The good prognostic features in childhood ALL are:
▪ age between one and 10
▪ female gender
▪ low white cell count (below 50 x 109/l)
▪ no evidence of central nervous system disease or particular chromosomal abnormalities
▪ complete response to early chemotherapy.
Haemoglobin and platelet counts have not been shown to significantly influence prognosis.
Showing posts with label oncology. Show all posts
Showing posts with label oncology. Show all posts
Carcinoid Syndrome
Carcinoid syndrome is due to an underlying carcinoid tumour. These tumours may contain and secrete a number of biologically active substances. Immunocytochemical or radioimmunoassay studies show that carcinoids can contain adrenocorticotrophic hormone (ACTH), gastrin, somatostatin, insulin, motilin, growth hormone, gastrin- releasing peptide, serotonin, calcitonin, neurotensin, melanocyte- stimulating hormone-beta, tachykinins (substance P, substance K, neuropeptide K), glucagon, pancreatic polypeptide (PP), vasoactive intestinal peptide (VIP), and prostaglandins. These substances may not be released in sufficient amounts to cause symptoms.
In various studies of patients with carcinoids, elevated serum concentrations of PP occur in 43%, motilin in 14%, and subunits of human chorionic gonadotropin (HCG) in 12%; a slightly elevated level of gastrin was reported in 15%, and none were reported with an elevated VIP or plasma gastrin-releasing peptide level. Even though these gastrointestinal (GI) peptides were present in the serum, it is not apparent that any of these peptides contributed to any clinical symptoms. Foregut carcinoids are more likely to produce various GI peptides than midgut carcinoids.
5-hydroxyindoleacetic acid is the metabolic product excreted in urine from the metabolism of serotonin.
Ectopic ACTH production with Cushing's syndrome is increasingly seen with foregut carcinoids, and in some studies, these tumours were the most common cause of the ectopic ACTH syndrome, accounting for 64% of all patients. Acromegaly due to release of growth hormone-releasing factors can occur with a number of carcinoids.
Reference
In various studies of patients with carcinoids, elevated serum concentrations of PP occur in 43%, motilin in 14%, and subunits of human chorionic gonadotropin (HCG) in 12%; a slightly elevated level of gastrin was reported in 15%, and none were reported with an elevated VIP or plasma gastrin-releasing peptide level. Even though these gastrointestinal (GI) peptides were present in the serum, it is not apparent that any of these peptides contributed to any clinical symptoms. Foregut carcinoids are more likely to produce various GI peptides than midgut carcinoids.
5-hydroxyindoleacetic acid is the metabolic product excreted in urine from the metabolism of serotonin.
Ectopic ACTH production with Cushing's syndrome is increasingly seen with foregut carcinoids, and in some studies, these tumours were the most common cause of the ectopic ACTH syndrome, accounting for 64% of all patients. Acromegaly due to release of growth hormone-releasing factors can occur with a number of carcinoids.
Reference
Risk factors for hepatocellular carcinoma (HCC)
Eighty per cent of cases of hepatocellular carcinoma (HCC) are associated with chronic hepatitis B infection. Most cases of HCC not associated with hepatitis B infection are associated with hepatitis C infection.
Alcoholic cirrhosis and autoimmune chronic active hepatitis also increase the risk of developing HCC.
Several metabolic diseases are also associated with an increased risk for the development of HCC, such as haemochromatosis (iron accumulation), Wilson's disease (copper accumulation), alpha-1-antitrypsin deficiency and glycogen storage diseases.
Alflatoxins are mycotoxins produced by the fungi Aspergillus flavus and Aspergillus parasiticus which contaminate food (e.g. peanuts and corn).
A less common association is with primary biliary cirrhosis which is more typically associated with the subsequent development of cholangiocarcinoma.
Reference
Alcoholic cirrhosis and autoimmune chronic active hepatitis also increase the risk of developing HCC.
Several metabolic diseases are also associated with an increased risk for the development of HCC, such as haemochromatosis (iron accumulation), Wilson's disease (copper accumulation), alpha-1-antitrypsin deficiency and glycogen storage diseases.
Alflatoxins are mycotoxins produced by the fungi Aspergillus flavus and Aspergillus parasiticus which contaminate food (e.g. peanuts and corn).
A less common association is with primary biliary cirrhosis which is more typically associated with the subsequent development of cholangiocarcinoma.
Reference
- DeVita VT, Hellman S, Rosenberg SA. Cancer Principles and Practice of Oncology, 5th edn. Philadelphia: Lippincott-Raven.
Risk Factors for Ovarian Cancer
Consistently identified risk factors for ovarian cancer include:
▪ a positive family history
▪ few or no children
▪ older age at first marriage and childbirth.
There is a protective effect for childbearing and use of the oral contraceptive pill.
There is some evidence that patients with HER-2 over-expression have a worse response to chemotherapy and a worse prognosis, but the reported studies are retrospective only and there is no evidence that the gene is a risk factor for the development of ovarian cancer.
Risk factor Relative risk
General population 1
Family history 17-50
Nulliparity 4-5
1-2 children 3
Obesity 2
Oral contraceptive 0.5
Relationship between ovarian germ cell tumours and serum markers
About 90% of persons with non-dysgerminomatous germ cell tumours produce either alpha-fetoprotein (AFP) or human chorionic gonadotropin (beta-hCG). In contrast, persons with pure dysgerminoma usually produce neither.
These tumour markers are present for some time after surgery. If the presurgical levels are high, 30 days or more may be required before meaningful postsurgical levels can be obtained. The half-lives of AFP and beta-hCG are six days and one day respectively. After treatment, unequal reduction of beta-hCG and AFP may occur, suggesting that the two markers are synthesized by heterogeneous clones of cells within the tumour; thus, both markers should be followed.
Beta-hCG is similar to luteinizing hormone except for its distinctive beta subunit.
These tumour markers are present for some time after surgery. If the presurgical levels are high, 30 days or more may be required before meaningful postsurgical levels can be obtained. The half-lives of AFP and beta-hCG are six days and one day respectively. After treatment, unequal reduction of beta-hCG and AFP may occur, suggesting that the two markers are synthesized by heterogeneous clones of cells within the tumour; thus, both markers should be followed.
Beta-hCG is similar to luteinizing hormone except for its distinctive beta subunit.
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