Athena Vale
Cancer treatment can cause long-term muscle problems, including muscle dysfunction, weakness, and wasting. This can be caused by the cancer itself, its treatment, or a combination of both. Chemotherapy-induced peripheral neuropathy, for example, can cause nerve and muscle effects, including weakness and fatigue in skeletal muscle. This can lead to a limited treatment regimen and increased morbidity. Furthermore, extended therapy with corticosteroids, a potent anti-inflammatory drug, may cause muscle wasting. Cancer-induced muscle wasting, or cachexia, can lead to drastic weight loss and increased mortality rates. While there is currently no effective treatment for cachexia, early and appropriate nutritional intervention may help attenuate and reverse muscle wasting. Exercise training has also been found to be a promising therapeutic countermeasure to cancer-related muscle dysfunction.
| Characteristics | Values |
|---|---|
| Cancer treatment causing long-term muscle problems | Chemotherapy-induced peripheral neuropathy |
| Muscle dysfunction | Prevalent phenomenon in oncology settings |
| Muscle wasting | Cancer-induced |
| Cancer cachexia | Multifactorial syndrome common in advanced malignancy |
| Corticosteroids | Anti-inflammatory drugs that may cause muscle wasting as a side effect |
| Thalidomide | Immunomodulatory and anti-inflammatory agent tested for cancer cachexia |
| Exercise training | Potential therapeutic countermeasure to cancer-related muscle dysfunction |
| Nutritional intervention | Potential strategy to counteract inflammation and interfere with cancer cachexia |
| Pharmacological intervention | MEK inhibitors, tyrosine kinase inhibitors, JAK/STAT3 pathway inhibitors |
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What You'll Learn
Cancer-induced muscle wasting
The causes of cancer-related muscle dysfunction are complex and vary depending on the patient's clinical setting. Tumours can cause muscle cells to self-destruct, releasing amino acids that can be used by other cells in the body. This slight increase in autophagy can result in a loss of muscle mass over time. Removing the tumour can reverse cachexia, but not all tumours can be removed due to the spread of cancer, inaccessibility, or ineffective treatment.
Research has focused on developing agents that target the activin type II B receptor (ActRIIB) pathway, which negatively regulates muscle mass. Blockade of this pathway has been shown to counteract muscle wasting and improve muscle strength without influencing tumour growth. However, initial clinical trials encountered bleeding issues. Other treatments, such as PD98059 (a MEK inhibitor) and selumetinib, have shown promise in restoring myogenesis and reducing muscle depletion.
Exercise training has also been explored as a therapeutic countermeasure to cancer-related muscle dysfunction. While it has shown potential in improving muscle function, there is a need for further studies to evaluate its long-term benefits on clinical outcomes. Nutritional interventions have been suggested, but additional investigations are required to determine their effectiveness in attenuating and reversing muscle wasting.
Overall, cancer-induced muscle wasting is a complex and challenging condition that requires further research to develop effective treatments and improve patient outcomes.
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Corticosteroids and thalidomide as treatments
Corticosteroids are potent anti-inflammatory drugs frequently used to treat cancer patients. They can help ease cancer-related fatigue and improve patients' energy levels. They can also boost appetite. However, extended therapy with corticosteroids is not recommended as they may cause muscle wasting.
Thalidomide is an agent with immunomodulatory, anti-inflammatory, and antiangiogenic properties. It has been investigated in a number of cancers, including multiple myeloma, myelodysplastic syndromes, gliomas, Kaposi's sarcoma, renal cell carcinoma, advanced breast cancer, and colon cancer. Its role has been best explored in myeloma, where it is remarkably active, causing clinically meaningful responses in one-third of extensively pretreated patients and in over half of patients treated early in the course of the disease. It also acts synergistically with corticosteroids and chemotherapy in myeloma. Thalidomide produces improvements in cytopenias characteristic of myelodysplastic syndrome, resulting in the reduction or elimination of transfusion dependence in some patients. Responses have also been seen in one-third of patients with Kaposi's sarcoma, a small proportion of patients with renal cell carcinoma and high-grade glioma, and in combination therapy for advanced breast cancer.
Thalidomide is currently being investigated in a number of clinical trials for cancer. Drowsiness, constipation, and fatigue are common adverse effects seen in 75% of patients. Symptoms of peripheral neuropathy and skin rash are seen in 30%. A minority of patients experience bradycardia and thrombotic phenomena. Despite the high frequency of adverse effects, those severe enough to necessitate cessation of therapy are seen in only 10 to 15% of patients.
Thalidomide and its analogs lenalidomide and pomalidomide have wide-ranging and seemingly disparate cellular actions, including induction of oxidative stress and inhibition of angiogenesis, as well as multiple effects on the immune system. Thalidomide was found to bind to the protein cereblon, which forms an E3 ubiquitin ligase complex with other proteins. This complex tags specific proteins with ubiquitin, thereby targeting them for proteolysis. The drug-protein interaction disrupts the activity of the E3 ubiquitin ligase complex, which underpins the cytotoxic and immune-modulating effects of IMiDs.
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Exercise as a countermeasure
Cancer-related muscle dysfunction is a common issue for patients, regardless of the tumour stage and nutritional state. This can be caused by the cancer itself, the tumour environment, chemotherapy, radiotherapy, and malnutrition. The mechanisms underlying these causes are complex and involve inflammation, autophagy, disrupted protein synthesis, and degradation.
Exercise training has been identified as a promising therapeutic countermeasure to cancer-related muscle dysfunction. Exercise intervention trials have shown that muscle function can be improved, which may also positively impact clinical outcomes such as time-to-progression, treatment toxicity, and mortality.
