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==Classification==
==Classification==
Embryonal rhabdomyosarcoma is the more common of two major sub-types of [[rhabdomyosarcoma]] and accounts for 60% to 70% of rhabdomyosarcoma, the other being [[alveolar rhabdomyosarcoma]] (ARMS), also known as ''PAX''-fusion positive or Fusion Positive rhabdomyosarcoma.<ref name="Yohe_2019" /><ref name="Rodeberg_2006">{{cite journal | vauthors = Rodeberg D, Paidas C | title = Childhood rhabdomyosarcoma | journal = Seminars in Pediatric Surgery | volume = 15 | issue = 1 | pages = 57–62 | date = February 2006 | pmid = 16458847 | doi = 10.1053/j.sempedsurg.2005.11.009 | series = Childhood Cancer | s2cid = 1220308 }}</ref> Most often, ERMS is found in children during ages 0 to 5 years old, however ERMS can develop throughout any stage of life.<ref>{{Cite web |title=What Is Rhabdomyosarcoma? |url=https://www.cancer.org/cancer/rhabdomyosarcoma/about/what-is-rhabdomyosarcoma.html |access-date=2022-07-28 |website=www.cancer.org |language=en}}</ref> Embryonal rhabdomyosarcoma can be further divided into three subcategories: the botryoid, spindle cell, and not-otherwise-specified (NOS).<ref>{{cite journal | vauthors = Ibrahim U, Saqib A, Mohammad F, Ding J, Salman B, Collado FK, Dhar M | title = Embryonal Rhabdomyosarcoma of the Cervix: A Rare Disease at an Uncommon Age | journal = Cureus | volume = 9 | issue = 11 | pages = e1864 | date = November 2017 | pmid = 29375950 | pmc = 5773277 | doi = 10.7759/cureus.1864 }}</ref> These two subtypes of rhabdomyosarcoma, ERMS and ARMS, each have multiple genetic variations.<ref name="Ricker_2020">{{cite journal | vauthors = Ricker CA, Crawford K, Matlock K, Lathara M, Seguin B, Rudzinski ER, Berlow NE, Keller C | display-authors = 6 | title = Defining an embryonal rhabdomyosarcoma endotype | journal = Cold Spring Harbor Molecular Case Studies | volume = 6 | issue = 2 | pages = a005066 | date = April 2020 | pmid = 32238403 | pmc = 7133750 | doi = 10.1101/mcs.a005066 }}</ref>
Embryonal rhabdomyosarcoma is the more common of two major sub-types of [[rhabdomyosarcoma]] and accounts for 60% to 70% of rhabdomyosarcoma, the other being [[alveolar rhabdomyosarcoma]] (ARMS), also known as ''PAX''-fusion positive or Fusion Positive rhabdomyosarcoma.<ref name="Yohe_2019" /><ref name="Rodeberg_2006">{{cite journal | vauthors = Rodeberg D, Paidas C | title = Childhood rhabdomyosarcoma | journal = Seminars in Pediatric Surgery | volume = 15 | issue = 1 | pages = 57–62 | date = February 2006 | pmid = 16458847 | doi = 10.1053/j.sempedsurg.2005.11.009 | series = Childhood Cancer | s2cid = 1220308 }}</ref> Most often, ERMS is found in children during ages 0 to 5 years old, however ERMS can develop throughout any stage of life.<ref>{{Cite web |title=What Is Rhabdomyosarcoma? |url=https://www.cancer.org/cancer/rhabdomyosarcoma/about/what-is-rhabdomyosarcoma.html |access-date=2022-07-28 |website=www.cancer.org |language=en}}</ref> Embryonal rhabdomyosarcoma can be further divided into three subcategories: the botryoid, spindle cell, and not-otherwise-specified (NOS).<ref>{{cite journal | vauthors = Ibrahim U, Saqib A, Mohammad F, Ding J, Salman B, Collado FK, Dhar M | title = Embryonal Rhabdomyosarcoma of the Cervix: A Rare Disease at an Uncommon Age | journal = Cureus | volume = 9 | issue = 11 | pages = e1864 | date = November 2017 | pmid = 29375950 | pmc = 5773277 | doi = 10.7759/cureus.1864 }}</ref> These two subtypes of rhabdomyosarcoma, ERMS and ARMS, each have multiple genetic variations.<ref name="Ricker_2020">{{cite journal | vauthors = Ricker CA, Crawford K, Matlock K, Lathara M, Seguin B, Rudzinski ER, Berlow NE, Keller C | display-authors = 6 | title = Defining an embryonal rhabdomyosarcoma endotype | journal = Cold Spring Harbor Molecular Case Studies | volume = 6 | issue = 2 | pages = a005066 | date = April 2020 | pmid = 32238403 | pmc = 7133750 | doi = 10.1101/mcs.a005066 }}</ref>

