The Prevalence and Prognostic Value of Low Muscle Mass in Cancer Patients: A Review of the Literature

Many studies underline the clinical value of low muscle mass as a prognostic factor for adverse outcomes in cancer patients, but there is no standardized approach for measuring muscle mass. This review summarizes the methods of diagnosing low muscle mass in cancer patients, the difference between underlying syndromes (sarcopenia and cachexia), and the association with clinical outcomes.

Abstract

In several diseases, low muscle mass has been revealed as an unfavorable prognostic factor for outcome. Whether this holds true in patients with solid malignancies as well has increasingly been explored recently. However, this research field is severely hampered by a lack of consensus on how to determine muscle mass in cancer patients and on the definition of low muscle mass. Consequently, the prevalence of low muscle mass varies widely across several studies. Nevertheless, most studies show that, in patients with solid malignancies, low muscle mass is associated with a poor outcome. In the future, more research is needed to get better insight into the best method to determine muscle mass, the exact prognostic value of low muscle mass in diverse tumor types and stages, pathophysiology of low muscle mass in patients with cancer, and ways to intervene and improve muscle mass in patients. This review addresses the current literature on the importance of muscle mass in cancer patients and the methods of muscle measurement.

Implications for Practice:

An increasing number of studies underline the clinical value of low muscle mass as a prognostic factor for adverse outcomes in cancer patients. However, studies show large heterogeneity because of the lack of a standardized approach to measure muscle mass and the lack of reference populations. As a result, the interpretation of data and further progress are severely hampered, hindering the implementation of muscle measurement in oncological care. This review summarizes the methods of diagnosing low muscle mass in cancer patients, the difference between underlying syndromes such as sarcopenia and cachexia, and the association with clinical outcomes described so far.

Introduction

Muscle mass starts to decline around the age of 40 years, resulting in a mean loss of 8% per decade until the age of 70 [1]. Above 70 years of age, this decline accelerates to 25%–40% muscle mass loss per decade [2, 3].

Loss of muscle mass is associated with unfavorable outcomes in chronic diseases, such as liver cirrhosis [4] and cardiovascular disease [5], and is frequently present in patients with rheumatoid arthritis [6], diabetes [7], and HIV/AIDS [8]. In surgical patients, low muscle mass is associated with postoperative complications and can be used to identify the risk level of patients before surgery [9]. Recently, the role of low muscle mass has become of interest in patients with cancer. In different tumor types and treatment settings, patients with low muscle mass appear to have worse survival compared with patients without low muscle mass [10–13]. Additionally, patients with low muscle mass are more likely to experience more severe toxicities from systemic antitumor agents [14]. Many chemotherapeutic drugs are distributed to the fat-free compartment of the body [15]. Because it is associated with a decline of the fat-free compartment, low muscle mass is thought to result in relatively higher drug concentrations with all accompanying toxicities [16]. Consequently, muscle mass could be an important new prognostic factor for survival and treatment tolerability in cancer patients.

In patients with cancer, muscle loss is probably the result of both sarcopenia and processes closely linked to cachexia. Sarcopenia is a geriatric syndrome with multifactorial etiology, consisting of low muscle mass combined with low muscle strength or impaired physical performance [17]. In older adults, sarcopenia is associated with mortality [18, 19] and physical disability [20]. Cachexia is a severe wasting of both fat and muscle mass and loss of weight, mediated by systemic inflammation in the presence of a severe chronic disease [21]. Several names have been used in the literature to describe muscle status, such as sarcopenia, low muscle mass, and muscle loss. In oncological studies, the term sarcopenia is frequently used, although most studies do not report impaired muscle function and physical performance, parameters that are crucial to diagnosing sarcopenia [17].

