interesting here is that in the absence of hypertension, we didn’t really see an increased risk despite having an elevated Lp(a),” said Dr. Shapiro. “What it may indicate is that really for Lp(a) to be associated with risk, there may already need to be some kind of arterial damage that allows the Lp(a) to have its atherogenic impact.

“In other words, in individuals who have totally normal arterial walls, potentially, maybe that is protective enough against Lp(a) that in the absence of any other injurious factor, maybe it’s not an issue,” he said. “That’s a big hypothesis-generating [statement], but hypertension is certainly one of those risk factors that’s known to cause endothelial injury and endothelial dysfunction.”

Dr. Shapiro pointed out that when first measured in MESA, Lp(a) was measured in 4,600 participants who were not on statins, which is important because statins can increase Lp(a) levels.

“When you look just at those participants, those 4,600, you actually do see a relationship between Lp(a) and cardiovascular disease,” he said. “When you look at the whole population, including the 17% who are baseline populations, even when you adjust for statin therapy, we fail to see that, at least in the long-term follow up.”

Nevertheless, he cautioned that hypertension is just one of many traditional cardiovascular risk factors that could affect the relationship between Lp(a) and CVD risk. “I don’t want to suggest that we believe there’s something specifically magical about hypertension and Lp(a). If we chose, say, diabetes or smoking or another traditional risk factor, we may or may not have seen kind of similar results.”

When the investigators stratified the analyses by sex and race/ethnicity, they found that Lp(a) was not associated with CVD risk, regardless of hypertension status. In Black participants, however, greater CVD risk was seen when both elevated Lp(a) and hypertension were present (HR, 2.07, 95% CI, 1.34-3.21; P = .001).

Asked whether the results support one-time universal screening for Lp(a), which is almost exclusively genetically determined, Dr. Shapiro said he supports screening but that this was a secondary analysis and its numbers were modest. He added that median Lp(a) level is higher in African Americans than any other racial/ethnic group but the “most recent data has clarified that, per any absolute level of Lp(a), it appears to confer the same absolute risk in any racial or ethnic group.”

The authors acknowledge that differential loss to follow-up could have resulted in selection bias in the study and that there were relatively few CVD events in group 2, which may have limited the ability to detect differences in groups without hypertension, particularly in the subgroup analyses. Other limitations are the potential for residual confounding and participants may have developed hypertension during follow-up, resulting in misclassification bias.

Further research is needed to better understand the mechanistic link between Lp(a), hypertension, and CVD, Dr. Shapiro said. Further insights also should be provided by the ongoing phase 3 Lp(a) HORIZON trial evaluating the effect of Lp(a) lowering with the investigational antisense drug, pelacarsen, on cardiovascular events in 8,324 patients with established CVD and elevated Lp(a). The study is expected to be completed in May 2025.

The study was supported by contracts from the National Heart, Lung, and Blood Institute and by grants from the National Center for Advanced Translational Sciences. Dr. Shapiro reports participating in scientific advisory boards with Amgen, Novartis, and Novo Nordisk, and consulting for Regeneron.

A version of this article first appeared on Medscape.com.

Key clinical point: Chronic exposure to heavy metals was not associated with an increased risk for breast cancer (BC) among never smokers in the general population.

Major finding: Serum levels of cobalt were inversely associated with the risk for BC (odds ratio 0.33; P = .033), with no association being observed between the risk for BC and exposure to other heavy metals.

Study details: Findings are from a prospective cohort study including 150 women with BC and without a smoking history and 150 matched control women without BC and smoking history.

Disclosures: This study was supported by the Tuscany Region, “Bando Ricerca Salute 2018.” The authors declared no conflicts of interest.

Source: Caini S et al. Serum heavy metals and breast cancer risk: A case-control study nested in the Florence cohort of the EPIC (European Prospective Investigation into Cancer and nutrition) study. Sci Total Environ. 2022;160568 (Dec 1). Doi: 10.1016/j.scitotenv.2022.160568

Key clinical point: Chronic exposure to heavy metals was not associated with an increased risk for breast cancer (BC) among never smokers in the general population.

Major finding: Serum levels of cobalt were inversely associated with the risk for BC (odds ratio 0.33; P = .033), with no association being observed between the risk for BC and exposure to other heavy metals.

Study details: Findings are from a prospective cohort study including 150 women with BC and without a smoking history and 150 matched control women without BC and smoking history.

