question: If muscles are built by cells repairing themselves after being ripped apart, how come cancer in muscles isn't more common?
comment: I actually found a TED talk referenced in another post under r/askscience. The talk discussed how muscles are naturally going to tear and reproduce so our ancestors who developed cancer in muscles died and the ones survived developed muscle cells that are more resistant to gene mutations.
passages: In a minority of patients with SPS, breast, ovarian, or lung cancer manifests paraneoplasticly as proximal muscle stiffness. These cancers are associated with the synaptic proteins amphiphysin and gephyrin. Paraneoplastic SPS with amphiphysin antibodies and breast adenocarcinoma tend to occur together. These patients tend not to have GAD antibodies. Passive transfer of the disease by plasma injection has been shown in paraneoplastic SPS but not classical SPS.
   Section::::Mechanism.
  
  Smooth muscle cells make up the involuntary muscles, which are found in most parts of the body, including the uterus, stomach and intestines, the walls of all blood vessels, and the skin. It is therefore possible for leiomyosarcomas to appear at any site in the body. They are most commonly found in the uterus, stomach, small intestine and retroperitoneum.
   The MYF6 gene is physically linked to the MYF5 gene on chromosome 12, and similar linkage is observed in all vertebrates. Mutations in the mouse Myf6 gene typically exhibit reduced levels of Myf5. Despite reductions in muscle mass of the back and defective rib formation, Myf6 mutants still exhibit fairly normal skeletal muscle. This demonstrates that Myf6 is not essential for the formation of most myofibers, at least in the strains of mice tested.
  
  In zebrafish, Myf6/Mrf4 is expressed in all terminally differentiated muscle examined, but expression has not been reported in muscle precursor cells.
  
  Section::::Clinical significance.
   The field of satellite cell biology suffers from the same technical difficulties as other stem cell fields. Studies rely almost exclusively on Flow cytometry and fluorescence activated cell sorting (FACS) analysis, which gives no information about cell lineage or behaviour. As such, the satellite cell niche is relatively ill-defined and it is likely that it consists of multiple sub-populations.
  
  Section::::Function.
  
  Section::::Function.:Muscle repair.
   Section::::Age-associated accumulation of DNA damage and decline in gene expression.:Muscle.
   Certain studies suggested a possible link between a high incidence of amyotrophic lateral sclerosis (ALS) among professional American football players and Italian soccer players, and certain sports supplements including BCAAs. In mouse studies, BCAAs were shown to cause cell hyper-excitability resembling that usually observed in ALS patients. The proposed underlying mechanism is that cell hyper-excitability results in increased calcium absorption by the cell and thus brings about cell death, specifically of neuronal cells which have particularly low calcium buffering capabilities.
   Other patients who received BTS-derived tissue and body parts include a Colorado woman who had to repeat her ACL replacement surgery after her first BTS tendon failed, an Ohio woman who developed syphilis after receiving a bone from BTS, and an Ohio man who developed both HIV and hepatitis C after receiving BTS bone implants in surgery.
   The process of muscle regeneration involves considerable remodeling of extracellular matrix and, where extensive damage occurs, is incomplete. Fibroblasts within the muscle deposit scar tissue, which can impair muscle function, and is a significant part of the pathology of muscular dystrophies.
   Accompanying the atrophy process noted above are the important observations that many (but not all) of the slow fibers in primarily antigravity-type muscles (such as SOL and VI) are also induced to express fast myosin isoforms. This transformation is largely manifested in the expression of hybrid fibers, in which both slow MHC and either fast type IIx or fast type IIa MHC become simultaneously co-expressed. These observations suggest that the slow MHC is targeted for degradation, evidenced by the net loss in slow MHC in the atrophying muscle (fibers), while at the same time, according to premRNA and mRNA analyses, up-regulation of the faster MHC genes by transcriptional and/or pretranslational processes occurs. More recent studies on this topic clearly suggest that the type IIx MHC, which is a faster isoform than the IIa type, is more abundantly expressed. From these observations it is apparent that the myofibrillar fraction, which is a key component of the muscle, is targeted for net degradation (as noted above) for two reasons:
   Protein synthesis and protein degradation decline with age in skeletal and heart muscle, as would be expected, since DNA damage blocks gene transcription. In 2005, Piec et al. found numerous changes in protein expression in rat skeletal muscle with age, including lower levels of several proteins related to myosin and actin. Force is generated in striated muscle by the interactions between myosin thick filaments and actin thin filaments.
  