Here, we review the current knowledge on diagnosing low muscle mass, its prevalence, and its prognostic value in cancer patients. To make the nomenclature in this review clear, we use the term low muscle mass to describe radiologically measured muscle mass (i.e., measured using radiation techniques). We use the term sarcopenia when describing the combination of radiologically measured muscle mass, impaired muscle function, and/or impaired physical performance. Because most of the literature on muscle mass and its association with outcome has been generated in studies on the elderly, special emphasis is put on the methods used in muscle measurement, which might be useful for studying the clinical relevance of low muscle mass in patients with cancer.

Sarcopenia and Aging

The probable mechanism of sarcopenia occurring in the elderly is an imbalance in muscle protein turnover [22], without the possibility of pointing out a single factor as the main cause (Table 1) [17]. Muscle protein synthesis decreases during aging, partly because of age-related endocrine changes, such as a reduction of sex hormones and growth factors [23]. Additionally, muscle protein breakdown increases, mainly because of age-related low-grade systemic inflammation [24], alongside other factors, such as physical inactivity and malnutrition [21]. This low-grade systemic inflammation, also called inflammaging [25], is characterized by elevated proinflammatory cytokines and is caused by age-related cell damage [25] and mitochondrial dysfunction, leading to accumulation of oxidative stress [26].

Table 1.

Etiological factors of sarcopenia^a

Middle-aged men (40–50 years old) have more muscle mass than women of the same age [1]. However, because of faster deterioration of muscle mass and muscle strength in men compared with women, at older age, men experience more absolute muscle loss and relatively greater losses of both muscle mass and muscle strength than women [2, 3]. A specific subgroup is patients suffering from sarcopenic obesity. Sarcopenic obesity is not just the combination of obesity and low muscle mass, but the result of unfavorable metabolic changes leading to both obesity and low muscle mass [27]. These patients may form a particularly worse prognostic group for adverse outcomes.

Diagnosing Sarcopenia in Geriatric Patients

Nowadays, deterioration of muscle mass alone is considered insufficient to establish the diagnosis of sarcopenia. A prospective cohort study in 2,292 community-dwelling elderly subjects showed that muscle strength had a higher association with mortality than muscle mass [28], whereas there was no linear correlation between muscle loss and reduced muscle strength [17]. Longitudinal studies reported dissociations in time between loss of muscle mass and loss of muscle strength [29], with muscle strength deteriorating more rapidly than muscle mass [20].

Therefore, it is recommended by the European Working Group on Sarcopenia in Older People (EWGSOP) to include muscle strength and physical performance in addition to muscle mass to diagnose sarcopenia in the elderly (Fig. 1) [17, 20, 21, 30]. A crucial shortcoming of this recommendation, however, is that no advice has been given on how to measure muscle mass and strength or which cutoff values should be used to define sarcopenia. Consequently, consensus about a definition of sarcopenia has not yet been reached, and various methods and definitions are used [17, 31]. Studies comparing the various definitions diagnosing sarcopenia, which includes muscle mass, muscle strength, and physical performance, showed a large variation of 0%–20% in the prevalence of sarcopenia in different populations [32–34].

Figure 1.

Diagnostic algorithm for sarcopenia according to the European Working Group on Sarcopenia in Older People [17]. ^aLow gait speed, ≤0.8 m/second; normal gait speed, >0.8 m/second.

Cachexia

In contrast to sarcopenia, cachexia is not caused by aging itself, but is a result of metabolic changes due to disease [35]. Cachexia is a combination of weight loss, muscle and adipose tissue loss, anorexia [35], hyperglycemia, hyperlipidemia, and anemia [36] (the two most widely used definitions of cachexia are listed in Table 2). Factors contributing to these metabolic changes and muscle protein degradation are proinflammatory cytokines, whereas in cancer patients, tumor metabolism contributes as well [36].

Table 2.

Definitions of cachexia

Both sarcopenia and cachexia feature the combined loss of muscle mass and muscle function; thus, distinguishing between these two syndromes in one patient can be difficult or even impossible [21, 37]. However, certain clinical features are more pathognomonic for cachexia, such as weight loss in a short time frame in combination with the failure of nutrition support [36, 38] and abnormal biochemistry. In general, muscle mass measurement alone, or even in combination with muscle function, is not sufficient to differentiate sarcopenia and cachexia; knowledge regarding metabolic state is essential [37].

