xColorectal cancer (CRC) is one of the leading causes of cancer deaths worldwide. This article reviews the aetiology and risk factors for CRC and focuses on strategies for prevention and early diagnosis. Prevention involves identifying and optimizing modifiable risk factors through public health awareness as well as population screening, for example using detection of occult blood in stool. Endoscopic surveillance in the UK is currently performed on a population basis with the bowel scope programme and faecal immunochemical testing, with colonoscopy reserved for patients known to be at higher risk of developing CRC.
In June 1948, Sidney Farber reported promising results in treatment of early childhood leukemia. Based on anecdotal evidence that children with acute leukemia worsened if they were given folic acid, he worked on blocking folic acid metabolism. His team gave 16 infants and children with acute lymphoblastic leukemia a folic acid inhibitor, aminopterin—10 showed improvement by clinical and hematologic parameters after three months.[11] In his article, Farber advised receiving the results cautiously: "It is again emphasized that these remissions are temporary in character and that the substance is toxic and may be productive of even greater disturbances than have been encountered so far in our studies," he wrote. "No evidence has been mentioned in this report that would justify the suggestion of the term 'cure' of acute leukemia in children."
xColorectal cancer (CRC) is common, affecting >40,000 people a year in the UK. Most cancers are sporadic but a few, such as those occurring at a younger age, have a clear genetic basis. Most are situated in the rectum or rectosigmoid and cause rectal bleeding, often with a looser or more frequent stool. Right-sided cancers typically result in anaemia, because the blood in the stool is occult and unnoticed by the patient. Almost all symptoms of malignancy can also be caused by benign disease. Diagnosis relies on luminal imaging, with colonoscopy being the gold standard.
Patients with interstitial lung disease associated with systemic sclerosis were treated with usual care plus placebo or nintedanib. The annual rate of change in forced vital capacity assessed over a 52-week period was −52.4 ml per year with nintedanib and −93.3 ml per year with placebo. There were no differences in other measures of systemic sclerosis.
In April 2001, Druker et al. reported a targeted therapy for chronic myelogenous leukemia. Based on the knowledge that BCR-ABL, a constitutively activated tyrosine kinase, causes CML, the authors tested with success an inhibitor of this tyrosine kinase in patients who had failed first-line therapy. The finding helped begin the era of designing cancer drugs to target specific molecular abnormalities.[18]
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