When examining Embroynal Rhabdomyosarcoma tumors vs. Alveolar Rhabdomyosarcoma tumors, a 2013 study had discovered that there were more rates of mutation in ERMS tumors.<ref>{{Cite journal |last=Chen |first=Xiang |last2=Stewart |first2=Elizabeth |last3=Shelat |first3=Anang A. |last4=Qu |first4=Chunxu |last5=Bahrami |first5=Armita |last6=Hatley |first6=Mark |last7=Wu |first7=Gang |last8=Bradley |first8=Cori |last9=McEvoy |first9=Justina |last10=Pappo |first10=Alberto |last11=Spunt |first11=Sheri |date=2013-12-09 |title=Targeting Oxidative Stress in Embryonal Rhabdomyosarcoma |url=https://www.cell.com/cancer-cell/abstract/S1535-6108(13)00490-X |journal=Cancer Cell |language=English |volume=24 |issue=6 |pages=710–724 |doi=10.1016/j.ccr.2013.11.002 |issn=1535-6108 |pmc=PMC3904731 |pmid=24332040}}</ref>


Embryonal rhabdomyosarcoma results from copy number alterations as well as mutations in the RAS pathway.<ref name="Leiner_2020" /> It is believed that some of the identifying genetic mutations that can cause ERMS include p53 loss, RAS pathway activation, MYOD1 mutations.<ref name="Ricker_2020" /> There have not been many studies linking the genetic profile and clinical outcome of ERMS. However in this report, the authors analyzed patient data from the Children's Oncology Group (COG) and European paediatric Soft tissue sarcoma Study Group (EpSSG), hoping to analyze the identify any relationship between clinical outcomes and genetic mutations.<ref name=":0">{{cite journal | vauthors = Shern JF, Selfe J, Izquierdo E, Patidar R, Chou HC, Song YK, Yohe ME, Sindiri S, Wei J, Wen X, Rudzinski ER, Barkauskas DA, Lo T, Hall D, Linardic CM, Hughes D, Jamal S, Jenney M, Chisholm J, Brown R, Jones K, Hicks B, Angelini P, George S, Chesler L, Hubank M, Kelsey A, Gatz SA, Skapek SX, Hawkins DS, Shipley JM, Khan J | display-authors = 6 | title = Genomic Classification and Clinical Outcome in Rhabdomyosarcoma: A Report From an International Consortium | language = EN | journal = Journal of Clinical Oncology | volume = 39 | issue = 26 | pages = 2859–2871 | date = September 2021 | pmid = 34166060 | pmc = 8425837 | doi = 10.1200/JCO.20.03060 }}</ref> The study comprised of 641 patients with sufficient data to analyze.<ref name=":0" /> The authors found that the patients in the fusion-negative group had different genetic mutation profiles than those in the fusion-positive group.<ref name=":0" /> Focusing on the fusion negative patients, it was shown that the most fusion-negative tumors was caused by RAS isoform mutations, making up more than 50% of the fusion-negative cases.<ref name=":0" /> Tumor suppressor genes such as TP53 mutations were shown in about 13% in the mutations and MYOD1 mutations were seen in about 3% of the mutations.<ref name=":0" />
Embryonal rhabdomyosarcoma results from copy number alterations as well as mutations in the RAS pathway.<ref name="Leiner_2020" /> It is believed that some of the identifying genetic mutations that can cause ERMS include p53 loss, RAS pathway activation, MYOD1 mutations.<ref name="Ricker_2020" /> There have not been many studies linking the genetic profile and clinical outcome of ERMS. However in this report, the authors analyzed patient data from the Children's Oncology Group (COG) and European paediatric Soft tissue sarcoma Study Group (EpSSG), hoping to analyze the identify any relationship between clinical outcomes and genetic mutations.<ref name=":0">{{cite journal | vauthors = Shern JF, Selfe J, Izquierdo E, Patidar R, Chou HC, Song YK, Yohe ME, Sindiri S, Wei J, Wen X, Rudzinski ER, Barkauskas DA, Lo T, Hall D, Linardic CM, Hughes D, Jamal S, Jenney M, Chisholm J, Brown R, Jones K, Hicks B, Angelini P, George S, Chesler L, Hubank M, Kelsey A, Gatz SA, Skapek SX, Hawkins DS, Shipley JM, Khan J | display-authors = 6 | title = Genomic Classification and Clinical Outcome in Rhabdomyosarcoma: A Report From an International Consortium | language = EN | journal = Journal of Clinical Oncology | volume = 39 | issue = 26 | pages = 2859–2871 | date = September 2021 | pmid = 34166060 | pmc = 8425837 | doi = 10.1200/JCO.20.03060 }}</ref> The study comprised of 641 patients with sufficient data to analyze.<ref name=":0" /> The authors found that the patients in the fusion-negative group had different genetic mutation profiles than those in the fusion-positive group.<ref name=":0" /> Focusing on the fusion negative patients, it was shown that the most fusion-negative tumors was caused by RAS isoform mutations, making up more than 50% of the fusion-negative cases.<ref name=":0" /> Tumor suppressor genes such as TP53 mutations were shown in about 13% in the mutations and MYOD1 mutations were seen in about 3% of the mutations.<ref name=":0" />