Determination of Muscle Mass in Noncancer Patients

Muscle mass is part of the fat-free mass (FFM) of the human body. Total body mass consists of several compartments: fat mass (FM), water, protein, and bone, with the latter three forming the fat-free compartment [39]. Body composition analyses focus on measuring these compartments individually rather than simply measuring total body weight. Distinguishing between the measurement of FM and FFM can be important, because alterations in both compartments do not occur synchronically [40]. Furthermore, body mass index [41] and body surface area [42] cannot be relied on to detect total lean body mass or muscle mass, which indicates the need to assess these conditions separately.

In geriatric studies, measurement of muscle mass is mostly performed by dual energy x-ray absorptiometry (DEXA) and bioelectrical impedance analysis (BIA) [30]. In oncological studies, computed tomography (CT) imaging is most often used. Other options are magnetic resonance imaging (MRI) [31] and ultrasound [43]. CT imaging and MRI are regarded as gold standards for muscle mass measurement [30, 44] after validation in cadavers (r = .99) [45]. Although DEXA has shown high correlation with MRI images (r = .94) [46], to the best of our knowledge, DEXA has never been validated in cadaver studies, and its accuracy decreases in obese patients [47]. Furthermore, a study in advanced cancer patients showed that appendicular skeletal muscle mass obtained from DEXA and muscle cross-sectional area at the lumbar vertebra 3 (L3) level measured by CT showed a moderate correlation (r = .70), but with a large difference in agreement after Bland-Altman analysis [48]. BIA is less accurate when measuring tissues with heterogeneous composition [30, 49, 50], often leading to overestimation of measured muscle mass [51]. Considering this and the high availability of CT images in cancer patients, we recommend CT imaging as the “gold standard” method to assess skeletal muscle in cancer patients.

Muscle mass measurement using DEXA in noncancer patients has been described in two ways, with different cutoff points to define low muscle mass. In the first method, appendicular skeletal muscle mass (ASM), which is the sum of the muscle mass of all limbs [52], is corrected for height. In one study, low muscle mass is defined as ASM two standard deviations below ASM in young adults, aged 30 years (mean), resulting in cutoffs of 7.26 kg/m² for men and 5.45 kg/m² for women [53]; these cutoff points are frequently used in studies. In other cutoff points commonly used, low muscle mass is defined as the 20th percentile of ASM in community-dwelling elderly subjects, resulting in cutoffs of 7.23 kg/m² for men and 5.67 kg/m² for women [54], which shows high similarity. In the second method, ASM is corrected for both height and fat mass by using linear regression. The residuals of the regression were used to identify the difference between expected muscle mass and true muscle mass. Low muscle mass was defined as the 20th percentile of the distribution of the residuals [54]. However, despite using 20th percentiles in both methods, almost 50% of a population of community-dwelling elderly subjects were identified as having low muscle mass by one method, but not by the other [54]. This discrepancy clearly stresses the high need for a standardized approach to measure muscle mass.

Determination of Low Muscle Mass in Cancer Patients

Little is known about the pathophysiology of low muscle mass in cancer patients [55]. Etiological factors seen during aging, such as physical inactivity and increased levels of proinflammatory cytokines, also contribute to cancer-related muscle wasting; however, the main cause is probably increased activity of the ubiquitin-proteasome system (UPS), resulting in increased muscle protein degradation. This can be present without the other determinants of cachexia, such as weight loss, metabolic changes, and loss of muscle and adipose tissue. Furthermore, cancer treatment frequently leads to vomiting, inappropriate food intake, and lack of physical activity, which can also result in the loss of both fat and muscle tissue [56]. In addition, corticosteroids, which are frequently used in cancer patients, stimulate the UPS and cause insulin resistance, both leading to muscle proteolysis [57].

