Yannick Deswysen^1,2*, Marc Van den Eynde^3,4, Nicolas Lanthier^2,4

¹UpperGI surgical unit, Service de chirurgie et transplantation abdominale, Cliniques universitaires Saint-Luc, Institut Roi Albert II, UCLouvain, Brussels, Belgium

²Laboratoire de gastroentérologie et d’hépatologie, Institut de Recherche Expérimentale et Clinique, Université catholique de Louvain, Brussels, Belgium

³Service d’Oncologie Médicale, Cliniques universitaires Saint-Luc, Institut Roi Albert II, UCLouvain, Brussels, Belgium

⁴Service d’Hépato-gastroentérologie, Cliniques universitaires Saint-Luc, UCLouvain, Brussels, Belgium

^*Corresponding Author: Yannick DESWYSEN, MD, Service de Chirurgie et Transplantation Abdominale,

Cliniques universitaires Saint-Luc, Université Catholique de Louvain 10, Avenue Hippocrate, B-1200 Bruxelles, Belgium.

Received: 09 July 2025; Accepted: 16 July 2025; Published: 15 August 2025

Article Information

Citation: Yannick Deswysen, Marc Van den Eynde, Nicolas Lanthier. Myosteatosis in Oesophagogastric Cancer: A Systematic Review. Journal of Cancer Science and Clinical Therapeutics. 9 (2025): 112-131.

DOI: 10.26502/jcsct.5079271

Abstract

Keywords

Oesophagogastric cancer; Sarcopenia; Myosteatosis; Muscle function; Oncological outcomes; Immune-inflammatory markers

Article Details

Introduction

Oesophageal and gastric cancer are associated with significant morbidity and mortality rates worldwide [1]. Despite advancements in surgical, medical, and therapeutic treatments, patient survival often remains limited, underscoring the urgent need to identify new prognostic factors and therapeutic targets [2]. Body composition, encompassing muscle mass, adipose tissue level, and inflammatory and nutritional parameters, plays a pivotal role in treatment response and survival outcomes among cancer patients. Variations in body composition primarily involve two main entities: sarcopenia and myosteatosis. Sarcopenia is defined by the loss of skeletal muscle mass and function [3], while myosteatosis is defined by an excessive accumulation of lipid within skeletal muscle tissue [4]. Sarcopenia, which is well-documented, is associated with poor clinical outcomes, including an increased risk of infection, loss of function, increased chemotherapy related toxicity and mortality [5-7].

Myosteatosis, reflective of deteriorating muscle composition, is increasingly acknowledged as a potential prognostic marker in the context of oesophagogastric cancer [8]. In various malignancies, such as hepatocellular, colorectal or bladder cancers, myosteatosis has been linked to reduced muscle quality, impaired metabolic function, and poorer clinical outcomes. These outcomes include higher rates of complications, reduced tolerance to treatments, and lower overall survival [9-11]. However, the precise impact on clinical outcomes, particularly in relation to inflammatory and nutritional parameters, as well as the physical functional status of patients, remains incompletely understood and subject to ongoing debate. Fat accumulation within muscles occurs predominantly in two areas: within muscle fibres (intramyocellular lipids) and in the interstitial spaces (intermuscular fat) [12]. This accumulation is particularly detrimental to locomotor and respiratory muscles, exacerbating functional decline and reducing patient autonomy [13]. Such effects may partly explain the association of myosteatosis with increased treatment morbidity and mortality.

In the context of cancer, myosteatosis may be driven by mechanisms distinct from those in metabolic diseases, such as metabolic dysfunction-associated steatotic liver disease (MASLD) or type 2 diabetes [14]. In cancer, tumour-induced systemic inflammation, mediated by cytokines such as interleukin-6 (IL-6) and tumour necrosis factor-α (TNF-α), contributes to muscle breakdown and lipid dysregulation [15]. Alterations in proteins such as perilipins, which regulate lipid storage, further exacerbated abnormal fat deposition in muscles [16]. Understanding the mechanics is essential to identifying actionable causes to improve patient care. A critical question of causality arises: does the tumour directly induce myosteatosis, or does pre-existing muscle fat accumulation create a pro-inflammatory environment that promotes tumour aggressiveness? Regardless of direction, the interaction appears to amplify both tumour progression and muscle degradation.