Revision as of 05:44, 1 August 2022

Embryonal rhabdomyosarcoma
SpecialtyOncology Edit this on Wikidata

Embryonal rhabdomyosarcoma (EMRS) is a rare histological form of cancer of connective tissue wherein the mesenchymally-derived malignant cells resemble the primitive developing skeletal muscle of the embryo. It is the most common soft tissue sarcoma occurring in children.[1] Embryonal rhabdomyosarcoma is also known as PAX-fusion negative or Fusion-Negative rhabdomyosarcoma, as tumors of this subtype are unified by their lack of a PAX3-FOXO1 fusion oncogene (or other PAX fusions seen in alveolar rhabdomyosarcoma).[2][3]

Classification

Embryonal rhabdomyosarcoma is the more common of two major sub-types of rhabdomyosarcoma and accounts for 60% to 70% of rhabdomyosarcoma, the other being alveolar rhabdomyosarcoma (ARMS), also known as PAX-fusion positive or Fusion Positive rhabdomyosarcoma.[3][4] Most often, ERMS is found in children during ages 0 to 5 years old, however ERMS can develop throughout any stage of life.[5] Embryonal rhabdomyosarcoma can be further divided into three subcategories: the botryoid, spindle cell, and not-otherwise-specified (NOS).[6] These two subtypes of rhabdomyosarcoma, ERMS and ARMS, each have multiple genetic variations.[7]

When examining Embroynal Rhabdomyosarcoma tumors vs. Alveolar Rhabdomyosarcoma tumors, a 2013 study had discovered that there were more rates of mutation in ERMS tumors.[8]

Embryonal rhabdomyosarcoma results from copy number alterations as well as mutations in the RAS pathway.[9] It is believed that some of the identifying genetic mutations that can cause ERMS include p53 loss, RAS pathway activation, MYOD1 mutations.[7] There have not been many studies linking the genetic profile and clinical outcome of ERMS. However in this report, the authors analyzed patient data from the Children's Oncology Group (COG) and European paediatric Soft tissue sarcoma Study Group (EpSSG), hoping to analyze the identify any relationship between clinical outcomes and genetic mutations.[10] The study comprised of 641 patients with sufficient data to analyze.[10] The authors found that the patients in the fusion-negative group had different genetic mutation profiles than those in the fusion-positive group.[10] Focusing on the fusion negative patients, it was shown that the most fusion-negative tumors was caused by RAS isoform mutations, making up more than 50% of the fusion-negative cases.[10] Tumor suppressor genes such as TP53 mutations were shown in about 13% in the mutations and MYOD1 mutations were seen in about 3% of the mutations.[10]