To measure muscle mass in cancer patients, CT imaging instead of DEXA is mostly used because of its high availability, given its frequent use to evaluate tumor growth. However, DEXA could be a valuable alternative to measure muscle mass in cancer patients. Unfortunately, as holds true for muscle measurement in the elderly, consensus for determining muscle mass by CT scanning is lacking.

Muscle mass has been determined by measuring either the total psoas cross-sectional area (TPA) at the L3 level [58–61] or the total abdominal muscle area (TAMA) at the L3 level [16, 42, 62, 63]. The TAMA at L3 is highly correlated with the total body muscle mass (r = .924) [64]. The TAMA is corrected for height, resulting in a skeletal muscle index (cm²/m²). Therefore, muscle mass quantification can be performed easily by using only one slice, avoiding analyses of multiple images and larger surfaces being exposed to radiation.

Importantly, the first cutoff points for TAMA measurement using the single slice technique were computed in an obese population [16], but the prevalence of obesity in later studies using these cutoff points varied from 14% [65] to 57% [66]. Several studies established their own cutoff points for both TAMA and TPA, resulting in a large variation of diagnosing low muscle mass (Table 3). Furthermore, cutoff points for low muscle mass are mostly established by optimum stratification to detect the association with mortality, but the sensitivity to detect survival differences is higher in obese patients [62]. However, few studies report the distribution of muscle loss according to body mass index (BMI) groups in cancer patients.

Table 3.

Cutoff points for low muscle mass associated with mortality

Importantly, the first cutoff points for TAMA measurement using the single slice technique were computed in an obese population, but the prevalence of obesity in later studies using these cutoff points varied from 14% to 57%.

Prevalence of Low Muscle Mass in Cancer Patients

Several large studies have reported on the prevalence of low muscle mass in cancer patients [42, 62, 67, 68]. Most studies used TAMA and TPA to describe the prevalence of low muscle mass. The prevalence of low muscle mass using TPA seems to be somewhat lower compared with the measurement of TAMA (Table 4). However, because there is no standard method for the quantification of muscle mass by CT imaging, reported prevalence of low muscle mass is difficult to compare and are highly dependent on the used definition for muscle measurement. Furthermore, the level of correlation between TPA and TAMA is unknown, which makes it hard to compare these results with other studies. Table 4 describes the reported prevalence of low muscle mass and the used definition per cancer type. The prevalence of low muscle mass was highly variable across cancer types, ranging from 5% to 89%.

Table 4.

Prevalence of low muscle mass in patients with cancer using CT imaging

In cancer patients, low muscle mass more often occurs in patients older than 65 years, although is not restricted to the elderly [16]. In patients with tumors of the respiratory and gastrointestinal tract, 68% of the patients with low muscle mass were older than 65 years. Among the group of patients without low muscle mass, 45% were above 65 years old [16]. Knowledge is lacking about the prognostic value of low muscle mass in different age groups in the presence of malignancy. According to gender, no difference in the prevalence of low muscle mass is objectivated [68–71]. Compared with women, however, susceptibility for muscle loss and adverse outcomes related to low muscle mass in males has been described on multiple occasions in patients with cancer [69, 72–74] and without cancer [19, 75].

In addition to taking into account gender and BMI, stratification of cutoff points for low muscle mass by ethnicity should be considered. It has been reported that the muscle mass of young healthy Chinese men was 17% lower than in Caucasian men [76]. In studies investigating Asian populations, lower cutoff points for low muscle mass are applied [68, 77] (Table 3).

Adding Functional Assessments to Muscle Mass Measurements in Cancer Patients

Importantly—like what has been done in studies in the elderly and according to the previously mentioned EWGSOP guidelines— the prognostic value of determining muscle mass can potentially be increased by adding functional tests to muscle mass measurement in cancer patients. Physical performance is mostly described by using the Eastern Cooperative Oncology Group (ECOG) performance score in cancer patients. Although a high ECOG performance score correlated well with impaired physical function according to geriatric assessment, 38% of the patients with low ECOG performance scores were limited in instrumental activities of daily living, which possibly would require additional parameters to assess functional status [78].