Myosteatosis profoundly impairs muscle function, reducing contractility, strength, and endurance. Additionally, the accumulation of intramuscular lipids promotes the release of free fatty acids, which, through oxidative processes, generate oxidative stress. This oxidative stress induces cellular damage and exacerbates local inflammation, further accelerating muscle degradation. These mechanisms can contribute to increased muscle stiffness and diminished mobility, particularly in the elderly [17]. Oxidative stress and inflammation are indeed recognised as key pathological features of ageing skeletal muscle, contributing to the progressive loss of muscle mass and function [18]. Addressing myosteatosis in oesophagogastric cancer could improve patient outcomes by targeting both the tumour and the associated muscle dysfunction. This approach may pave the way for integrated therapies aimed at enhancing metabolic and functional recovery.

This systematic review aims to synthesize the current evidence regarding the multifaceted role of myosteatosis, alongside inflammatory and nutritional parameters, and the physical functional status in oesophagogastric cancer. We will explore the current implications of myosteatosis on survival, postoperative complications, and systemic immuno-inflammatory response.

Methods

Search strategy

A systematic literature research was conducted independently by two investigators based on the PubMed/Medline, Embase, Scopus, and Cochrane databases until 31 October, 2024. The search keywords (« myosteatosis » OR « muscle fat infiltration » AND « oesophageal cancer ») and (« myosteatosis » OR « muscle fat infiltration » AND « gastric cancer »). Additionally, the citation lists of review articles were manually analysed for potentially eligible studies.

Inclusion and exclusion criteria

The inclusion criteria were studies published in English exploring the impact of myosteatosis in gastric and/or esophageal cancer in adult’s patients. Exclusion criteria were: 1) non-human study, 2) duplicative studies, 3) letter, review, case reports, conference abstracts, 4) unusable data.

Study selection

Two authors independently selected studies on title and abstract. Studies that met inclusion data have been included to analyse the full-text. The 2 investigators analysed the full-texts, and a third reviewer resolved any disagreements.

Data extraction

Data extracted from selected articles included study characteristics (authors, journal, country, study design, sample size, type of cancer, cancer stage, type of treatment performed, follow-up), patient demographics (gender, age), body composition measurements (body component analysis method, index, cutoff, anatomical location of analysis, software used), functional physical evaluation, prognostic value (overall survival, recurrence free survival, disease free survival, progression free survival), treatment complications and immuno-inflammatory response (C-reactive protein (CRP), neutrophils, lymphocytes, platelets, neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR)).

Results

1) Data collection

Of the 132 manuscripts evaluated, 34 articles met the inclusion criteria totalling 9,814 patients [8, 19-51] (Figure 1). Depending on the trials, sample sizes ranged between 45 and 1,147 patients. Among these, 22 studies included patients with gastric cancer [28-45, 49-51], 7 with oesophageal cancer [19, 21-24, 46, 48] and 6 with both [8, 20, 25-27, 47].

All studies, including the type of cancer, treatment modalities, methods for assessing sarcopenia and myosteatosis, cut-off values for their diagnosis, and main findings are listed in Table 1. Most studies used computed tomography (CT) images at the third lumbar level (L3). One study employed a combination of CT and magnetic resonance imaging (MRI) [38], while two analysed images at the L4 level [22, 31]. Six studies evaluated the psoas major and paraspinal muscles in the abdominal region [19, 22, 26, 39, 41, 43], but the majority measured the total abdominal muscle area (TAMA) without specifying which muscles were assessed [8, 20, 21, 23-25, 27-38, 40, 42, 44-51].

Figure 1: Flow chart

2) Myosteatosis prevalence in oesophagogastric cancer

In terms of muscle quality, different terminologies were used by authors, such as mean attenuation, Hounsfield units, skeletal muscle (SM) attenuation, intramuscular adipose concentration, or skeletal muscle radiation attenuation. For consistency, we standardised the terminology as “skeletal muscle density” (SMD).