  Section::::Age-associated accumulation of DNA damage and decline in gene expression.:Liver.
   In undamaged muscle, the majority of satellite cells are "quiescent"; they neither differentiate nor undergo cell division. In response to mechanical strain, satellite cells become "activated". Activated satellite cells initially proliferate as skeletal myoblasts before undergoing myogenic differentiation.
  
  Section::::Structure.
  
  Section::::Structure.:Genetic markers.
   Several studies published since 1990 indicate that cooking muscle meat creates heterocyclic amines (HCAs), which are thought to increase cancer risk in humans. Researchers at the National Cancer Institute published results of a study which found that human subjects who ate beef rare or medium-rare had less than one third the risk of stomach cancer than those who ate beef medium-well or well-done. While eating muscle meat raw may be the only way to avoid HCAs fully, the National Cancer Institute states that cooking meat below creates "negligible amounts" of HCAs. Also, microwaving meat before cooking may reduce HCAs by 90%.
   In experimental evaluation of specific DNA repair deficiencies in cancers, many specific DNA repair deficiencies were also shown to occur in the field defects surrounding those cancers. The Table, below, gives examples for which the DNA repair deficiency in a cancer was shown to be caused by an epigenetic alteration, and the somewhat lower frequencies with which the same epigenetically caused DNA repair deficiency was found in the surrounding field defect.
   The first step to understanding the importance of macrophages in muscle repair, growth, and regeneration is that there are two "waves" of macrophages with the onset of damageable muscle use – subpopulations that do and do not directly have an influence on repairing muscle. The initial wave is a phagocytic population that comes along during periods of increased muscle use that are sufficient to cause muscle membrane lysis and membrane inflammation, which can enter and degrade the contents of injured muscle fibers. These early-invading, phagocytic macrophages reach their highest concentration about 24 hours following the onset of some form of muscle cell injury or reloading. Their concentration rapidly declines after 48 hours. The second group is the non-phagocytic types that are distributed near regenerative fibers. These peak between two and four days and remain elevated for several days during the hopeful muscle rebuilding. The first subpopulation has no direct benefit to repairing muscle, while the second non-phagocytic group does.
   BULLET::::- Canadian comedian Irwin Barker, who was featured in a documentary, "That's my Time", which chronicled his battle with leiomyosarcoma. In Barker's own words. "Cancer has my body but not my spirit, and I'll continue to make jokes, not so much about cancer, but in spite of it."
  
  BULLET::::- E. J. McGuire Long time professional ice hockey coach, scout, and VP of the NHL Central Scouting Bureau
  
  BULLET::::- Dr. Amy Reed (US physician who campaigned for discontinuing the use of morcellators, which have been shown to spread the disease)
  
  BULLET::::- Patricia Elliott, Tony-winning theatre and soap opera actress
   In humans with weakness and low muscle tone, a muscle biopsy can help distinguish between myopathies (where the pathology is in the muscle tissue itself) and neuropathies (where the pathology is at the nerves innervating those muscles). Muscle biopsies can also help to distinguish among various types of myopathies, by microscopic analysis for differing characteristics when exposed to a variety of chemical reactions and stains.
   Spinal muscular atrophy (SMA) and ageing-related motor degeneration share clear parallels with ALS in the patterns and specificity of motor neuron loss. Though it is completely distinct from ALS in its pathogenesis, SMA leads to a similar rapid death of FF motor neurons, with S type neurons being generally spared. Further, motor pools controlling facial muscles (including those of the eye) and voluntary excretory muscles are spared. Motor neuron degeneration caused by ageing similarly affects FF types but not S types; ageing also seems to spare ocular motor pools. These similar patterns of neurodegeneration in three different diseases have led researchers to speculate that slow-twitch motor neurons, along with motor pools of the eyes and excretory muscles, have intrinsic neuroprotective properties that are not disease-specific. Research is currently being conducted to discover a possible molecular basis for neuroprotection in these cell types.
   Section::::Clinical significance.:Other diseases.
  
  Pectoralis major muscle in rare occasions may develop intramuscular lipomas. Such rare tumors may mimic malignant breast tumors as they look like enlargements of the breasts. They are well-encapsulated radiolucent tumours of fat density. Their location can be accurately identified through computed tomography and magnetic resonance imaging (MRI). The treatment in these cases involves complete surgical excision because of the risk of liposarcoma they post especially large intramuscular liposomas. Partial excision is risky because recurrence may occur.
  