However, so far, only two studies among cancer patients combined muscle mass determination and functional assessments (gait speed and handgrip strength) according to the EWGSOP guidelines, and they reported that the combination of radiological muscle mass and functional assessments had more predictive power for postoperative complications than radiological muscle mass alone in patients with colorectal cancer [12] and gastric cancer [79]. Although the EWGSOP guidelines do not recommend devices to determine handgrip strength, the Jamar hand dynamometer (Lafayette Instrument Co., Lafayette, IN, http://www.lafayetteinstrument.com) is the most widely used and is considered the gold standard to measure handgrip strength [80].

Functional tests actually reflect muscle quality, and several mechanisms of muscle quality are reported in the literature, such as decrease in muscle fiber size and number (resulting in reduced gait speed), reduction of muscle fiber contractility (resulting in reduced strength), mitochondrial dysfunction, and microfatty or macrofatty infiltration of muscle. Further research is warranted to determine whether adding functional tests improves the clinical value of muscle mass determination in cancer patients and, if so, to establish the most appropriate way to determine muscle quality.

Association of Low Muscle Mass With Chemotherapeutic Toxicity and Survival

Low muscle mass might be of emerging clinical significance in the oncology field because of its association with clinical endpoints such as toxicity and cancer-related mortality [81]. A summary of studies reporting on the prognostic value of low muscle mass for survival and treatment toxicity in cancer patients undergoing chemotherapeutic treatment is provided in Table 5. The studies are characterized by a variation of muscle-measurement methods, and the knowledge regarding prognosis is described per cancer type.

Table 5.

Prognostic impact of low muscle mass in patients undergoing chemotherapeutic treatment

Breast Cancer

After the introduction of muscle mass measurement using CT imaging, the first study that reported on the association of low muscle mass and oncological outcome was conducted among 55 younger patients with metastatic breast cancer and a mean age of 55 years [82]. All patients received a fixed dose of capecitabine, and toxicity was determined after one cycle to avoid the influence of treatment adjustments. Patients with low muscle mass had a calculated higher capecitabine dose per kilogram of lean body mass and had a three times greater risk of chemotherapeutic toxicity, such as diarrhea and stomatitis. Moreover, low muscle mass was the only independent predictor of toxicity in a model with age, body surface area, and ECOG performance score. In the same study, low muscle mass was associated with a shorter time to tumor progression (62 vs. 105 days). The authors mentioned that chemotherapeutic dose interruption or reduction for toxicity, which was more prevalent in patients with low muscle mass, could be responsible for a shorter time to tumor progression. Alternatively, the low muscle mass before starting treatment itself could be a sign of aggressive or advanced underlying disease [82].

In contrast, patients with localized breast cancer and low muscle mass achieved higher rates of pathological complete response after neo-adjuvant chemotherapeutic treatment compared with those without low muscle mass [83]. It is possible that patients with low muscle mass received a relatively higher dose of chemotherapeutic agents per kilogram of lean body mass (LBM), resulting in better chemotherapeutic efficacy on tumor eradication [83]. The systemic clearance and systemic drug levels of hydrophilic chemotherapeutic agents correlate well with the LBM [15, 84], and in patients with low LBM in relation to their length and weight, a lower volume of distribution of chemotherapeutic drugs can be seen, resulting in higher systemic drug levels and consequently more chemotherapeutic toxicity [14, 85, 86]. Likewise, it can be hypothesized that patients with low muscle mass will also have higher systemic drug levels, which might lead not only to more toxicity, but to better antitumor effects as well, in this case translated into a higher pathological response rate in patients with low muscle mass.