However, there is a discrepancy between the timing of these exercise intervention trials and the study populations. Most trials have been conducted on early-stage breast and prostate cancer patients, while observational studies have shown that muscle function is a critical prognostic factor for advanced-stage patients. Therefore, future exercise trials should focus on evaluating the long-term benefits of improved muscle function on clinical outcomes in early-stage patients and be promoted in advanced-stage settings to potentially reverse cancer-related muscle dysfunction.
In addition to exercise, nutritional interventions have been explored as a potential strategy to prevent and treat cancer-induced muscle wasting. While increased nutrient intake alone may not compensate for drastic weight loss in patients with cachexia, specific nutrients or nutraceuticals may help counteract inflammation and interfere with the molecular mechanisms of cancer cachexia. For example, fish oil-derived fatty acids have been studied for their potential ability to modulate pro-inflammatory cytokines and increase insulin sensitivity.
Overall, exercise training and nutritional interventions show potential as countermeasures to cancer-related muscle dysfunction and wasting. Further research and clinical trials are needed to optimize these approaches and evaluate their long-term benefits for cancer patients.
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Bone metastases and muscle weakness
Cancer patients experience muscle dysfunction and wasting across all stages of their disease trajectory. This is caused by a combination of tumour- and therapy-related factors. Tumours can cause muscle cells in the body to self-destruct, leading to muscle wasting and cachexia. This results in a loss of muscle mass and weight, and increased toxicity from cancer treatment.
Bone metastases occur when cancer cells break away from where they started and spread to a bone. Nearly all types of cancer can spread to the bones, but some types are more likely to do so, including breast cancer, kidney cancer, lung cancer, multiple myeloma, prostate cancer, and thyroid cancer. Bone metastases are often incurable and can cause pain, hypercalcemia, and bone destruction.
Bone metastases can result in muscle weakness, which is often associated with cancer cachexia. Tumour cells in the bone stimulate excessive osteoclast activity, causing the release of growth factors that fuel tumour growth and bone destruction. These bone-derived growth factors can act systemically to cause muscle weakness. Muscle weakness can be caused by reduced muscle mass or reduced muscle function, and in advanced disease, it is likely due to a combination of both.
Treatments for bone metastases include bone-targeted anti-resorptive therapy, chemotherapy, hormonal therapy, radiation, and surgery. While these treatments can shrink tumours and relieve symptoms, they do not cure the disease. Exercise training has been proposed as a therapeutic countermeasure to cancer-related muscle dysfunction, but more research is needed to determine its effectiveness in advanced-stage patients.
In summary, bone metastases can cause muscle weakness through a combination of reduced muscle mass and function. This can be a debilitating co-morbidity of bone metastases, further limiting treatment options and increasing the risk of fracture. While treatments for bone metastases can help relieve symptoms, there is currently no cure for this condition.
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Chemotherapy-induced peripheral neuropathy
Cancer treatment can cause long-term muscle problems. Chemotherapy-induced peripheral neuropathy (CIPN) is one of the most common side effects of cancer treatment, affecting 19% to over 85% of patients. It is a challenging complication that arises from treatment with many commonly used anti-cancer agents. CIPN is a mostly sensory neuropathy, but it can also present with motor and autonomic changes of varying intensity and duration. The feet and hands are often affected simultaneously, with predominant pain, and symptoms tend to progress rapidly.
The mechanisms underlying CIPN involve damage to peripheral sensory, motor, and autonomic neurons. Six main substance groups are known to cause this damage, resulting in the development of CIPN: platinum-based antineoplastic agents, vinca alkaloids, epothilones (ixabepilone), taxanes, proteasome inhibitors (bortezomib), and immunomodulatory drugs (thalidomide). Platinum-based drugs, for example, induce the activation of glia cells, leading to immune cell activation and the release of pro-inflammatory cytokines. This results in nociceptor sensitization and hyperexcitability of peripheral neurons, causing neuroinflammation. Mitochondrial damage caused by platinum-based drugs also increases reactive oxygen species (ROS), leading to enzyme, protein, and lipid damage within neurons and dysregulation of calcium homeostasis, which induces apoptotic changes in peripheral nerves.
CIPN is a significant problem for cancer patients, survivors, and their healthcare providers. Currently, there is no single effective method for preventing CIPN, and treatment options are limited. Acute CIPN can occur during chemotherapy, sometimes requiring dose reduction or cessation of treatment. Approximately 30% of patients will still experience CIPN a year or more after completing chemotherapy.
Some therapies have been used to prevent or limit the effects of CIPN, but more research is needed to prove their effectiveness. These include cold therapy (cryotherapy) and compression therapy during chemotherapy infusions. Cold therapy involves using ice packs, special socks, and mittens or gloves to cool down the hands and feet. Compression therapy involves wearing tight-fitting gloves to compress the fingertips during chemotherapy. These therapies may reduce circulation in the hands and feet, potentially lowering the amount of chemotherapy drugs that reach these areas.
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Frequently asked questions
Yes, cancer treatment can cause long-term muscle weakness and fatigue. This is due to oxidative stress, which affects non-targeted tissues such as striated muscle.
Long-term muscle problems caused by cancer treatment include muscle weakness, fatigue, and reduced muscle function. These problems can persist from 6 months to 2 years following remission.
Cancer treatment, such as chemotherapy, can cause oxidative stress in skeletal muscle, leading to muscle weakness and fatigue. Chemotherapy drugs such as doxorubicin have been linked to skeletal muscle weakness.
Exercise training has been suggested as a therapeutic countermeasure to cancer-related muscle dysfunction. Additionally, nutritional interventions and specific nutrients/nutraceuticals may help attenuate and reverse cancer-related muscle wasting.
Yes, if symptoms are severe, medications may be prescribed to provide relief. It is important to discuss this with your doctor to determine the most appropriate treatment option.