The variability in cut-off values used to define sarcopenia and myosteatosis presents a challenge for data comparison. A significant portion of studies [20, 23, 25, 27, 29, 35, 36, 42] relied on the data from Martin et al [52], while others established cut-offs specific to their populations through statistical analyses [19, 30, 32, 39, 43-45, 49-51]. For reference, Martin's criteria for defining sarcopenia are based on gender and BMI without measuring muscle strength, which is usually recommended when diagnosing sarcopenia, and solely on BMI for measuring myosteatosis. Thus, sarcopenia is defined as a SMI <43 cm2/m2 in men with a BMI <25 kg/m2, <53 cm2/m2 in men with a BMI ≥25 kg/m2, and <41 cm2/m2 in women. Low MA was defined as a mean attenuation <41 HU in patients with a BMI <25 kg/m2 and <33 HU in those with a BMI ≥25 kg/m2 (Table 1.) [52]. Some studies categorised patients using tertiles, whereas others utilised continuous data for group definitions. Based on the criteria set by the researchers, the prevalence rate for sarcopenia ranged from 15.4 to 69.9% while the prevalence of myosteatosis ranged from 11.0 to 84.0%. When data are available, the percentage of women presenting sarcopenia and/or myosteatosis is higher than that of men [20, 25].

Table 1: Incidence of myosteatosis and sarcopenia.

CSA = cross sectional area (cm²) ; CT = chemotherapy ; RCT = radiochemotherapy ; IMAC = intramuscular adipose concentration (HU) ; HUAC = Hounsfield unit average calculation (HU); IT = immunotherapy ; PMA = psoas muscle attenuation (HU) ; PMI = psoas muscle mass index (cm²/m²); SMD = skeletal muscle density (HU) ; SMI = skeletal muscle mass index (cm²/m²); SM-RA = skeletal muscle radiation attenuation (HU) ; TAMA = total abdominal muscle area ; TPA = total psoas area (mm² /m²) ; NDA = no data available ; None = using continuous variables.

3) Association between sarcopenia, myosteatosis and oncological outcomes

Twenty-nine studies reported the prognostic impact of sarcopenia and myosteatosis [8, 19, 21-32, 34, 36, 38-46, 48-51]. These findings are summarised in Table 2. The pooled analysis demonstrated that patients with myosteatosis faced a higher risk of mortality compared with those without myosteatosis. Low SMD was identified as an independent prognostic factors for overall survival (OS) [19, 22, 26, 29, 31, 32, 40-45, 48-51], disease free survival (DFS) [19, 29, 31, 45, 50], progression-free survival (PFS) [49, 51], and cancer-specific survival (CSS) [41, 44].

Table 2: Prognostic impact of myosteatosis and sarcopenia.

CSS= cancer-specific survival ; DFS : disease free-survival ; HUAC = Hounsfield unit average calculation ; IMAC : intramuscular adipose tissue content ; MA = muscle attenuation ; mIMAC = modified intramuscular adipose tissue content ; OS = overall survival ; PFS : progression-free survival ; PMI = psoas muscle index (cm²/m²) ; PMMA= mean attenuation within paraspinal muscle ; PMRA = paraspinal muscle radiation attenuation ; PNI = prognostic nutritional index = Albumin+5 x total lymphocyte count (x 10⁹/L) ; SMD = skeletal muscle density ; SMI = skeletal muscle index ; SMRA = skeletal muscle radiation attenuation ; TPA = total psoas area

However, five studies reported no significant association between myosteatosis and OS [27, 30, 34, 36, 46]. Additionally, one study observed improved OS and PFS in patients with myosteatosis treated with definitive chemoradiotherapy, when the latter is not associated with systemic inflammation. The authors suggested that the positive impact of myosteatosis on OS could be attributed to factors such as the low prevalence of overweight or obese patients, a reduced proportion of visceral fat, and the predominance of squamous cell carcinoma—a histological type less commonly associated with obesity [23].

Findings for sarcopenia were also reported in the Table 2. Low skeletal muscle index (SMI) was identified as an independent prognostic factors for overall survival (OS) [19, 21, 24, 25, 28, 30, 32, 34, 39-41, 43, 44, 46, 48-51], disease free survival (DFS) [28, 32, 39, 40, 50] and progression-free survival (PFS) [38, 49, 51]. No significant association between sarcopenia and OS was find in eight studies [22, 26, 27, 29, 36, 38, 42, 45].