Disclosures: This study was supported by the Tuscany Region, “Bando Ricerca Salute 2018.” The authors declared no conflicts of interest.

Source: Caini S et al. Serum heavy metals and breast cancer risk: A case-control study nested in the Florence cohort of the EPIC (European Prospective Investigation into Cancer and nutrition) study. Sci Total Environ. 2022;160568 (Dec 1). Doi: 10.1016/j.scitotenv.2022.160568

Key clinical point: Chronic exposure to heavy metals was not associated with an increased risk for breast cancer (BC) among never smokers in the general population.

Major finding: Serum levels of cobalt were inversely associated with the risk for BC (odds ratio 0.33; P = .033), with no association being observed between the risk for BC and exposure to other heavy metals.

Study details: Findings are from a prospective cohort study including 150 women with BC and without a smoking history and 150 matched control women without BC and smoking history.

Disclosures: This study was supported by the Tuscany Region, “Bando Ricerca Salute 2018.” The authors declared no conflicts of interest.

Source: Caini S et al. Serum heavy metals and breast cancer risk: A case-control study nested in the Florence cohort of the EPIC (European Prospective Investigation into Cancer and nutrition) study. Sci Total Environ. 2022;160568 (Dec 1). Doi: 10.1016/j.scitotenv.2022.160568

Key clinical point: Patients with human epidermal growth factor receptor 2-positive (HER2+) metastatic breast cancer (BC) who had an isolated brain metastasis as their first metastatic event reported worse survival outcomes than those with concurrent progressive or stable/responding extracranial disease (ECD).

Major finding: Patients with isolated brain relapse or no evidence of ECD (28.4 months; P = .0028) reported worse overall survival from metastatic diagnosis to death than patients with concurrent progressive ECD (48.8 months) or stable/responding disease (71.5 months).

Study details: Findings are from a retrospective analysis including 126 patients with HER2+ BC, brain metastasis, and known ECD status.

Disclosures: This study was funded by the Duke University Department of Medicine and other sources. Some authors declared receiving royalties or serving as consultants at various sources.

Source: Noteware L et al. Brain metastasis as the first and only metastatic relapse site portends worse survival in patients with advanced HER2 + breast cancer. Breast Cancer Res Treat. 2022 (Nov 20). Doi: 10.1007/s10549-022-06799-7

Key clinical point: Patients with human epidermal growth factor receptor 2-positive (HER2+) metastatic breast cancer (BC) who had an isolated brain metastasis as their first metastatic event reported worse survival outcomes than those with concurrent progressive or stable/responding extracranial disease (ECD).

Major finding: Patients with isolated brain relapse or no evidence of ECD (28.4 months; P = .0028) reported worse overall survival from metastatic diagnosis to death than patients with concurrent progressive ECD (48.8 months) or stable/responding disease (71.5 months).

Study details: Findings are from a retrospective analysis including 126 patients with HER2+ BC, brain metastasis, and known ECD status.

Disclosures: This study was funded by the Duke University Department of Medicine and other sources. Some authors declared receiving royalties or serving as consultants at various sources.

Source: Noteware L et al. Brain metastasis as the first and only metastatic relapse site portends worse survival in patients with advanced HER2 + breast cancer. Breast Cancer Res Treat. 2022 (Nov 20). Doi: 10.1007/s10549-022-06799-7

Key clinical point: Patients with human epidermal growth factor receptor 2-positive (HER2+) metastatic breast cancer (BC) who had an isolated brain metastasis as their first metastatic event reported worse survival outcomes than those with concurrent progressive or stable/responding extracranial disease (ECD).

Major finding: Patients with isolated brain relapse or no evidence of ECD (28.4 months; P = .0028) reported worse overall survival from metastatic diagnosis to death than patients with concurrent progressive ECD (48.8 months) or stable/responding disease (71.5 months).

Study details: Findings are from a retrospective analysis including 126 patients with HER2+ BC, brain metastasis, and known ECD status.

Disclosures: This study was funded by the Duke University Department of Medicine and other sources. Some authors declared receiving royalties or serving as consultants at various sources.

Source: Noteware L et al. Brain metastasis as the first and only metastatic relapse site portends worse survival in patients with advanced HER2 + breast cancer. Breast Cancer Res Treat. 2022 (Nov 20). Doi: 10.1007/s10549-022-06799-7

Key clinical point: Breast conserving surgery (BCS) plus radiotherapy (RT) demonstrated superior survival outcomes compared to mastectomy in patients with ductal carcinoma in situ with microinvasion (DCIS-MI).

