Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0476089 (endometrial cancer)
 11,379 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present study investigated comparatively the relation between host age and age-specific incidence rate (ASIR) of breast cancer in the United Kingdom and Japan. Comparison was also made between breast cancer and 5 non-mammary neoplasias as regards the cancer incidence/age profile. The results obtained are as follows: 1) the ASIR profile of breast cancer in the age range of 22.5 years to 47.5 years was characterized by a rapid rise versus age which was common between the United Kingdom and Japan. By use of the log-log plot, the growth of breast cancer risk was found to be quasi-exponential, and the above time range was termed the stage of exponential growth. 2) From 47.5 years of age on, the stage of stagnation ensued: the ASIR for the United Kingdom kept on rising with a much reduced inclination, whereas that for Japan followed the way of gradual decline. In the log-log plot, the junction between the 2 stages was recognized as a distinct break point. 3) A similar two-stage structure was found in the ASIR profiles of cancers of the stomach, lung, cervix uteri, and corpus uteri. The break points for the first 2 neoplasias were located at senescent ages, and those for cervical cancer and endometrial cancer were located at the pre- and peri-menopausal ages respectively (27.5-32.5 and 52.5 years). The profile of lymphoid leukemia gave 2 distinct surges at the ages of infancy and senescence, regardless of the country. The significance of the break point in the ASIR profile of breast cancer was discussed in relation to the two-step carcinogenesis theory.
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PMID:The genesis of breast cancer is a two-step phenomenon. I. Differential effects of aging on the cancer incidence in the United Kingdom and Japan. 156 61

The epipodophyllotoxin derivatives, etoposide (VP-16) and teniposide (VM-26), are highly lipophilic anticancer drugs supplied with novel commercial solvent systems. A BALB/c mouse skin toxicity model was used to evaluate the ulcerative potential of intradermal (ID) VP-16 and its lipophilic solvent system along with the main ingredient of the VM-26 solvent, polyethoxylated castor oil (PECO). ID VP-16 caused dose-dependent ulceration following 0.17 mg, 0.33 mg (50 mg/M2) or 1.0 mg (150 mg/M2). Both normal saline (0.05 ml ID) and hyaluronidase (7.5 u ID) were effective as local VP-16 antidotes, presumably by diluting out the extravasated drug. The VP-16 solvent alone was as toxic as the 1.0 mg (undiluted) ID VP-16 injection. ID PECO was mildly ulcerative in mouse skin. When given to P-388 lymphocytic leukemia-bearing mice, both VP-16 (24 mg/kg IP for 3 doses) and VM-26 (8 mg/kg IP for 2 doses) were active, producing increased life spans (ILS) of 160% and 90%, respectively. The solvents, given IP at the same schedule, did not increase or decrease the life span of tumor-bearing mice, but did increase morbidity. In an in vitro human tumor clonogenic assay (WiDr colon carcinoma and HEC-1A endometrial carcinoma in soft agar), both VP-16 and VM-26 showed moderate to complete inhibition of tumor colony forming units (TCFUs) by continuous exposure. 1-h drug exposures were marginally active at reducing TCFUs. None of the epipodophyllotoxin diluents at clinical concentrations reduced TCFUs. At very high concentrations, both epipodophyllotoxins were cytotoxic. They were more effective at reducing TCFUs when plated as a continuous exposure rather than a 1-h exposure.
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PMID:Skin ulceration potential without therapeutic anticancer activity for epipodophyllotoxin commercial diluents. 667 64