The toxicity and many side effects of the drugs, and the uncertain outcome of chemotherapy in brain tumors puts this treatment further down the line of treatment options with surgery and radiation therapy preferred.UCLA Neuro-Oncology publishes real-time survival data for patients with a diagnosis of glioblastoma multiforme. They are the only institution in the United States that displays how brain tumor patients are performing on current therapies. They also show a listing of chemotherapy agents used to treat high-grade glioma tumors.Genetic mutations have significant effects on the effectiveness of chemotherapy. Gliomas with IDH1 or IDH2 mutations respond better to chemotherapy than those without the mutation. Loss of chromosome arms 1p and 19q also indicate better response to chemoradiation. Other
A shunt may be used to relieve symptoms caused by intracranial pressure, by reducing the build-up of fluid (hydrocephalus) caused by the blockage of the free flow of cerebrospinal fluid. Prognosis
The prognosis of brain cancer depends on the type of cancer diagnosed. Medulloblastoma has a good prognosis with chemotherapy, radiotherapy, and surgical resection while glioblastoma multiforme has a median survival of only 12 months even with aggressive chemoradiotherapy and surgery. Brainstem gliomas have the poorest prognosis of any form of brain cancer, with most patients dying within one year, even with therapy that typically consists of radiation to the tumor along with corticosteroids. However, one type, focal brainstem gliomas in children, seems open to exceptional prognosis and long-term survival has frequently been reported.Prognosis is also affected by presentation of genetic mutations. Certain mutations provide better prognosis than others.
Its mucinous cells resemble the normal cervical lining, while its tuboendometrial cells resemble the lining of normal fallopian tubes or endometrium.It is sometimes considered a precancerous lesion, given clear-cell adenocarcinoma patients present these lesions in close proximity to atypical tuboendometrial glands, and microglandular hyperplasia has been seen to arise from these lesions. References
Further reading
OBrien, P. C.; Noller, K. L.; Robboy, S. J.; Barnes, A. B.; Kaufman, R. H.; Tilley, B. C.; Townsend, D. E. (March 1979). "Vaginal epithelial changes in young women enrolled in the National Cooperative Diethylstilbestrol Adenosis (DESAD) project". Obstetrics & Gynecology. 53 (3): 300–308. PMID 424101. Laronda, Monica M.; Unno, Kenji; Butler, Lindsey M.; Kurita, Takeshi (2012). "The development of cervical and vaginal adenosis as a result of diethylstilbestrol exposure in utero". Differentiation. 84 (3): 252–260. doi:10.1016/j.diff.2012.05.004. ISSN 0301-4681. PMC 3443265. PMID 22682699. PMID 22682699. Ganesan, R.; Ferryman, S. R.; Waddell, C. A. (1999). "Vaginal adenosis in a patient on Tamoxifen therapy: a case report". Cytopathology. 10 (2): 127–130. doi:10.1046/j.1365-2303.1999.00162.x. ISSN 0956-5507. PMID 10211619. S2CID 33999959. Laronda, M. M.; Unno, K.; Ishi, K.; Serna, V. A.; Butler, L. M; Mills, A. A.; Orvis, G. D.; Behringer, R. R.; Deng, C.; Sinha, S.; Kurita, T. (2013). "Diethylstilbestrol induces vaginal adenosis by disrupting SMAD/RUNX1-mediated cell fate decision in the Müllerian duct epithelium". Developmental Biology 381(1): 5-16. doi: 10.1016/j.ydbio.2013.06.024. PMID 23830984.