Major finding: Overall survival (hazard ratio [HR] 0.676; P < .001) and breast cancer-specific survival (HR 0.565; P = .017) were significantly improved in the BCS+RT vs mastectomy group.

Study details: This study analyzed the data of 5432 patients with DCIS-MI from the Surveillance, Epidemiology, and End Results (SEER) database, of which 52.17% of patients had received BCS+RT.

Disclosures: This study did not report a source of funding. The authors declared no conflicts of interest.

Source: Xia LY et al. Survival outcomes after breast-conserving surgery plus radiotherapy compared with mastectomy in breast ductal carcinoma in situ with microinvasion. Sci Rep. 2022;12:20132 (Nov 22). Doi: 10.1038/s41598-022-24630-7

Key clinical point: Breast conserving surgery (BCS) plus radiotherapy (RT) demonstrated superior survival outcomes compared to mastectomy in patients with ductal carcinoma in situ with microinvasion (DCIS-MI).

Major finding: Overall survival (hazard ratio [HR] 0.676; P < .001) and breast cancer-specific survival (HR 0.565; P = .017) were significantly improved in the BCS+RT vs mastectomy group.

Study details: This study analyzed the data of 5432 patients with DCIS-MI from the Surveillance, Epidemiology, and End Results (SEER) database, of which 52.17% of patients had received BCS+RT.

Disclosures: This study did not report a source of funding. The authors declared no conflicts of interest.

Source: Xia LY et al. Survival outcomes after breast-conserving surgery plus radiotherapy compared with mastectomy in breast ductal carcinoma in situ with microinvasion. Sci Rep. 2022;12:20132 (Nov 22). Doi: 10.1038/s41598-022-24630-7

Key clinical point: Breast conserving surgery (BCS) plus radiotherapy (RT) demonstrated superior survival outcomes compared to mastectomy in patients with ductal carcinoma in situ with microinvasion (DCIS-MI).

Major finding: Overall survival (hazard ratio [HR] 0.676; P < .001) and breast cancer-specific survival (HR 0.565; P = .017) were significantly improved in the BCS+RT vs mastectomy group.

Study details: This study analyzed the data of 5432 patients with DCIS-MI from the Surveillance, Epidemiology, and End Results (SEER) database, of which 52.17% of patients had received BCS+RT.

Disclosures: This study did not report a source of funding. The authors declared no conflicts of interest.

Source: Xia LY et al. Survival outcomes after breast-conserving surgery plus radiotherapy compared with mastectomy in breast ductal carcinoma in situ with microinvasion. Sci Rep. 2022;12:20132 (Nov 22). Doi: 10.1038/s41598-022-24630-7

Key clinical point: Palbociclib plus endocrine therapy (ET) improved progression-free survival (PFS) across all subgroups of patients with hormone receptor-positive/human epidermal growth factor receptor 2-negative (HR+/HER2−) advanced breast cancer (BC).

Major finding: Median PFS was longer in patients receiving palbociclib+letrozole vs placebo+letrozole (hazard ratio [HR] 0.56; 95% CI 0.46-0.69) or palbociclib+fulvestrant vs placebo+fulvestrant (HR 0.50; 95% CI 0.40-0.62), with similar outcomes observed in subgroups of patients reporting a disease-free interval of ≤12 months, visceral disease, or ET resistance.

Study details: Findings are from a post hoc analysis of two phase 3 trials including women with HR+/HER2− advanced BC who were randomly assigned to receive letrozole with palbociclib or placebo (n = 666; PALOMA-2) or fulvestrant with palbociclib or placebo (n = 521; PALOMA-3).

Disclosures: This study was funded by Pfizer Inc. Four authors declared being employees and stockholders of Pfizer, and the other authors reported ties with several sources, including Pfizer.

Source: Rugo HS et al. Effect of palbociclib plus endocrine therapy on time to chemotherapy across subgroups of patients with hormone receptor‒positive/human epidermal growth factor receptor 2‒negative advanced breast cancer: Post hoc analyses from PALOMA-2 and PALOMA-3. Breast. 2022;66:324-331 (Nov 15). Doi: 10.1016/j.breast.2022.11.005

Key clinical point: Palbociclib plus endocrine therapy (ET) improved progression-free survival (PFS) across all subgroups of patients with hormone receptor-positive/human epidermal growth factor receptor 2-negative (HR+/HER2−) advanced breast cancer (BC).

