User:Jchhen/sandbox

7/25:

Changes to make:

- Simplify lead section, less medical jargon

- rewrite classification section to make it more clear and easier to read

- define Rhabdomyosarcoma

- add images

- add more information such as treatment, life expectancy, mortality,

- link wikipedia oncogene/define oncogene

- where does this disease most commonly occur

- Add more subheadings such as diagnosis, management/therapy, epidemiology of disease

--where does this disease most commonly occur

-- what does it look like

- add images of cells and what it looks like on a body

- explain medical jargon/define terms

Edits

- adding citation

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"

- making edits

Under Prognosis

The prognosis for rhabdomyosarcoma has improved greatly in recent decades, with over 70% of patients people surviving for five years after diagnosis.

- changed "patients" to people

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Under classification section

Embryonal rhabdomyosarcoma can be further divided into 3 different subcategories: the botryoid, spindle cell, and not-otherwise-specified (NOS).

These two subtypes of rhabdomyosarcoma, ERMS and ARMS, are comprised of different genetic variations. It is believed that some of the identifying genetic mutations that can cause ERMS include p53 loss, RAS pathway activation, and MYOD1 mutations.

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Under classification, add "(ARMS)" next to Alveolar rhabdomyosarcoma

under classification, add

Most often, ERMS is found in children during ages 0 to 5 years old, however ERMS can develop throughout any stage of life. Under classication

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. The study comprised of 641 patients with sufficient data to analyze. The authors found that the patients in the fusion-negative group had different genetic mutation profiles than those in the fusion-positive group. 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. 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.

Contrary to previous research, the findings of this study suggest that having RAS isoform mutations did not necessarily equate to a poor development of the disease. However, a pattern was found between the RAS isoform mutation seen and ones stage in life; HRAS isoform in infants, KRAS isoform in toddlers, and NRAS isoform in adolescence. This clinical study also found similar results as previous studies with the correlation of TP53 mutations and clinical outcome. TP53 mutations tended to result in a worsening development and clinical outcome of the disease. Although MYOD1 mutations make up a small percentage of ERMS, these mutations have been seen to have a negative prognosis and more studies should be conducted to understand how to treat the clinical condition of this specific mutation.

Tumor suppressors singal the cell to stop the cell cycle and start apoptosis, known as programmed cell death, when the cell senses damage or irregular cell cycle growth patterns.

These types of tumors are called embryonal rhabdomyosarcoma "because of their remarkable resemblance to developing embryonic and fetal skeletal muscle."