4) Association between myosteatosis and immuno-inflammatory markers

Among 34 articles included in this review, 8 examined the relationship between body composition and immune-inflammatory parameters - 7 in gastric cancer [28-30, 33, 36, 39, 44] and 1 in oesophageal cancer [23]. Various scores derived from simple markers, such as CRP, NLR, PLR, lymphocyte-to-monocyte ratio (LMR), prognostic nutritional index (PNI). In the only study concerned, there was no correlation between CRP and myosteatosis [33].

In gastric cancer, immunoinflammatory markers appear to influence tumour outcome by affecting progression or survival. For instance, a high NLR has been linked to poorer OS and recurrence-free survival (RFS), as has a high PLR [29, 30, 39] although this association was not observed in another study [36]. The combination of sarcopenia or myosteatosis with elevated NLR or PLR further exacerbates the negative impact on survival. High NLR may correlate with poorer physical condition, commonly seen in patients with muscle mass loss or myosteatosis. Sarcopenic patients often exhibit a more pronounced inflammatory response. Two studies found that a high LMR ratio negatively impacts survival [30, 39]. When combined with myosteatosis, the risk of progression doubled. A reduced lymphocyte count and increased monocyte count reflect an immunosuppressive and inflammatory environment, which may reflect a low LMR [39]. The PNI, a multiparametric marker combining nutritional and immune factors, was first introduced by Buzby et al. [53]. A low PNI ratio suggests a compromised nutritional status and/or immunosuppression and is associated with sarcopenia and myosteatosis and reduced OS in gastric cancer patients [28, 30].

Finally, as noted earlier, myosteatosis was significantly associated with favourable PFS and OS in one study of patients treated with definitive chemoradiotherapy for locally advanced esophageal cancer. Increased NLR was more frequently observed in patients without myosteatosis. In subgroups analyses, patients with myosteatosis and low NLR demonstrated a reduced risk of tumour progression and mortality, suggesting that myosteatosis in the absence of systemic inflammation predicts a favourable prognosis [23].

5) Association between myosteatosis and muscle function

Few studies have comprehensively analysed the correlations between body composition, muscle strength and physical performance in patients treated for oesophagogastric cancer. Most studies adopted the muscle mass as a single parameter for evaluating sarcopenia, overlooking the critical role of muscle strength and functional physical capacity. Five studies assessed muscle function by using the hand-grip-test (HGT) to measure muscle strength [35, 37, 40, 41, 47], and only one study evaluated preoperative physical performance status by using the six-minute walk test (6MWT) [40].

Waki et al reported an inverse correlation between myosteatosis, represented by intramuscular adipose tissue content (IMAC), and high HGT in both men (r=-0.373, p<0.001) and women (r=-0.400, p<0.001) [41]. Sales-Balaguer et al confirmed the association between low HGT and both myosteatosis and sarcopenia [47]. Dong et al. highlighted the lack of consensus regarding the predictive value of different functional parameters for postoperative complications. Indeed, while low SMD and 6MWT are associated with post-operative complications in univariate analysis, skeletal muscle index (SMI) and HGT seem superior (in multivariate analysis) in predicting surgical morbidity. Conversely, the team found a greater impact of SMD and 6MWT than SMI and HGT on survival [40].

Regarding complications, Carvalho et al. and Lin et al. identified a correlation between low HGT and low SMI or SMD in predicting postoperative complications. However, only SMD was found to be predictive of severe complications [35, 37].

6) Impact of muscle parameters on treatment’s morbidity in oesophagogastric cancer.

An evaluation of the impact of sarcopenia and myosteatosis on treatment was conducted in 15 studies. Details are provided in Table 3.

Table 3: Relationship between myosteatosis and treatment’s outcomes, muscle function and immune-inflammatory markers

CRP = C-reactive protein ; CSS = cancer-specific survival ; CT = chemotherapy ; dRCT = definitive radiochemotherapy ; HGT = hand grip test ; HUAC = Hounsfield unit average calculation ; LMR = lymphocyte to monocyte ratio ; NLR = neutrophil to lymphocyte ratio ; NPR = neutrophil to platelet ratio ; OS = overall survival ; PLR = platelet to lymphocyte ratio ; PNI = prognostic nutritional index ; RBP = retinol-binding protein ; RCT = radiochemotherapy ; RFS = recurrence-free survival ; SII = systemic immuno-inflammation index; TPA = total psoas area ; TPG = total psoas gauge (TPA X HUAC)

