Correct me if I am wrong from veteran posters, but I thought giving medical advices without a medical residency is illegal? Is that why the Dr.Jarvis guy is getting investigated?
Does your pathology articles have medical advices?
No, I didnt say to take this and that. I cited information. I enjoyed doing this type of writing and I would to build a career writing articles like this (for pay....but I have to go to medical school or get a PhD for most high level positions (work from home types)
Let me give you a sample
🙁this is just part of an article)
Familial Melanoma Syndromes: Several genetic syndromes can lead to development of melanoma. Some of these syndromes, such as Familial Dysplastic Nevi Syndrome, have been recognized as associated with malignant melanoma for decades. Other syndromes, such as Malignant Melanoma-Pancreatic Carcinoma syndrome, are more recently discovered.
- Xeroderma Pigmentosum [3] is characterized by mutations in DNA repair genes. Such mutations lead to skin's inability to repair itself. The DNA's capacity for repair is important for individuals with other strong genetic risk factors, such as low tanning ability and presence of dysplastic nevi-premalignant moles.
- Familial Dysplastic Nevus Syndrome [3] is an autosomal dominant condition, which markedly increases an individual's risk for developing melanoma. A patient with Familial Dysplastic syndrome usually has two or more first-degree relatives with melanoma, and a large number of moles - between 10 and 100.
- In Familial Melanoma [3], several genes are rearranged or deleted on chromosomes 9 and 10. Such changes lead to uncontrolled cell proliferation. Often in this syndrome, cellular cycle is altered as well. In a healthy cell, the repair of the damaged or mutated DNA takes place between G1 (growth) and S (synthesis) stages. The stage between G1 and S stages is called the transition stage. Normally, the transition stage takes longer time in order for the cell to check and repair its DNA. In familial melanoma, the transition stage does not last long enough for repair to occur. Genetic mutations in familial melanoma are not absolutely penetrant. It has been found that the degree of expression of the mutation depends on the geographic location and the level of exposure to the ultraviolet light [2].
- Melanoma-Astrocytoma Syndrome is inherited in an autosomal dominant fashion. Expression of this condition may vary, often presenting with different clinical characteristics. Families with both melanoma and CNS tumors can have alterations in the CDKN2A that affect the expression of the tumor suppressor gene p14 and the alternate reading frame (p14ARF) [4].
- Atypical Mole Melanoma-Pancreatic Carcinoma Syndrome is a newly identified condition, which appears to be inherited in an autosomal dominant fashion. This syndrome is characterized by a high degree of expression. Affected individuals harbor mutations in the CDKN2A gene and often present with either melanoma or pancreatic cancer, or both. A 2003 study from the University of Washington found that offspring of affected parents have much higher risk of developing skin or pancreatic neoplasm as compared with offspring of unaffected parents - 48.9% vs. 16.7% [5]
Non-syndrome hereditary melanoma: A non-syndrome hereditary condition, which is associated with increased risk for developing melanoma, is caused by a certain genetic variation in melanocortin-1 receptor gene. It is more common in individuals of Germanic and Celtic descents. This variation has been shown to lead to a decreased response of melanocytes to melanotropin, the major hormone that regulates skin pigmentation. Studies suggest that this factor makes melanocytes more sensitive to damaging effects of UV light [3].
Difference from other familial cancer syndromes: Hereditary skin cancers differ from other familial cancer syndromes. Most cancer syndromes, like breast cancer syndrome, are typically diagnosed before the age of 40, whereas in carriers of familial melanoma mutations, melanoma may develop at any age, including old age. Such cases then are often considered sporadic and attributed to spontaneous mutations, resulting in a delayed screening of other family members.
Individual gene involvement in melanoma: Approximately 10% of melanoma cases occur in familial clusters, the remaining 90% are either sporadic in nature, or involve mutation in individual genes. Several of such genes have been identified so far.
- CDKN2A (Cyclin Dependant Kinase inhibitor 2A) gene: It is the best researched melanoma susceptibility gene. This gene is located on chromosome 9, segment p21.
- BRAF: BRAF gene is another melanoma-related gene that is also associated with benign moles, but when mutated, may lead to malignant changes. Located on chromosome 7, segment q34.
- NRAS: Neuroblastoma RAS viral (v-ras) oncogene homolog. Located on chromosome 1, segment p13.2.
- PTEN/MMAC1: phosphatase and tensin homolog (mutated in multiple advanced cancers) Located on chromosome 10, segment q23.3.
- hOGG1: Human oxoguanine glycosylase 1 has a role in repairing a DNA damage. Defects in the DNA repair mechanism can increase the rate at which a primary tumor can develop.
- Monosomy of chromosome 3: Research has shown that a tumor with monosomy of chromosome 3 can lead to the development of an inflammatory phenotype, resulting in neoplastic changes. [6]
- A study [7] found that majority of all melanoma cell lines - 85%- had mutations in NRAS, BRAF or PTEN/MMAC1 genes. These genes regulate cellular repair and division mechanism, and alteration in their function leads to development of malignant skin lesions.
- Unlike in other malignancies, the alterations or loss of function of the main tumor suppression gene, the p53 gene, do not occur frequently in melanoma [8].
A good number of my articles like this are a good 15 pages long+ single spaced.
I may write articles like this for my own enjoyment in the future and just allow people to read them.