Major finding: Median PFS was longer in patients receiving palbociclib+letrozole vs placebo+letrozole (hazard ratio [HR] 0.56; 95% CI 0.46-0.69) or palbociclib+fulvestrant vs placebo+fulvestrant (HR 0.50; 95% CI 0.40-0.62), with similar outcomes observed in subgroups of patients reporting a disease-free interval of ≤12 months, visceral disease, or ET resistance.

Study details: Findings are from a post hoc analysis of two phase 3 trials including women with HR+/HER2− advanced BC who were randomly assigned to receive letrozole with palbociclib or placebo (n = 666; PALOMA-2) or fulvestrant with palbociclib or placebo (n = 521; PALOMA-3).

Disclosures: This study was funded by Pfizer Inc. Four authors declared being employees and stockholders of Pfizer, and the other authors reported ties with several sources, including Pfizer.

Source: Rugo HS et al. Effect of palbociclib plus endocrine therapy on time to chemotherapy across subgroups of patients with hormone receptor‒positive/human epidermal growth factor receptor 2‒negative advanced breast cancer: Post hoc analyses from PALOMA-2 and PALOMA-3. Breast. 2022;66:324-331 (Nov 15). Doi: 10.1016/j.breast.2022.11.005

Key clinical point: Palbociclib plus endocrine therapy (ET) improved progression-free survival (PFS) across all subgroups of patients with hormone receptor-positive/human epidermal growth factor receptor 2-negative (HR+/HER2−) advanced breast cancer (BC).

Major finding: Median PFS was longer in patients receiving palbociclib+letrozole vs placebo+letrozole (hazard ratio [HR] 0.56; 95% CI 0.46-0.69) or palbociclib+fulvestrant vs placebo+fulvestrant (HR 0.50; 95% CI 0.40-0.62), with similar outcomes observed in subgroups of patients reporting a disease-free interval of ≤12 months, visceral disease, or ET resistance.

Study details: Findings are from a post hoc analysis of two phase 3 trials including women with HR+/HER2− advanced BC who were randomly assigned to receive letrozole with palbociclib or placebo (n = 666; PALOMA-2) or fulvestrant with palbociclib or placebo (n = 521; PALOMA-3).

Disclosures: This study was funded by Pfizer Inc. Four authors declared being employees and stockholders of Pfizer, and the other authors reported ties with several sources, including Pfizer.

Source: Rugo HS et al. Effect of palbociclib plus endocrine therapy on time to chemotherapy across subgroups of patients with hormone receptor‒positive/human epidermal growth factor receptor 2‒negative advanced breast cancer: Post hoc analyses from PALOMA-2 and PALOMA-3. Breast. 2022;66:324-331 (Nov 15). Doi: 10.1016/j.breast.2022.11.005

Key clinical point: Q-122, a novel nonhormonal oral treatment, significantly improved vasomotor symptoms and was well-tolerated in women with breast cancer (BC) who received oral adjuvant endocrine therapy (ET).

Major finding: After 28 days, Q-122 led to a significantly higher improvement in the mean Vasomotor Symptom Severity Score of moderate and severe hot flushes and night sweats than placebo (−39% vs −26%; P = .018). Q-122 was well tolerated, and most adverse events were mild-to-moderate in severity.

Study details: Findings are from a multicenter, phase 2 study including 131 women with BC who were receiving oral adjuvant ET and were randomly assigned to receive 100 mg oral Q-122 or identical placebo, twice daily for 28 days.

Disclosures: This study was funded by QUE Oncology. The authors declared delivering lectures or receiving honoraria, grant funding, or personal fees from several sources. Two authors declared being current or former employees of QUE Oncology.

Source: Vrselja A et al. Q-122 as a novel, non-hormonal, oral treatment for vasomotor symptoms in women taking tamoxifen or an aromatase inhibitor after breast cancer: A phase 2, randomised, double-blind, placebo-controlled trial. Lancet. 2022;400(10364):1704-1711 (Nov 12). Doi: 10.1016/S0140-6736(22)01977-8

Key clinical point: Q-122, a novel nonhormonal oral treatment, significantly improved vasomotor symptoms and was well-tolerated in women with breast cancer (BC) who received oral adjuvant endocrine therapy (ET).