The evolution of the body component was analysed in 4 studies before and after the different neoadjuvant treatment modalities [20, 25, 27, 48]: one evaluated outcomes before and after neoadjuvant treatment [20], another at diagnostic and 100 days after treatment [25], another before and after chemotherapy for metastatic cancers [27], and the last before and after radiotherapy [48]. West et al and Daly et al reported a significant impact of systemic treatments on both muscle mass and muscle quality [20, 25]. Daly et al observed a greater increase in sarcopenia among patients undergoing neoadjuvant treatment compared to those receiving palliative care [25]. Yang et al found an increase of sarcopenia prevalence but a decrease myosteatosis prevalence, whereas Dijksterhuis et al noted a decrease in myosteatosis over time in patients receiving palliative treatment [27]. Thus, all demonstrated an increase in sarcopenia due to muscle mass loss during neoadjuvant treatment. Myosteatosis appeared to follow a similar trend under the influence of non-surgical treatments [20, 25, 27], except in the study by Yang et al, which observed a slight, non-significant decrease [48].

Adverse events related to neoadjuvant or systemic treatment in patients with myosteatosis or sarcopenia were analysed in one study. Dijksterhuis et al observed a significant correlation between low SMD and toxicity grade 3 or 4. Others parameters were not associated with toxicity [27]. No data were found on the impact of surgery on the body component. Studies have focused on correlations between sarcopenia/myosteatosis and the occurrence of complications. Surgical postoperative complications were assessed in 12 studies. Most of them reported a negative impact of myosteatosis on surgical complications in patients who underwent surgery. Low SMD were strongly associated with surgical complications, including overall complications [8, 21, 32, 33, 35, 37, 40, 41, 50], severe complications (≥ grade 2-3) [8, 32, 35, 41, 46, 50], and anastomotic leaks [8]. Srpcic et al, however, found no association with respiratory complications and even reported fewer conduit complications in the myosteatosis group compared with patients without myosteatosis (6,9 vs 23,9 %, OR 0,238 (0,082-0,692), p=0,005) [21]. Conversely, two studies did not identify any impact of low SMD on surgical outcomes [43, 44]. Lu et al, however, highlighted a significant impact of the total Psoas Gauge (TPG), defined by the product of the Total Psoas Area (”TPA”) by the density measurement in Hounsfield units (“HUAC”) on severe and overall complications for sarcopenia et myosteatosis.

Sarcopenia was associated with overall postoperative complications in several studies [33, 37, 40, 50], although others did not report any significant relationship [21, 35, 43, 44].

Discussion

This systematic review highlights the prognostic significance of myosteatosis in oesophagogastric cancer and its treatment while underscoring the challenges in interpreting existing data. The considerable heterogeneity in defining body composition variables, analytical methodologies, and study populations complicates the interpretation of findings and does not allow all the results to be presented in a uniform and standardised manner.

Myosteatosis can be assessed non-invasively through imaging techniques such as computed tomography (CT), magnetic resonance imaging (MRI), and quantitative ultrasound. Each method has its advantages and limitations [12]. While there is no gold standard for measuring myosteatosis, CT remains the most commonly used tool in large-scale research. However, CT provides only an indirect assessment by analysing muscle density and cannot differentiate between intermuscular and intramuscular fat [14, 54, 55], Although Hounsfield unit (HU) cut-off values have been linked to prognostic outcomes in cancer populations [52], no universally accepted cut-offs exist, leading to inconsistencies in defining sarcopenia and myosteatosis, thereby complicating data comparison.

The prevalence of myosteatosis remains debated due to the lack of standardised measurement methods, but evidence suggests it is as significant as sarcopenia. Some studies report that up to 84% of patients with oesophagogastric cancer exhibit myosteatosis. In our review, sarcopenia prevalence ranged from 15.4% to 69.9%, while myosteatosis prevalence varied between 11.0% and 84.0%. These discrepancies stem from multiple factors. Firstly, many studies do not stratify patients by age, despite age-related progression of muscle mass and myosteatosis. Secondly, inconsistencies in cut-off values for defining these conditions lead to differing prevalence estimates. Thirdly, comorbidities such as diabetes or neuromuscular diseases could also influence muscle measurements. Finally, variations in tumour stages and treatment regimens impact muscle health and, consequently, prevalence estimates.