  Section::::See also.
  
  BULLET::::- Pectoralis minor, an inferior, smaller muscle to the pectoralis major
   About 1 in 100,000 people gets diagnosed with LMS each year. Leiomyosarcoma is one of the more common types of soft-tissue sarcoma, representing 10 percent to 20 percent of new cases. (Leiomyosarcoma of the bone is more rare.) Sarcoma is rare, consisting of only 1 percent of cancer cases in adults. Leiomyosarcomas can be very unpredictable. They can remain dormant for long periods of time and recur after years. It is a resistant cancer, meaning generally not very responsive to chemotherapy or radiation. The best outcomes occur when it can be removed surgically with wide margins early, while small and still in situ.
   Currently, there is no association between myoferlin mutations and human diseases. However, it has been shown experimentally that loss of myoferlin results in reduced myoblast fusion and muscle size. There is also a correlation between myoferlin overexpression and several types of cancers such as lung cancer and breast cancer. In pancreatic ductal adenocarcinoma (PDAC) myoferlin increases cell proliferation and promotes tumorigenesis and its expression negatively correlates with tumor size. Breast cancer patients with overexpressed myoferlin have a lower survival rate. Although it is not yet clear how myoferlin contributes in cancer pathology in a molecular level, there are scientific evidences that myoferlin overexpression is associated with tumor growth and metastasis. In fact, myoferlin depletion in cancer cell lines can result in reduced tumor size and metastasis rate.
   These forms of cancer have been hypothesized to be highly sensitive to ferroptosis, or react to erastin or Xc- in a way that minimizes the tumor cells or responds to this treatment with a result of cell death. An upregulation of iron levels has also been seen to induce ferroptosis in certain types of cancer, such as breast cancer. Breast cancer cells have exhibited vulnerability to ferroptosis via a combination of siramesine and lapatinib. These cells also exhibited an autophagic cycle independent of ferroptotic activity, indicating that the two different forms of cell death could be controlled to activate at specific times following treatment.
   The pathogenesis of this myopathy is very varied. Many mutations occur in the region of actin's indentation near to its nucleotide binding sites, while others occur in Domain 2, or in the areas where interaction occurs with associated proteins. This goes some way to explain the great variety of clumps that form in these cases, such as Nemaline or Intranuclear Bodies or Zebra Bodies. Changes in actin's folding occur in nemaline myopathy as well as changes in its aggregation and there are also changes in the expression of other associated proteins. In some variants where intranuclear bodies are found the changes in the folding masks the nucleus's protein exportation signal so that the accumulation of actin's mutated form occurs in the cell nucleus. On the other hand, it appears that mutations to "ACTA1" that give rise to a CFTDM have a greater effect on sarcomeric function than on its structure. Recent investigations have tried to understand this apparent paradox, which suggests there is no clear correlation between the number of rods and muscular weakness. It appears that some mutations are able to induce a greater apoptosis rate in type II muscular fibres.
   Leiomyosarcoma
  
  Leiomyosarcoma, is a malignant (cancerous) smooth muscle tumor. A benign tumor originating from the same tissue is termed leiomyoma. While it has been believed that leiomyosarcomas do not arise from leiomyomas, there are leiomyoma variants for which classification is evolving. 
   Another study demonstrated that skeletal muscle fibres of collagen VI knockout mice showed signs of degeneration due to an insufficiency of autophagy which led to an accumulation of damaged mitochondria and excessive cell death. Exercise-induced autophagy was unsuccessful however; but when autophagy was induced artificially post-exercise, the accumulation of damaged organelles in collagen VI deficient muscle fibres was prevented and cellular homeostasis was maintained. Both studies demonstrate that autophagy induction may contribute to the beneficial metabolic effects of exercise and that it is essential in the maintaining of muscle homeostasis during exercise, particularly in collagen VI fibres.
   Aged muscle cells in mammalian hearts constantly regenerate, albeit at a very low rate. Within 18 months around five percent of the heart muscle cells regenerated themselves originating from Sca-1 stem cells
  
  Section::::Effects of exercise.
  
raw_presuppositions: Cancer in muscles is not common Cancer doesn't develop in muscles.
raw_corrections: Cancer in muscles was common to our ancestors, but those who survived developed muscle cells that are more resistant to gene mutations. It used to develop in muscles but because of evolution it stopped.