Editorial: ["Obesity and Cancer: The Possible Molecular Links"]

Biswarup Basu ^1* Debanjan Chakroborty ^2* Chandrani Sarkar ^2*

• ¹ Chittaranjan National Cancer Institute, Kolkata, India
• ² University of South Alabama, Mobile, United States

Obesity is a global public health issue that adversely affects several disease pathogenesis and prognosis, including cancer, by increasing the risk and the number of deaths associated with cancer (1). The underlying molecular mechanisms of obesity-associated cancer progression are unclear. With worldwide growing obesity, the obese tumor microenvironment, in addition to cancer patients' socio-economical or ethnic perspectives, has emerged as a new area for understanding the dynamics of cancer initiation and outcomes obtained and for developing improved approaches to cancer management. The collection "Obesity and Cancer: The Possible Molecular Links" was developed to highlight novel, original research findings, and critical reviews focusing on identifying the link between obesity and cancers. With three original research studies and one review article, this collection highlights the interconnecting issues regulating obesity and cancer progression.Furthermore, the collection has included epidemiological findings that reinforce the role of obesity in cancer progression by assessing the effect of neighborhood obesogenic environment on cancer risk and mortalities.Obese breast cancer (BCa) patients, particularly postmenopausal women, have an increased risk of hormone receptor (HR)-positive BCa compared to lean women and often demonstrate more aggressive forms of the disease and face numerous challenges during therapy (2). Though in premenopausal women, obesity is reported to reduce the risk of BCa, after BCa diagnosis, obesity worsens overall survival (OS) in all BCa subtypes (2). The interplay between adipocytes and tumor cells contributing to the adipose microenvironment significantly influences tumor growth and response to therapy (3). Kakkat et al. reviewed the complex relationship between BCa cells and adipocytes during tumor development, progression, and therapeutic response. The review discusses how circulating adipokines influence BCa progression. While adipokines like leptin, resistin, chemerin, visfatin, osteopontin, apelin, and lipocalin 2 promote BCa pathogenesis, adiponectin confers a protective effect by suppressing breast carcinogenesis (4). As leptin exerts an opposite effect by promoting BCa initiation, growth, and metastasis, the adiponectin-leptin ratio plays a critical role in breast tumorigenesis (5). Cancer-associated adipocytes (CAAs) secrete factors influencing immune cell recruitment, functions, differentiation, and immune escape, thereby promoting tumor progression. Adipocytes also contribute to the formation of extracellular matrix (ECM), which in turn promotes metastatic dissemination and cancer advancement. Furthermore, adipocytes stimulate resistance to therapy by activating multiple signaling pathways that promote angiogenesis, increase tumor cell proliferation, and decrease apoptosis. A thorough investigation of the effects of strategies in weight loss on BCa progression and therapeutic response and the molecular pathways affected is essential for the development of novel therapeutic approaches for BCa patients.In their original research article, Wu et al. studied the impact of body mass index (BMI) on malignant lymphoma. Numerous prior reports indicate a positive link between high BMI and both B cell derived Hodgkin's lymphoma (HL) and non-Hodgkin's lymphoma (NHL), derived from B cells and T cells, indicating that obesity is a potential risk towards malignant lymphoma (6,7).Interestingly, some studies also indicate that obese or overweight patients have a better favorable prognosis in malignant lymphoma, making the role of obesity in lymphoma controversial (8,9). In However, a strong association between obesity and other comorbidities was identified, which influenced cancer progression. The study findings indicate that the chances of having chronic comorbidities were higher among obese cancer compared to lean patients. The findings further suggest that weight reduction is a measure to limit added complications and reduce cancer progression. It also provides interesting information about the lower incidence of comorbidities in cancer patients in Eastern Ethiopia, which suggests that different lifestyles and differences in genetic background can affect cancer incidence and progression differently. The observation underscores the critical need for more studies in underdeveloped and developing countries to help better understand the role of obesity and other comorbidities in cancer and other diseases.Obesity has been reported to be associated with aggressive and high-grade prostate cancer (PCa) and increased PCa-associated deaths (12). Taken together, the findings from these studies clearly indicate the complex relationship between body weight and cancer progression. Further research is needed to comprehend the molecular pathways underlying obesity-associated cancer progression, identify novel biomarkers in different groups at risk, and identify new targets that can lead to the design of improved therapeutic approaches for successful clinical management of cancer. We believe that this collection of research studies will serve as a valuable resource to drive further advancement in this field.