Examining myosteatosis alongside sarcopenia offers a more comprehensive understanding of muscle health in cancer patients. For reference, Martin's criteria for defining sarcopenia are based on gender and BMI, and solely on BMI for measuring myosteatosis. Thus, sarcopenia is defined without measuring muscle strength, which is usually recommended when diagnosing sarcopenia. In clinical practice, sarcopenia is often assessed without considering muscle strength, in which case it is referred to as myopenia [54, 55]. While sarcopenia refers to the loss of muscle mass and function, myosteatosis is characterised by pathological fat accumulation within muscle tissue, which can occur even in the absence of significant muscle mass reduction. Their coexistence exacerbates muscle weakness, accelerates functional decline, and negatively affects overall health outcomes. However, it remains unclear whether sarcopenia or myosteatosis serves as the better prognostic indicator [56]. Moreover, few studies have focused on the relationship between muscle and its function in oesogastric cancer. Although a potential link between muscle function and myosteatosis exists, the lack of data prevents any firm conclusions. Further research is needed to explore this association. Prospective studies combining body composition imaging and muscle function assessment would be valuable. Such investigations could provide a more comprehensive understanding of muscle health in this context. Importantly, low muscle density has been associated with poorer survival compared to normal muscle attenuation. Most studies in this review highlight the negative impact of myosteatosis and/or sarcopenia on overall survival (OS) and/or progression-free or disease-free survival (PFS/DFS). However, some studies report no significant association between myosteatosis and OS [27, 30, 34, 36, 46]. Interestingly, Gabiatti et al. observed improved OS and PFS in patients with myosteatosis undergoing definitive chemoradiotherapy, provided systemic inflammation (NLR < 2.8) was absent [23]. This unexpected finding suggests a dual role of visceral fat in malignancies: it serves as an energy reserve and indicator of nutritional status, but also contributes to pro-inflammatory processes and tumour growth. Systemic inflammation may further exacerbate survival outcomes by promoting insulin resistance or impairing mitochondrial oxidation [23]. However, Gabiatti’s study focused exclusively on patients treated with chemoradiotherapy, a group potentially too frail for multimodal treatment, including surgery, which remains the standard of care.

As shown in this review, tumour-associated inflammation plays a crucial role in cancer initiation, progression, and metastasis. Several inflammatory markers, such as CRP, PLS, PNI, NLR, NPR, and LMR, have been strongly linked to poor outcomes in oesophagogastric cancer [30, 54, 55]. Beyond its systemic effects, inflammation contributes to skeletal muscle depletion and cachexia [56, 57]. Emerging mechanistic insights suggest that skeletal muscle functions as a secretory organ, releasing myokines that regulate inflammation [58]. In myosteatosis, impaired muscle quality may disrupt myokine production, exacerbating pro-inflammatory cytokine activity. Evidence from colorectal cancer cohorts has shown a direct association between myosteatosis, increased NLR, and low albumin levels—both markers of systemic inflammation [59].

Further research should investigate the role of local muscle inflammation in the development of myosteatosis and its potential impact on cancer progression. Understanding the crosstalk between intramuscular inflammatory pathways and tumour-related systemic inflammation could provide insights into disease mechanisms and reveal novel therapeutic strategies.

The pathophysiological mechanisms behind increased intramyocellular lipid deposits in cancer-related weight loss are not yet fully understood, though enhanced lipolysis, insulin resistance, and impaired mitochondrial oxidation are commonly implicated [57]. Recent mouse model studies suggest cancer cachexia induces myosteatosis via dysregulated lipid metabolism and altered lipid droplet-associated proteins. Myosteatosis may impair fatty acid oxidation by reducing lipid droplet interactions with mitochondria, thereby worsening metabolic dysfunction [16]. Parallels can also be drawn with cancer-associated adipocytes (CAAs) present in the tumour microenvironment, which exhibit similar morphological and functional changes. Research in breast cancer patients has shown that CAAs enhance tumour aggressiveness by altering their phenotype upon contact with cancer cells, secreting proteases and inflammatory cytokines (e.g. IL-6, IL-1beta) [58]. However, these mechanisms require further investigation in human studies.