Genetic conditions such as Gorlin syndrome, neurofibromatosis type 1, and Beckwith-Wiedemann syndrome have been shown to predispose individuals to embryonal rhabdomyosarcoma.[9] Risk Factors associated with possible increased Embryonal Rhabdomyosarcoma include cigarette smoking, older age of mother, x-ray exposure, and maternal drug use.[11]

Embryonal rhabdomyosarcoma is commonly driven by a mutation in the RAS family of proto-oncogenes, creating a powerful signal which is now known to promote tumor growth by preventing muscle lineage progression by blocking expression of the transcription factor myogenin.[12] Inhibition of this signaling pathway with trametinib has been recently shown to overcome this differentiation block and reduce tumor progression in animal models of embryonal rhabdomyosarcoma.[12]

Embryonal rhabdomyosarcoma has been informally classified as a "small round blue cell tumor"[1] because of the characteristic microscopic appearance of its cells after histological staining with hematoxylin and eosin. Histologically, embryonal rhabdomyosarcoma commonly presents as alternating loose and dense patches of cells, including round cell and spindle cell components encapsulated in a myxoid stroma.[13][14] The heterogenous structure resembles striated muscle at various embryonal developmental stages.[15]

Embryonal rhabdomyosarcoma can develop in soft tissues throughout the body, however, it is commonly found in the "head and neck area or in the genital or urinary organs" [4][16]

Diagnosis

Rhabdomyosarcoma is diagnosed through the presence of embryonic myogenesis, which can be identified through morphological examination as well as assays containing myogenic markers.[17][18] Immunohistochemical assays use protein expression to determine the fusion status of the growth, differentiating fusion-negative rhabdomyosarcoma from fusion-positive rhabdomyosarcoma.[17] In the recent years, there has been a shift to use molecular classification over histological classification as histology alone does not predict the fusion type of rhabdomyosarcoma.[19] Fusion-status is determined through the expression of certain proteins, such as myogenin, although the specific assay panel used for diagnosis depends on the tumor morphology.[17][18] Embryonal rhabdomyosarcoma can be classified by its lack of PAX3–FOXO1 or PAX7–FOXO1 gene fusions, but approximately 20% of alveolar rhabdomyosarcomas are also determined to be fusion-negative.[20] However, it is suggested that these "fusion-negative" alveolar rhabdomyosarcomas may be a misclassification of embryonal rhabdomyosarcomas with predominantly dense morphology.[14] In either case, "fusion-negative" alveolar rhabdomyosarcoma have similar clinical presentation and outcome as embryonal rhabdomyosarcoma, risk stratification is now determined by fusion-status instead of histological classification.[20]

After a physical exam, formal diagnosis of RMS in adult patients requires a computed tomography (CT) scan, which can assess the areas affected and to delineate the tumor.[19] In children, physicians may opt for magnetic resonance imaging (MRI) to limit radiation exposure in younger populations.[19] In the majority of individuals diagnosed with Rhabdomyosarcoma, more than half are diagnosed before the age of 10.[21]

Prognosis

The prognosis for rhabdomyosarcoma has improved greatly in recent decades, with over 70% of people surviving for five years after diagnosis.[22] Embryonal rhabdomyosarcoma is generally associated with better prognosis than alveolar rhabdomyosarcoma, with a 5-year survival prognosis of 82% and 53%, respectively.[23][9] This may be due to the more aggressive and metastatic nature of ARMS that can be attributed to its PAX3–FOXO1 or PAX7–FOXO1 gene fusions.[24] Nevertheless, some embryonal rhabdomyosarcoma patients with a rare Leu122Arg mutation in MYOD1 gene have a very poor outcome.[25] In two different studies, none of the subjects with the MYOD1 mutation survived.[26]  Tumors due to this mutation commonly manifest in the head and neck area, causing the mutated protein to behave like an oncogene.[26]

In a 2020 case study of 464 adolescents aged 0–19 years diagnosed with rhabdomyosarcoma between 1988 to 2016, children who were diagnosed between ages 5–9 years had the most promising prognosis.[27] In contrast, infants less than 1 years old had the worst outcome, which may be associated to the lower doses of chemotherapy and radiotherapy administered and naive immune system.[27]

