Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0178874 (tumor progression)
 40,807 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Second-look operations for glioblastomas, one of the most malignant types of brain tumor, were performed after the administration of chemotherapeutic treatments of general-VM 26 plus ACNU, local-MTX, or interferon-beta in each of ten, two, and three cases, respectively. Patients who had received the treatments were divided into two groups, living and deceased, as of August 1982. Therapeutic evaluation was performed with clinical parameters. Among the cases of CR, one (a 14-year-old female) had undergone surgery four times in the four years following onset, and no trace of tumor shadow appeared on the CT grams that were taken one month after the last surgery. Her performance was evaluated as almost 100% (ECOG). In cases of local administration, one case, which had been treated with IFN-beta, demonstrated an apparent decrease in the growth fraction and a pronounced decrease in tumor progression potency. Cell kinetic analyses were also performed, and cell cycle time and growth fraction were estimated by computer with the aid of flow cytometry. Efficacious chemotherapy yielded a decreased value of the growth fraction and an increase in cell cycle time. The decreased value of the growth fraction demonstrates especially well the effectiveness of a chemotherapeutic regimen. The cell kinetic analyses aided in the rational establishment of a chemotherapeutic regimen. Second-look operations for malignant brain tumors will enable more effective refinements in chemotherapeutic regimens and more successful results.
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PMID:[Second-look operations and chemotherapy for malignant tumors of the brain]. 657 17

Infection with HPV (human papillomavirus) 16 is the cause of 50% or more of cervical cancers in women. HPV16 infection, however, is very common in young sexually active women, but the majority mount an effective immune response and clear infection. Approx. 10% of individuals develop a persistent infection, and it is this cohort who are at risk of cancer progression, with the development of high-grade precursor lesions and eventually invasive carcinoma. Effective evasion of innate immune recognition seems to be the hallmark of HPV infections, since the infectious cycle is one in which viral replication and release is not associated with inflammation. Furthermore, HPV infections disrupt cytokine expression and signalling with the E6 and E7 oncoproteins particularly targeting the type I IFN (interferon) pathway. High doses of IFN can overcome the HPV-mediated abrogation of signalling, and this may be the basis for the therapeutic effects on HPV infections of immune-response modulators such as the imidazoquinolones that induce high levels of type I IFNs by activation of TLR (Toll-like receptor) 7. Using the unique W12 model of cervical carcinogenesis, some of these IFN-related interactions and their relevance in the selection of cells with integrated viral DNA in cancer progression have been investigated. Our data show that episome loss associated with induction of antiviral response genes is a key event in the spontaneous selection of cervical keratinocytes containing integrated HPV16. Exogenous IFN-beta treatment of W12 keratinocytes in which the majority of the population contain episomes results only in the rapid emergence of IFN-resistant cells, loss of episome-containing cells and a selection of cells containing integrated HPV16 in which the expression of the transcriptional repressor E2 is down-regulated, but in which E6 and E7 are up-regulated.
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PMID:HPV: from infection to cancer. 1803 Dec 45