Our review found a strong association between myosteatosis and treatment outcomes, although some studies failed to establish such links. The mechanisms underlying the impact of myosteatosis or sarcopenia on postoperative complications remain uncertain, but two hypotheses have been proposed. Firstly, myosteatosis reflects a decline in muscle quality, leading to reduced strength and mobility [59]. Secondly, it is linked to systemic inflammation, which is exacerbated by the catabolic stress of surgery and postoperative complications [60]. Beyond general complications, the association between myosteatosis and severe surgical complications—known to impact oncological survival—is particularly significant. This suggests that improving patients’ muscle status prior to surgery could enhance postoperative outcomes and treatment tolerance. In a non-oncological geriatric population, Taaffe et al. demonstrated that exercise significantly improved skeletal muscle density (HU) and quadriceps strength [61]. Similarly, Shaver et al. found an association between myosteatosis and reduced physical function in head and neck cancer patients, indicating that prehabilitation programmes could optimise functional capacity [62]. In oesophageal cancer, prehabilitation has been shown to reduce muscle mass loss during neoadjuvant therapy while also decreasing subcutaneous and intra-abdominal fat, which correlates with a lower risk of postoperative complications [63]. Prospective studies will make it possible to verify the beneficial impact of these improved parameters on outcomes such as mortality in oesophagogastric cancer. Recently, multimodal prehabilitation interventions—including nutrition and exercise—prior to oesophagogastric cancer surgery have been shown to improve fitness and postoperative outcomes [64]. Prehabilitation may help limit muscle mass decline and reduce visceral adipose tissue [63], thereby lowering treatment-related toxicity. Given that many patients are elderly and weakened by disease, physical preparation before treatment is crucial for improving postoperative recovery and overall resilience to oncological therapies.

Conclusion

This review highlights the significant impact of myosteatosis on oncological and treatment outcomes in patients with oesophagogastric cancer, in addition to sarcopenia (already well known and described). Further prospective studies are essential to uncover the mechanisms by which myosteatosis influences cancer progression, paving the way for the development of targeted interventions in cancer care.

Conflict Of Interest

The authors declare no conflicts of interest.

Author Contributions

YD conceived and designed the analysis, collected data, performed the analysis and wrote the manuscript. NL conceived and designed the analysis, collected data, performed the manuscript review with revisions for important intellectual content. MVD conceived and designed the analysis, performed the manuscript review with revisions for important intellectual content. All authors have read and agreed to the published version of the manuscript.

Funding Information

This work was supported by the IRA II grant (Centre du Cancer “Institut Roi Albert II”, Cliniques universitaires Saint-Luc) attributed to the principal author.

Institutional Review Board Statement

This retrospective study was conducted in accordance with the Declaration of Helsinki and approved by the Hospital-faculty Ethics Committee Saint-Luc – UCL (2023/31MAI/240 – B403).