Treatment

Treatment for Embryonal rhabdomyosarcoma involves the use of combination therapy consisting of chemotherapy, surgery, and/or radiation therapy.[28] In the US, a combination of Vincristine, Dactinomycin, and cyclophosphamide are often the chemotherapeutics used to treat rhabdomyosarcoma.[29] Radiation therapy continues to be an integral component of rhabdomyosarcoma treatment, however, the long-term safety and treatment related complications remain a concern.[30]

In individuals with localized rhabdomyosarcoma, surgery and/or radiation therapy are primarily use to eliminate the tumor. Localized rhabdomyosarcoma can typically be treated successfully with the current standard of care.[31]

In individuals with metastatic rhabdomyosarcoma, combination therapy is not able to treat specific sites such as bone marrow or the lungs.[28] Treatment for metastatic rhabdomyosarcoma has not changed over the last 3 decades and 5-year survival outcomes in those with high-risk rhabdomyosarcoma remain less than 40%.[32] In a European study on 174 adolescents with metastatic rhabdomyosarcoma, high dose chemotherapy compared to standard chemotherapy did not show a statistical difference in 5 year overall survival rates.[20] In fact, those who received the high dose chemotherapy had experienced an increase in adverse events such as myelosuppression, peripheral neuropathy and/or required a dose reduction.[20] In individuals with more resistant rhabdomyosarcoma, more targeted therapies and immunotherapies have been of interest to gain better survival outcomes and reduce toxicities and treatment resistance.[32]

