Precision Nutrition in Cancer: From Metabolic Dysregulation to Biomarker-Guided Interventions

OK, dear friends, good morning, good afternoon, good evening. Welcome to join the second webinar symposium of ISPH. Today, we are very pleased to invite Dr. Camelia Munteanu to be our keynote speaker, and also Dr. Danny Dhanasekaran to be the chair and Dr. Ben Tsang to be the panelist.

I believe today the title could be very attractive. This is about precision nutrition in cancer. So again, I welcome everyone to join this webinar symposium. Now I will move to the chair, Dr. Danny. Please.

Hi, I'm really glad to have the privilege of sharing this session, and especially to be with all of our friends. So it's my great pleasure to welcome all of you today to this webinar on Precision Nutrition and Cancer: From Metabolic Dysregulation to Biomarker-Guided Interventions.

I'm really delighted to have with us today Dr. Camelia Munteanu as our featured speaker. Dr. Munteanu is an internationally active nutrition scientist and faculty at the University of Agricultural Sciences and Veterinary Medicine in Cluj-Napoca, Romania. Her work sits at the exciting interface of precision nutrition, metabolism, and cancer biology.

Dr. Munteanu completed her PhD in Physical Education and Sport and Biology at Babeș-Bolyai University, Cluj-Napoca, and holds a master's degree in nutrition. Her research focuses on understanding how nutrition and obesity-driven metabolic networks influence cancer risk, progression, and therapeutic response. What makes her work particularly impactful is its integrative nature — combining nutrition science with advanced molecular approaches, including lncRNA-based transcriptomics and systems-level analysis, to uncover mechanistic links between diet, metabolic dysregulation, obesity, and cancer.

She has authored more than 33 peer-reviewed publications in leading journals including Cancers, Nutrients, and Obesity Reviews, serves as a reviewer for several international journals including the Journal of Ovarian Research, and is actively leading multiple national and international research initiatives, including Horizon Europe proposals. Dr. Munteanu, thank you so much for accepting our invitation. We all look forward to your talk.

Thank you so much for the warm introduction. It is truly an honour to be here with the ISPH community today.

I want to start with a fact that I think should alarm all of us: obesity is now established as a major modifiable risk factor for at least 13 types of cancer. In Romania, the data are particularly striking — approximately 58% of men and 41% of women are classified as overweight or obese, placing Romania among the highest in the European Union. We see particularly high incidence rates of postmenopausal breast cancer, endometrial cancer, ovarian cancer, and colorectal cancer, with especially vulnerable populations such as the Roma community carrying a disproportionate share of that burden.

The urgency is clear. We cannot talk about cancer prevention and treatment without talking about metabolic health and nutrition — and yet, until recently, these conversations have remained largely separate. My work is about bridging that gap.

So how exactly does obesity promote cancer? The mechanisms are multiple and interconnected. Chronic low-grade inflammation is a key driver — the adipose tissue in obese individuals is infiltrated by pro-inflammatory immune cells and secretes elevated levels of TNF-α, IL-6, and other cytokines that create a permissive environment for tumor growth.

Insulin resistance is another critical pathway. Hyperinsulinaemia and elevated IGF-1 activate proliferative and anti-apoptotic signalling cascades. And then there is the role of adipokines — leptin promotes proliferation and angiogenesis, while adiponectin — which is typically anti-tumorigenic — is paradoxically reduced in obese individuals.

What has become increasingly clear is that adipocytes are not passive bystanders — they are active endocrine players in the tumor microenvironment. They secrete lipids, cytokines, and — crucially — exosomes. These exosomes carry lncRNAs, DNA, and proteins that can be taken up by adjacent tumor cells and drive their progression. This is a central focus of our research.

The limitations of our current approach are significant. Traditional nutritional guidelines are essentially "one-size-fits-all" — they do not account for tumor heterogeneity, genetic and epigenetic profiles, metabolic status, the microbiome, the phase of treatment, or individual patient characteristics. A dietary intervention that benefits one patient may be neutral or even harmful in another.

Precision nutrition asks us to do better. It asks us to integrate multiple layers of biological information — genomic, epigenomic, metabolomic, microbiomic — to develop dietary and metabolic interventions that are tailored to the individual. And increasingly, we believe that tumor-specific molecular signatures, particularly lncRNA expression profiles, can be the key to unlocking this precision.

Let me now turn to our experimental work. We focused on high-grade serous ovarian cancer — HGSOC — which is the most common and lethal subtype of ovarian cancer and is known to be strongly influenced by the adipose-rich peritoneal microenvironment.

We used an adipocyte-conditioned medium, or ACM, model, in which we exposed HGSOC cell lines — OVCAR4, Kuramochi, and TYKnu — to media conditioned by mature adipocytes. This mimics the obese visceral adiposity microenvironment by providing the secretions of adipocytes — lipids, cytokines, and exosomal cargo — to the cancer cells.

Using lncRNA-based transcriptomics, we identified four lncRNAs that are differentially regulated by adipocyte-secreted factors: CCAT1, H19, LINC00887, and PCAT1. These are not random candidates — they are functionally linked to tumour-relevant processes, including proliferation, stemness, immune evasion, and metabolic reprogramming across glucose, lipid, and amino acid pathways.

Importantly, these lncRNAs are overexpressed in a substantial proportion of ovarian cancer patients, and their expression levels correlate with advanced disease stage and poorer overall survival. This gives them strong potential as diagnostic biomarkers, prognostic indicators, and therapeutic targets.

My take-home message is this: cancer metabolism is actionable. The era of generic nutritional advice in oncology must give way to precision nutrition guided by tumor-specific molecular signatures — and lncRNA profiles, integrated with metabolic data, offer a powerful framework for doing exactly that.

Looking ahead, we are working to validate urine-based detection of these lncRNA biomarkers using patient samples, develop metabolic profiling to complement the lncRNA signatures, and integrate exosome, lncRNA, and metabolic data with bioinformatic tools to build personalised cancer risk and prevention profiles. Our collaborations with bioinformaticians are already under way.

I believe that precision nutrition — grounded in the molecular biology of the tumor and the metabolic reality of the patient — can meaningfully improve outcomes, especially for obese patients who carry both the highest cancer risk and the least tailored support. I look forward to the discussion. Thank you.