Major finding: After 28 days, Q-122 led to a significantly higher improvement in the mean Vasomotor Symptom Severity Score of moderate and severe hot flushes and night sweats than placebo (−39% vs −26%; P = .018). Q-122 was well tolerated, and most adverse events were mild-to-moderate in severity.

Study details: Findings are from a multicenter, phase 2 study including 131 women with BC who were receiving oral adjuvant ET and were randomly assigned to receive 100 mg oral Q-122 or identical placebo, twice daily for 28 days.

Disclosures: This study was funded by QUE Oncology. The authors declared delivering lectures or receiving honoraria, grant funding, or personal fees from several sources. Two authors declared being current or former employees of QUE Oncology.

Source: Vrselja A et al. Q-122 as a novel, non-hormonal, oral treatment for vasomotor symptoms in women taking tamoxifen or an aromatase inhibitor after breast cancer: A phase 2, randomised, double-blind, placebo-controlled trial. Lancet. 2022;400(10364):1704-1711 (Nov 12). Doi: 10.1016/S0140-6736(22)01977-8

Key clinical point: Q-122, a novel nonhormonal oral treatment, significantly improved vasomotor symptoms and was well-tolerated in women with breast cancer (BC) who received oral adjuvant endocrine therapy (ET).

Major finding: After 28 days, Q-122 led to a significantly higher improvement in the mean Vasomotor Symptom Severity Score of moderate and severe hot flushes and night sweats than placebo (−39% vs −26%; P = .018). Q-122 was well tolerated, and most adverse events were mild-to-moderate in severity.

Study details: Findings are from a multicenter, phase 2 study including 131 women with BC who were receiving oral adjuvant ET and were randomly assigned to receive 100 mg oral Q-122 or identical placebo, twice daily for 28 days.

Disclosures: This study was funded by QUE Oncology. The authors declared delivering lectures or receiving honoraria, grant funding, or personal fees from several sources. Two authors declared being current or former employees of QUE Oncology.

Source: Vrselja A et al. Q-122 as a novel, non-hormonal, oral treatment for vasomotor symptoms in women taking tamoxifen or an aromatase inhibitor after breast cancer: A phase 2, randomised, double-blind, placebo-controlled trial. Lancet. 2022;400(10364):1704-1711 (Nov 12). Doi: 10.1016/S0140-6736(22)01977-8

Key clinical point: Margetuximab failed to demonstrate a survival advantage over trastuzumab in patients with previously treated human epidermal growth factor receptor 2-positive (HER2+) advanced breast cancer (BC).

Major finding: After a median follow-up of 20.2 months, no benefit in overall survival (OS) was observed with margetuximab vs trastuzumab (hazard ratio [HR] 0.95; P = .620). The safety profile of margetuximab was acceptable and comparable to that of trastuzumab.

Study details: Findings are from the phase 3 SOPHIA study including 536 patients with HER2+ advanced BC who received ≥2 prior anti-HER2 regimens and were randomly assigned to receive chemotherapy with margetuximab or trastuzumab.

Disclosures: This study was supported by MacroGenics, Inc. The authors declared serving as employees, consultants, or on speaker’s bureaus, holding stock options, or receiving honoraria, research funding, or travel or accommodation expenses from several sources, including MacroGenics.

Source: Rugo HS et al  on behalf of the SOPHIA Study Group. Margetuximab versus trastuzumab in patients with previously treated her2-positive advanced breast cancer (SOPHIA): Final overall survival results from a randomized phase 3 trial. J Clin Oncol. 2022 (Nov 4). Doi: 10.1200/JCO.21.02937

Key clinical point: Margetuximab failed to demonstrate a survival advantage over trastuzumab in patients with previously treated human epidermal growth factor receptor 2-positive (HER2+) advanced breast cancer (BC).

Major finding: After a median follow-up of 20.2 months, no benefit in overall survival (OS) was observed with margetuximab vs trastuzumab (hazard ratio [HR] 0.95; P = .620). The safety profile of margetuximab was acceptable and comparable to that of trastuzumab.

Study details: Findings are from the phase 3 SOPHIA study including 536 patients with HER2+ advanced BC who received ≥2 prior anti-HER2 regimens and were randomly assigned to receive chemotherapy with margetuximab or trastuzumab.