References

  1. ^ a b Masola V, Maran C, Tassone E, Zin A, Rosolen A, Onisto M (August 2009). "Heparanase activity in alveolar and embryonal rhabdomyosarcoma: implications for tumor invasion". BMC Cancer. 9: 304. doi:10.1186/1471-2407-9-304. PMC 2743710. PMID 19715595.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  2. ^ Shern JF, Chen L, Chmielecki J, Wei JS, Patidar R, Rosenberg M, et al. (February 2014). "Comprehensive genomic analysis of rhabdomyosarcoma reveals a landscape of alterations affecting a common genetic axis in fusion-positive and fusion-negative tumors". Cancer Discovery. 4 (2): 216–231. doi:10.1158/2159-8290.CD-13-0639. PMC 4462130. PMID 24436047.
  3. ^ a b Yohe ME, Heske CM, Stewart E, Adamson PC, Ahmed N, Antonescu CR, et al. (October 2019). "Insights into pediatric rhabdomyosarcoma research: Challenges and goals". Pediatric Blood & Cancer. 66 (10): e27869. doi:10.1002/pbc.27869. PMC 6707829. PMID 31222885.
  4. ^ a b Rodeberg D, Paidas C (February 2006). "Childhood rhabdomyosarcoma". Seminars in Pediatric Surgery. Childhood Cancer. 15 (1): 57–62. doi:10.1053/j.sempedsurg.2005.11.009. PMID 16458847. S2CID 1220308.
  5. ^ "What Is Rhabdomyosarcoma?". www.cancer.org. Retrieved 2022-07-28.
  6. ^ Ibrahim U, Saqib A, Mohammad F, Ding J, Salman B, Collado FK, Dhar M (November 2017). "Embryonal Rhabdomyosarcoma of the Cervix: A Rare Disease at an Uncommon Age". Cureus. 9 (11): e1864. doi:10.7759/cureus.1864. PMC 5773277. PMID 29375950.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  7. ^ a b Ricker CA, Crawford K, Matlock K, Lathara M, Seguin B, Rudzinski ER, et al. (April 2020). "Defining an embryonal rhabdomyosarcoma endotype". Cold Spring Harbor Molecular Case Studies. 6 (2): a005066. doi:10.1101/mcs.a005066. PMC 7133750. PMID 32238403.
  8. ^ Chen, Xiang; Stewart, Elizabeth; Shelat, Anang A.; Qu, Chunxu; Bahrami, Armita; Hatley, Mark; Wu, Gang; Bradley, Cori; McEvoy, Justina; Pappo, Alberto; Spunt, Sheri (2013-12-09). "Targeting Oxidative Stress in Embryonal Rhabdomyosarcoma". Cancer Cell. 24 (6): 710–724. doi:10.1016/j.ccr.2013.11.002. ISSN 1535-6108. PMC 3904731. PMID 24332040.{{cite journal}}: CS1 maint: PMC format (link)
  9. ^ a b c Leiner J, Le Loarer F (January 2020). "The current landscape of rhabdomyosarcomas: an update". Virchows Archiv. 476 (1): 97–108. doi:10.1007/s00428-019-02676-9. PMID 31696361. S2CID 207911529.
  10. ^ a b c d e Shern JF, Selfe J, Izquierdo E, Patidar R, Chou HC, Song YK, et al. (September 2021). "Genomic Classification and Clinical Outcome in Rhabdomyosarcoma: A Report From an International Consortium". Journal of Clinical Oncology. 39 (26): 2859–2871. doi:10.1200/JCO.20.03060. PMC 8425837. PMID 34166060.
  11. ^ Ognjanovic, Simona; Linabery, Amy M.; Charbonneau, Bridget; Ross, Julie A. (2009-09-15). "Trends in childhood rhabdomyosarcoma incidence and survival in the United States, 1975-2005". Cancer. 115 (18): 4218–4226. doi:10.1002/cncr.24465.
  12. ^ a b Yohe ME, Gryder BE, Shern JF, Song YK, Chou HC, Sindiri S, et al. (July 2018). "MEK inhibition induces MYOG and remodels super-enhancers in RAS-driven rhabdomyosarcoma". Science Translational Medicine. 10 (448): eaan4470. doi:10.1126/scitranslmed.aan4470. PMC 8054766. PMID 29973406.
  13. ^ Arnold MA, Barr FG (February 2017). "Molecular diagnostics in the management of rhabdomyosarcoma". Expert Review of Molecular Diagnostics. 17 (2): 189–194. doi:10.1080/14737159.2017.1275965. PMC 5657295. PMID 28058850.
  14. ^ a b Fan R, Parham DM, Wang LL (August 2022). "An Integrative Morphologic and Molecular Approach for Diagnosis and Subclassification of Rhabdomyosarcoma". Archives of Pathology & Laboratory Medicine. 146 (8): 953–959. doi:10.5858/arpa.2021-0183-RA. PMID 35051261. S2CID 246078793.
  15. ^ Dziuba I, Kurzawa P, Dopierała M, Larque AB, Januszkiewicz-Lewandowska D (2018). "Rhabdomyosarcoma in children - current pathologic and molecular classification". Polish Journal of Pathology. 69 (1): 20–32. doi:10.5114/pjp.2018.75333. PMID 29895123.
  16. ^ "Childhood Rhabdomyosarcoma Treatment (PDQ®)–Patient Version - NCI". www.cancer.gov. 2022. Retrieved 2022-07-25.