Non-Hodgkin Lymphoma

Three studies described the prognosis of patients with non-Hodgkin lymphoma undergoing chemotherapeutic treatment [63, 73, 87]. Only one study investigated the association between low muscle mass and treatment tolerability. Low muscle mass was a predictive factor of cancellation of chemotherapy compared with normal muscle mass, although the reasons for treatment interruption were not mentioned (40% vs. 16%, p = .02) [63]. In all studies, muscle mass was measured before the start of chemotherapy, and low muscle mass was associated with a worse overall survival compared with patients with normal muscle masses. In one study, the unfavorable survival effect was only detected in males [87].

Gastrointestinal Tumors

In colorectal cancer, low muscle mass was associated with a higher incidence of grade 3–4 chemotherapeutic toxicity during both adjuvant [88] and palliative treatment [72, 89]. Furthermore, most studies report impaired overall survival in patients with low muscle mass. Two studies showed an association between low muscle mass and mortality due to disease progression in patients with stage III colon cancer receiving adjuvant chemotherapy (hazard ratio [HR] 1.85, p = .022) [88] and in a large cohort of 1,473 patients (HR 1.34, p < .001) [62]. A third study showed that muscle loss greater than 5% during chemotherapy resulted in a two times higher mortality rate [89]. Remarkably, no association with recurrence-free survival was reported [88, 89].

In colorectal cancer, low muscle mass was associated with a higher incidence of grade 3–4 chemotherapeutic toxicity during both adjuvant and palliative treatment. Furthermore, most studies report impaired overall survival in patients with low muscle mass.

In patients with esophageal cancer, the association of low muscle mass with a higher incidence of chemotherapeutic toxicity was further confirmed [66, 70]. Among obese patients, those with low muscle mass had a five times higher risk of treatment toxicity compared with obese patients without low muscle mass before neo-adjuvant chemotherapy. Risk of toxicity did not reach significance in patients with low muscle mass and normal weight, also indicating that especially obese patients with low muscle mass are the worst prognostic group [66]. Another study containing 47 patients with esophago-gastric cancer reported that 57% were diagnosed with low muscle mass before the start of neo-adjuvant chemotherapy, and these patients suffered further reduction of muscle mass during chemotherapy. There was no association with reduced completion of chemotherapy or mortality, although this should be interpreted with caution, because the study was not powered to detect differences in clinical outcome [90].

Only one study determined the association between muscle mass and survival in patients with gastric cancer [91]. In this study, involving 152 patients before surgery, low muscle mass was not associated with mortality during hospital admission and 6-month mortality, although other studies have reported a higher incidence of postoperative complications in patients with low muscle mass after gastrectomy [92, 93].

Pancreatic and Hepatocellular Cancer

Associations of low muscle mass with treatment toxicity in patients with pancreatic and hepatocellular cancer have not been described yet. In patients with pancreatic cancer in a palliative setting, impaired overall survival has been reported in obese patients with low muscle mass. Of note, these results mostly could not be extended to patients with low muscle mass and normal weight [94, 95] (Table 5). In patients with hepatocellular carcinoma, low muscle mass was associated with both overall and progression-free survival [69, 96].

Discussion

Muscle mass loss occurs during aging, and in cancer patients it is possibly due to cachexia-associated processes. Accordingly, in cancer patients, low muscle mass is prevalent across all ages, but particularly in the elderly. The number of studies in cancer patients investigating the relationship between low muscle mass and clinical outcome is rapidly increasing, and promising results on the use of muscle mass measurement as a prognostic factor have been reported.