Disclosures: This study was supported by MacroGenics, Inc. The authors declared serving as employees, consultants, or on speaker’s bureaus, holding stock options, or receiving honoraria, research funding, or travel or accommodation expenses from several sources, including MacroGenics.

Source: Rugo HS et al  on behalf of the SOPHIA Study Group. Margetuximab versus trastuzumab in patients with previously treated her2-positive advanced breast cancer (SOPHIA): Final overall survival results from a randomized phase 3 trial. J Clin Oncol. 2022 (Nov 4). Doi: 10.1200/JCO.21.02937

Key clinical point: Margetuximab failed to demonstrate a survival advantage over trastuzumab in patients with previously treated human epidermal growth factor receptor 2-positive (HER2+) advanced breast cancer (BC).

Major finding: After a median follow-up of 20.2 months, no benefit in overall survival (OS) was observed with margetuximab vs trastuzumab (hazard ratio [HR] 0.95; P = .620). The safety profile of margetuximab was acceptable and comparable to that of trastuzumab.

Study details: Findings are from the phase 3 SOPHIA study including 536 patients with HER2+ advanced BC who received ≥2 prior anti-HER2 regimens and were randomly assigned to receive chemotherapy with margetuximab or trastuzumab.

Disclosures: This study was supported by MacroGenics, Inc. The authors declared serving as employees, consultants, or on speaker’s bureaus, holding stock options, or receiving honoraria, research funding, or travel or accommodation expenses from several sources, including MacroGenics.

Source: Rugo HS et al  on behalf of the SOPHIA Study Group. Margetuximab versus trastuzumab in patients with previously treated her2-positive advanced breast cancer (SOPHIA): Final overall survival results from a randomized phase 3 trial. J Clin Oncol. 2022 (Nov 4). Doi: 10.1200/JCO.21.02937

Key clinical point: The risk for uterine diseases was significantly increased in premenopausal women with breast cancer (BC) who received tamoxifen as an adjuvant hormone therapy.

Major finding: Compared with patients who did not receive adjuvant hormone therapy, those who received tamoxifen had a significantly higher risk for endometrial cancer (hazard ratio [HR] 3.77; 95% CI 3.04-4.66), endometrial polyps (HR 3.90; 95% CI 3.65-4.16), hyperplasia (HR 5.56; 95% CI 5.06-6.12), and other uterine cancers (HR 2.27; 95% CI 1.54-3.33).

Study details: Findings are from a nationwide, retrospective, longitudinal cohort study including 78,320 premenopausal women with BC who received (tamoxifen only; n = 34,637) or did not receive (n = 43,683) an adjuvant hormone treatment.

Disclosures: This study was supported by a National Research Foundation of Korea grant. The authors declared no conflicts of interest.

Source: Ryu KJ et al. Risk of endometrial polyps, hyperplasia, carcinoma, and uterine cancer after tamoxifen treatment in premenopausal women with breast cancer. JAMA Netw Open. 2022 5(11):e2243951 (Nov 28). Doi: 10.1001/jamanetworkopen.2022.43951

Key clinical point: The risk for uterine diseases was significantly increased in premenopausal women with breast cancer (BC) who received tamoxifen as an adjuvant hormone therapy.

Major finding: Compared with patients who did not receive adjuvant hormone therapy, those who received tamoxifen had a significantly higher risk for endometrial cancer (hazard ratio [HR] 3.77; 95% CI 3.04-4.66), endometrial polyps (HR 3.90; 95% CI 3.65-4.16), hyperplasia (HR 5.56; 95% CI 5.06-6.12), and other uterine cancers (HR 2.27; 95% CI 1.54-3.33).

Study details: Findings are from a nationwide, retrospective, longitudinal cohort study including 78,320 premenopausal women with BC who received (tamoxifen only; n = 34,637) or did not receive (n = 43,683) an adjuvant hormone treatment.

Disclosures: This study was supported by a National Research Foundation of Korea grant. The authors declared no conflicts of interest.

Source: Ryu KJ et al. Risk of endometrial polyps, hyperplasia, carcinoma, and uterine cancer after tamoxifen treatment in premenopausal women with breast cancer. JAMA Netw Open. 2022 5(11):e2243951 (Nov 28). Doi: 10.1001/jamanetworkopen.2022.43951

Key clinical point: The risk for uterine diseases was significantly increased in premenopausal women with breast cancer (BC) who received tamoxifen as an adjuvant hormone therapy.