  17. ^ a b c Parham DM, Barr FG (November 2013). "Classification of rhabdomyosarcoma and its molecular basis". Advances in Anatomic Pathology. 20 (6): 387–397. doi:10.1097/PAP.0b013e3182a92d0d. PMC 6637949. PMID 24113309.
  18. ^ a b Agaram NP (January 2022). "Evolving classification of rhabdomyosarcoma". Histopathology. 80 (1): 98–108. doi:10.1111/his.14449. PMID 34958505. S2CID 245501811.
  19. ^ a b c Frankart, Andrew J.; Breneman, John C.; Pater, Luke E. (2021). "Radiation Therapy in the Treatment of Head and Neck Rhabdomyosarcoma". Cancers. 13 (14): 3567. doi:10.3390/cancers13143567. ISSN 2072-6694.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  20. ^ a b c d Jawad N, McHugh K (October 2019). "The clinical and radiologic features of paediatric rhabdomyosarcoma". Pediatric Radiology. 49 (11): 1516–1523. doi:10.1007/s00247-019-04386-5. PMID 31620851. S2CID 204709484.
  21. ^ Ognjanovic, Simona; Linabery, Amy M.; Charbonneau, Bridget; Ross, Julie A. (2009-09-15). "Trends in childhood rhabdomyosarcoma incidence and survival in the United States, 1975-2005". Cancer. 115 (18): 4218–4226. doi:10.1002/cncr.24465. PMC 2953716. PMID 19536876.{{cite journal}}: CS1 maint: PMC format (link)
  22. ^ Breitfeld PP, Meyer WH (August 2005). "Rhabdomyosarcoma: new windows of opportunity". The Oncologist. 10 (7): 518–527. doi:10.1634/theoncologist.10-7-518. PMID 16079319. S2CID 24136175.
  23. ^ Frankart AJ, Breneman JC, Pater LE (July 2021). "Radiation Therapy in the Treatment of Head and Neck Rhabdomyosarcoma". Cancers. 13 (14): 3567. doi:10.3390/cancers13143567. PMC 8305800. PMID 34298780.
  24. ^ Yu PY, Guttridge DC (2018). "Dysregulated Myogenesis in Rhabdomyosarcoma". Current Topics in Developmental Biology. 126: 285–297. doi:10.1016/bs.ctdb.2017.10.007. ISBN 9780128092156. PMID 29305002.
  25. ^ Kohsaka S, Shukla N, Ameur N, Ito T, Ng CK, Wang L, et al. (June 2014). "A recurrent neomorphic mutation in MYOD1 defines a clinically aggressive subset of embryonal rhabdomyosarcoma associated with PI3K-AKT pathway mutations". Nature Genetics. 46 (6): 595–600. doi:10.1038/ng.2969. PMC 4231202. PMID 24793135.
  26. ^ a b Rudzinski ER, Anderson JR, Hawkins DS, Skapek SX, Parham DM, Teot LA (October 2015). "The World Health Organization Classification of Skeletal Muscle Tumors in Pediatric Rhabdomyosarcoma: A Report From the Children's Oncology Group". Archives of Pathology & Laboratory Medicine. 139 (10): 1281–1287. doi:10.5858/arpa.2014-0475-OA. PMC 4651658. PMID 25989287.
  27. ^ a b Wang X, Feng J, Li Z, Zhang X, Chen J, Feng G (December 2020). "Characteristics and prognosis of embryonal rhabdomyosarcoma in children and adolescents: An analysis of 464 cases from the SEER database". Pediatric Investigation. 4 (4): 242–249. doi:10.1002/ped4.12220. PMC 7768301. PMID 33376951.
  28. ^ a b Chen C, Dorado Garcia H, Scheer M, Henssen AG (2019). "Current and Future Treatment Strategies for Rhabdomyosarcoma". Frontiers in Oncology. 9: 1458. doi:10.3389/fonc.2019.01458. PMC 6933601. PMID 31921698.
  29. ^ Chen C, Dorado Garcia H, Scheer M, Henssen AG (2019). "Current and Future Treatment Strategies for Rhabdomyosarcoma". Frontiers in Oncology. 9: 1458. doi:10.3389/fonc.2019.01458. PMC 6933601. PMID 31921698.
  30. ^ Miwa S, Yamamoto N, Hayashi K, Takeuchi A, Igarashi K, Tsuchiya H (July 2020). "Recent Advances and Challenges in the Treatment of Rhabdomyosarcoma". Cancers. 12 (7): 1758. doi:10.3390/cancers12071758. PMC 7409313. PMID 32630642.
  31. ^ Miwa S, Yamamoto N, Hayashi K, Takeuchi A, Igarashi K, Tsuchiya H (July 2020). "Recent Advances and Challenges in the Treatment of Rhabdomyosarcoma". Cancers. 12 (7): 1758. doi:10.3390/cancers12071758. PMC 7409313. PMID 32630642.
  32. ^ a b van Erp AE, Versleijen-Jonkers YM, van der Graaf WT, Fleuren ED (July 2018). "Targeted Therapy-based Combination Treatment in Rhabdomyosarcoma". Molecular Cancer Therapeutics. 17 (7): 1365–1380. doi:10.1158/1535-7163.MCT-17-1131. PMID 29967215. S2CID 49648448.

External links

Retrieved from "https://en.wikipedia.org/w/index.php?title=Embryonal_rhabdomyosarcoma&oldid=1101662342"