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1.
J Surg Res ; 2024 Jun 10.
Artigo em Inglês | MEDLINE | ID: mdl-38862305

RESUMO

INTRODUCTION: Lung cancer is consistently the leading cause of cancer death among women in the United States, yet lung cancer screening (LCS) rates remain low. By contrast, screening mammography rates are reliably high, suggesting that screening mammography can be a "teachable moment" to increase LCS uptake among dual-eligible women. MATERIALS AND METHODS: This is a prospective survey study conducted at two academic institutions. Patients undergoing screening mammography were evaluated for LCS eligibility and offered enrollment in a pilot dual-cancer screening program. A series of surveys was administered to characterize participants' knowledge, perceptions, and attitudes about LCS before and after undergoing dual screening. Data were descriptively summarized. RESULTS: Between August 2022 and July 2023, 54 LCS-eligible patients were enrolled. The study cohort was 100% female and predominantly White (81%), with a median age of 57 y and median of 36 pack-y of smoking. Survey results showed that 98% felt they were at risk for lung cancer, with most (80%) motivated by early detection of potential cancer. Regarding screening barriers, 58% of patients lacked knowledge about LCS eligibility and 47% reported concerns about screening cost. Prior to undergoing LCS, 87% of patients expressed interest in combined breast and lung screening. Encouragingly, after LCS, 84% were likely or very likely to undergo dual screening again and 93% found the shared decision-making visit helpful or very helpful. CONCLUSIONS: Pairing breast and LCS is a feasible, acceptable intervention that, along with increasing patient and provider education about LCS, can increase LCS uptake and reduce lung cancer mortality.

2.
Biochim Biophys Acta Mol Basis Dis ; 1870(7): 167325, 2024 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-38925485

RESUMO

The mechanism(s) underlying obesity-related postmenopausal (PM) breast cancer (BC) are not clearly understood. We hypothesized that the increased local presence of 'obese' mammary adipocytes within the BC microenvironment promotes the acquisition of an invasive and angiogenic BC cell phenotype and accelerates tumor proliferation and progression. BC cells, treated with primary mammary adipocyte secretome from premenopausal (Pre-M) and PM obese women (ObAdCM; obese adipocyte conditioned-media) upregulated the expression of several pro-tumorigenic factors including VEGF, lipocalin-2 and IL-6. Both Pre-M and PM ObAdCM stimulated endothelial cell recruitment and proliferation and significantly stimulated BC cell proliferation, migration and invasion. IL-6 and LCN2 induced STAT3/Akt signaling in BC cells and STAT3 inhibition abrogated the ObAdCM-stimulated BC cell proliferation and migration. Expression of proangiogenic regulators including VEGF, NRP1, NRP2, IL8RB, TGFß2, and TSP-1 were found to be differentially regulated in mammary adipocytes from obese PM women. Comparative RNAseq indicated an upregulation of PI3K/Akt signaling, ECM-receptor interactions and lipid/fatty acid metabolism in PM versus Pre-M mammary adipocytes. Our results demonstrate that irrespective of menopausal status, cross-talk between obese mammary adipocytes and BC cells promotes tumor aggressiveness and suggest that targeting the LCN2/IL-6/STAT3 signaling axis may be a useful strategy in obesity-driven breast tumorigenesis.


Assuntos
Adipócitos , Neoplasias da Mama , Movimento Celular , Proliferação de Células , Neovascularização Patológica , Obesidade , Fator de Transcrição STAT3 , Feminino , Humanos , Adipócitos/metabolismo , Adipócitos/patologia , Neoplasias da Mama/patologia , Neoplasias da Mama/metabolismo , Linhagem Celular Tumoral , Interleucina-6/metabolismo , Lipocalina-2/metabolismo , Lipocalina-2/genética , Menopausa/metabolismo , Invasividade Neoplásica , Neovascularização Patológica/metabolismo , Neovascularização Patológica/patologia , Obesidade/metabolismo , Obesidade/patologia , Proteínas Proto-Oncogênicas c-akt/metabolismo , Transdução de Sinais , Fator de Transcrição STAT3/metabolismo , Microambiente Tumoral
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