References

1. Bray F, Laversanne M, Sung H, et al. Global cancer statistics 2022: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries. CA Cancer J Clin 74 (2024): 229-263.
2. Webb PM, Jordan SJ. Global epidemiology of epithelial ovarian cancer. Nat Rev Clin Oncol 21(2024): 389-400.
3. Lheureux S, Braunstein M, Oza AM. Epithelial ovarian cancer: Evolution of management in the era of precision medicine. CA Cancer J Clin 69 (2019): 280-304.
4. Cortez AJ, Tudrej P, Kujawa KA, et al. Advances in ovarian cancer therapy. Cancer Chemother Pharmacol [Internet] 81 (2018): 17-38.
5. Custódio N, Savisaar R, Carvalho C, et al. Expression Profiling in Ovarian Cancer Reveals Coordinated Regulation of BRCA1/2 and Homologous Recombination Genes. Biomedicines 10 (2022): 1-17.
6. Siegel RL, Miller KD, Jemal A. Cancer statistics, 2020. CA Cancer J Clin 70 (2020): 7-30.
7. Kurman RJ, Shih IM. The dualistic model of ovarian carcinogenesis revisited, revised, and expanded. Am J Pathol [Internet] 186 (2016): 733-747.
8. Zamwar UM, Anjankar AP. Aetiology, Epidemiology, Histopathology, Classification, Detailed Evaluation, and Treatment of Ovarian Cancer. Cureus 14 (2022).
9. Kast K, Rhiem K, Wappenschmidt B, et al. German Consortium for Hereditary Breast and Ovarian Cancer (GC-HBOC). Prevalence of BRCA1/2 germline mutations in 21 401 families with breast and ovarian cancer. J Med Genet 53 (2016): 465-471.
10. Grzymski JJ, Elhanan G, Morales Rosado JA, et al. Population genetic screening efficiently identifies carriers of autosomal dominant diseases. Nat Med 26 (2020): 1235-1239.
11. Roy R, Chun J PS. BRCA1 and BRCA2: different roles in a common pathway of genome protection. Nat Rev Cancer 23 (2011): 68-78.
12. Gorodetska I, Kozeretska I, Dubrovska A. BRCA genes: The role in genome stability, cancer stemness and therapy resistance. J Cancer 10 (2019): 2109-2127.
13. Harter P, Johnson T, Berton-Rigaud D, et al. BRCA1/2 mutations associated with progression-free survival in ovarian cancer patients in the AGO-OVAR 16 study. Gynecol Oncol [Internet] 140 (2016): 443-449.
14. Ledermann JA. PARP inhibitors in ovarian cancer. Ann Oncol [Internet] 27 (2016): 40-44.
15. Mateo J, Lord CJ, Serra V, et al. A decade of clinical development of PARP inhibitors in perspective. Ann Oncol 30 (2019): 1437-1447.
16. Tsibulak I, Wieser V, Degasper C, et al. BRCA1 and BRCA2 mRNA-expression prove to be of clinical impact in ovarian cancer. Br J Cancer [Internet] 119 (2018): 683-692.
17. Hospital Cancer Registry Report (2018-2020). National Institute of Cancer Research and Hospital, Dhaka (2022).
18. Christina IM, Philipp F, Hauptmann S, et al. The new WHO classification of ovarian , fallopian tube , and primary peritoneal cancer and its clinical implications. Arch Gynecol Obstet 293 (2016): 695-700.
19. Matsuno RK, Sherman ME, Visvanathan K, et al. Agreement for tumor grade of ovarian carcinoma: analysis of archival tissues from the surveillance, epidemiology, and end results residual tissue repository. Cancer Causes Control 24 (2013): 749-757.
20. Prat J, Belhadj H, Berek J, et al. Figo’s staging classification for cancer of the ovary, fallopian tube, and peritoneum: Abridged republication. J Gynecol Oncol 26 (2015): 87-89.
21. Wang Z, Zhang J, Zhang Y, et al. Expression and mutations of BRCA in breast cancer and ovarian cancer: Evidence from bioinformatics analyses. Int J Mol Med 42 (2018): 3542-3550.
22. Sorrells S, McKinnon KE, McBratney A, et al. Longitudinal and multi-tissue molecular diagnostics track somatic BRCA2 reversion mutations that correct the open reading frame of germline alteration upon clinical relapse. npj Genomic Med [Internet] 6 (2021).
23. Murciano-Goroff YR, Schram AM, Rosen EY, et al. Reversion mutations in germline BRCA1/2-mutant tumors reveal a BRCA-mediated phenotype in non-canonical histologies. Nat Commun 13 (2022): 1-10.
24. Lheureux S, Bruce JP, Burnier J V, et al. Somatic BRCA1/2 recovery as a resistance mechanism after exceptional response to poly (ADP-ribose) polymerase inhibition. J Clin Oncol 35 (2017): 1240-1249.
25. Maxwell KN, Wubbenhorst B, Wenz BM, et al. BRCA locus-specific loss of heterozygosity in germline BRCA1 and BRCA2 Nat Commun [Internet] 8 (2017): 1-11.
26. He W, Zhu H, Zhang S, et al. Promoter Methylation Changes in DNA Damage-Response Genes in Ovarian Cancer and Their Correlation with Prognosis. Clin Exp Obstet Gynecol 51 (2024).
27. Egawa C, Miyoshi Y, Taguchi T, et al. Quantitative analysis of BRCA1 and BRCA2 mRNA expression in sporadic breast carcinomas and its relationship with clinicopathological characteristics. Japanese J Cancer Res 92 (2001): 624-630.
28. Jin TY, Park KS, Nam SE, et al. BRCA1/2 Serves as a Biomarker for Poor Prognosis in Breast Carcinoma. Int J Mol Sci 23 (2022): 1-14.