Major finding: Compared with patients who did not receive adjuvant hormone therapy, those who received tamoxifen had a significantly higher risk for endometrial cancer (hazard ratio [HR] 3.77; 95% CI 3.04-4.66), endometrial polyps (HR 3.90; 95% CI 3.65-4.16), hyperplasia (HR 5.56; 95% CI 5.06-6.12), and other uterine cancers (HR 2.27; 95% CI 1.54-3.33).

Study details: Findings are from a nationwide, retrospective, longitudinal cohort study including 78,320 premenopausal women with BC who received (tamoxifen only; n = 34,637) or did not receive (n = 43,683) an adjuvant hormone treatment.

Disclosures: This study was supported by a National Research Foundation of Korea grant. The authors declared no conflicts of interest.

Source: Ryu KJ et al. Risk of endometrial polyps, hyperplasia, carcinoma, and uterine cancer after tamoxifen treatment in premenopausal women with breast cancer. JAMA Netw Open. 2022 5(11):e2243951 (Nov 28). Doi: 10.1001/jamanetworkopen.2022.43951

Key clinical point: The addition of weekly carboplatin to standard anthracycline-weekly paclitaxel-based neoadjuvant chemotherapy improved pathological complete response (pCR) rates in patients with triple-negative breast cancer (TNBC).

Major finding: The rate of pCR was significantly higher in the anthracycline-paclitaxel+carboplatin vs anthracycline-paclitaxel treatment group (51.9% vs 34.2%; odds ratio 2.40; P = .01); however, no significant differences were observed in grade ≥3 hematological toxicities between both groups.

Study details: Findings are from a multicenter study including 247 patients with TNBC who received sequential treatment with anthracycline and weekly paclitaxel with or without weekly carboplatin.

Disclosures: This study was supported by the Italian Ministry of Health. The authors declared receiving personal fees, grants, or non-financial support from several sources.

Source: Dieci MV et al. Incorporating weekly carboplatin in anthracycline and paclitaxel-containing neoadjuvant chemotherapy for triple-negative breast cancer: Propensity-score matching analysis and TIL evaluation. Br J Cancer. 2022 (Nov 17). Doi: 10.1038/s41416-022-02050-8

Key clinical point: The addition of weekly carboplatin to standard anthracycline-weekly paclitaxel-based neoadjuvant chemotherapy improved pathological complete response (pCR) rates in patients with triple-negative breast cancer (TNBC).

Major finding: The rate of pCR was significantly higher in the anthracycline-paclitaxel+carboplatin vs anthracycline-paclitaxel treatment group (51.9% vs 34.2%; odds ratio 2.40; P = .01); however, no significant differences were observed in grade ≥3 hematological toxicities between both groups.

Study details: Findings are from a multicenter study including 247 patients with TNBC who received sequential treatment with anthracycline and weekly paclitaxel with or without weekly carboplatin.

Disclosures: This study was supported by the Italian Ministry of Health. The authors declared receiving personal fees, grants, or non-financial support from several sources.

Source: Dieci MV et al. Incorporating weekly carboplatin in anthracycline and paclitaxel-containing neoadjuvant chemotherapy for triple-negative breast cancer: Propensity-score matching analysis and TIL evaluation. Br J Cancer. 2022 (Nov 17). Doi: 10.1038/s41416-022-02050-8

Key clinical point: The addition of weekly carboplatin to standard anthracycline-weekly paclitaxel-based neoadjuvant chemotherapy improved pathological complete response (pCR) rates in patients with triple-negative breast cancer (TNBC).

Major finding: The rate of pCR was significantly higher in the anthracycline-paclitaxel+carboplatin vs anthracycline-paclitaxel treatment group (51.9% vs 34.2%; odds ratio 2.40; P = .01); however, no significant differences were observed in grade ≥3 hematological toxicities between both groups.

Study details: Findings are from a multicenter study including 247 patients with TNBC who received sequential treatment with anthracycline and weekly paclitaxel with or without weekly carboplatin.

Disclosures: This study was supported by the Italian Ministry of Health. The authors declared receiving personal fees, grants, or non-financial support from several sources.

Source: Dieci MV et al. Incorporating weekly carboplatin in anthracycline and paclitaxel-containing neoadjuvant chemotherapy for triple-negative breast cancer: Propensity-score matching analysis and TIL evaluation. Br J Cancer. 2022 (Nov 17). Doi: 10.1038/s41416-022-02050-8