However, there are a few limitations. There is no consensus on a standard approach to measure muscle mass, and different cutoff points and devices are used. Furthermore, the current terminology of muscle mass in the literature is confusing. Radiological low muscle mass is part of the sarcopenia syndrome and is often called sarcopenia. However, sarcopenia is more than low muscle mass alone and consists of a triad of radiological low muscle mass, low muscle strength, and impaired physical performance [17]. Unfortunately, there is also no consensus on a definition of sarcopenia. Although low muscle mass seems like a good prognostic marker, it is possible that the prognostic value can be improved further by measuring muscle function and physical performance. This needs further investigation. Functional measures such as gait speed and handgrip strength are easy to perform, but are not yet widely available in oncological care. Nevertheless, many studies report a prognostic significance on measuring muscle mass, and establishing low muscle mass as a prognostic factor could be a valuable addition in estimating treatment risks and survival effects.

In cancer patients, CT imaging is mostly used to measure muscle mass, but a reference population for this evaluation has never been described. Consequently, the prevalence of low muscle mass and/or sarcopenia and their association with clinical outcomes is highly variable across the different studies and difficult to put into perspective. Studies are needed to construct reference populations for muscle mass measurement by CT imaging, adjusted for age, gender, race, and body mass index. Furthermore, the usage of devices to measure muscle mass, such as DEXA, which, like CT imaging, are widely available, could be explored in cancer patients. DEXA is highly available across cancer patients, in particular in postmenopausal, hormone receptor-positive breast cancer patients treated with endocrine therapy, and reference populations for muscle measurement using this device are well described.

To further study the prognostic value of low muscle mass in cancer patients, investigating the pathophysiology of muscle loss and the accompanying functional impairments in cancer patients is crucial. Studies investigating the impact of other well-known etiological factors of low muscle mass—such as low androgen levels, physical inactivity, and impaired nutritional intake—or on the effects of antitumor agents or comedication frequently used in cancer patients—such as corticosteroids—on muscle mass in cancer patients are lacking. Better insight into the mechanisms underlying low muscle mass in cancer patients is crucial because this might provide strategies to improve muscle mass and function and thereby potentially improve outcomes. Current treatment strategies to increase muscle mass in the elderly mainly involve resistance training and stimulation of nutritional intake [97]. Another possibility might be the investigation of low androgen levels in cancer patients with low muscle mass and whether this can be used as an intervention strategy. However, whether such strategies actually work in cancer patients—and, if so, what the optimal timing of such strategies should be—remains to be established.

Conclusion

Low muscle mass among cancer patients seems to be an important prognostic factor for outcomes in terms of treatment-induced toxicity and survival, but consensus about a definition of impaired muscle mass and a standardized approach to measure this are urgently warranted. Functional tests need to be measured to use the term sarcopenia, but the added value of these tests in cancer patients are yet to be established. Until a consensus on these items has been reached, reported prevalence of low muscle mass in populations and between cancer sites remains difficult to put into perspective. Consensus about a definition of low muscle mass and knowledge about its prognostic value and the underlying mechanisms are likely to contribute to strategies to develop a more personalized treatment approach and to novel interventions improving outcome.

This article is available for continuing medical education credit at CME.TheOncologist.com.

Author Contributions

Conception/Design: Hánah N. Rier, Agnes Jager, Stefan Sleijfer, Andrea B. Maier, Mark-David Levin

Provision of study material or patients: Hánah N. Rier, Agnes Jager, Stefan Sleijfer, Mark-David Levin

Collection and/or assembly of data: Hánah N. Rier

Data analysis and interpretation: Hánah N. Rier, Agnes Jager, Stefan Sleijfer, Mark-David Levin

Manuscript writing: Hánah N. Rier, Agnes Jager, Stefan Sleijfer, Andrea B. Maier, Mark-David Levin

Final approval of manuscript: Hánah N. Rier, Agnes Jager, Stefan Sleijfer, Andrea B. Maier, Mark-David Levin

Disclosures

Mark-David Levin: Abbvie, Roche (C/A). The other authors indicated no financial relationships.

(C/A) Consulting/advisory relationship; (RF) Research funding; (E) Employment; (ET) Expert testimony; (H) Honoraria received; (OI) Ownership interests; (IP) Intellectual property rights/inventor/patent holder; (SAB) Scientific advisory board