Malignancy Information and Courses from MediaLab, Inc.
These are the MediaLab courses that cover Malignancy and links to relevant pages within the course.
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|What is the most important modifiable risk factor for enteric colonization with vancomycin-resistant Enterococcus faecium (VREF)?||View Page|
Citron DM. Appelbaum PC.: How far should a clinical laboratory go in identifying anaerobic isolates, and who should pay? Clinical Infectious Diseases. 16 Suppl 4:S435-8, 1993 Identification of anaerobic bacteria in specimens from sites of infection due to mixed organisms can be time-consuming and expensive. Laboratories should limit anaerobic workups by testing only those specimens that have been properly collected and transported to the laboratory. Use of selective and differential media for initial processing can provide rapid and relevant information to the clinician. Anaerobes isolated from normally sterile sites and sites of serious infection should always be completely identified. Group-or genus-level identifications may suffice in other instances. The Bacteroides fragilis group of organisms should always be identified because of their virulence and resistance to many antimicrobial agents. Some of the other organisms that warrant identification include Clostridium septicum (associated with gastrointestinal malignancy); Clostridium ramosum, Clostridium innocuum, and Clostridium clostridioforme (which are resistant to antibiotics); Clostridium perfringens (a cause of myonecrosis and gas gangrene,potentially serious infection); anaerobic cocci (which may be resistant to metronidazole and clindamycin); and fusobacteria (which may be virulent and resistant to clindamycin and penicillin).
Kornbluth AA. Danzig JB. Bernstein LH.: Clostridium septicum infection and associated malignancy. Report of 2 cases and review of the literature. Medicine. 68(1):30-7, 1989 We report 2 patients with myonecrosis due to Clostridium septicum and associated colon carcinoma and have reviewed the English language literature for all reported cases of atraumatic C. septicum infection. A total of 162 cases of C. septicum infection have been reported. Eighty-one percent of these patients had an associated malignancy. Thirty-four percent of all patients had associated colon carcinoma, while 40% had a hematologic malignancy. Thirty-seven percent of reported patients had an occult malignancy at the time of their infection with C. septicum. In many patients, the portal of entry was found in the large intestine. In a particularly lethal form (79% mortality) of C. septicum infection, known as "distant myonecrosis," infection metastatic from the initial site of infection causes severe myonecrosis, gangrene, and often death within hours of clinical detection. Overall, survival of patients with C. septicum infection is only 35%. Review of all cases of C. septicum infection suggests several conclusions. 1) Patients with malignancy, particularly colonic or hematologic, and patients with cyclic neutropenia who develop signs and symptoms of sepsis, especially with associated findings of abdominal pain or pain in an extremity, should be treated for possible clostridial infection. 2) C. septicum infection does not appear to be a result of a single specific defect in either humoral or cell-mediated immunity. Rather, it may occur in patients who are granulocytopenic and therefore prone to an enterocolitis. 3) Patients in whom an infection with C. septicum is found must undergo a vigorous search for malignancy.
|Each of the following statements is true concerning Clostridium septicum infections EXCEPT:||View Page|
Malignant cells that have broken away from a tumor within the brain or meninges may also be present in spinal fluid. Tumor cells may be difficult to distinguish from macrophages or pia arachnoid mesothelial cells. While blasts in the CSF also indicate malignancy, in particular leukemia, for the purposes of this discussion, they are considered separately.
|High Sensitivity-C-Reactive Protein|
C-reactive protein (CRP) is a very sensitive acute phase reactant. Serum CRP levels increase following a variety of pro-inflammatory events such as infection, tissue necrosis, trauma, surgery and even malignancy. CRP levels can increase quickly and dramatically (often 100 fold) during inflammation. CRP can activate compliment, bind Fc receptors and can function as an opsonin, enhancing phagocytosis with certain infections. Measurement of CRP is not new, it has been on clinical laboratory testing menus for decades. However, a newer version of the CRP test is now in use to assess cardiovascular risk.High sensitivity-CRP (hs-CRP) assays have been developed that are more sensitive to the more subtle changes that can occur during chronic vascular inflammation. (Recall that atherosclerosis is an inflammatory process.) By measuring hsCRP we can get a glimpse at vascular function. CRP has been shown to be an independent risk factor for atherosclerotic disease and cardiac death. A 2002 prospective study of more than 27,000 patients showed that the CRP concentration is a stronger predictor of cardiovascular events than the LDL-cholesterol level.
|HPV Genome and Proteins|
When HPV infects host cells, several HPV DNA-coded proteins initiate cellular changes. Two such areas in the genome are the open reading frames E1 to E7 and the late open reading frames L1 and L2. The proteins encoded by E1 to E7 regions of the genome are responsible for HPV-gene regulation and cell transformation. Proteins resulting from L1 and L2 form the viral shell.E6 and E7 encoded proteins are the most important HPV proteins in malignancy transformations. These viral proteins work together to convert normal host cells to malignant cells. E6 proteins interact with intracellular protein p53 and E7 proteins interact with intracellular retinoblastoma (Rb) protein. Intracellular proteins p53 and Rb regulate cellular growth. Both p53 and Rb are tumor suppressor proteins.When chromosomal damage occurs in normal cellular growth, p53 halts cellular growth and allows DNA repair enzymes to repair damage. Rb also halts cellular growth in DNA damage by inducing apoptosis (cellular death). When HPV E6 proteins bind to p53 and HPV E7 to Rb, mutations accumulate, unchecked cellular growth occurs, and a state of chromosomal instability results. This instability and unregulated cellular growth increases the chance of forming malignant cells. Viral E1, E2, and E5 encoded proteins may also damage cellular processes when HPV infects cells and can lead to malignant transformations.
|Review: Tumor Suppressor Genes, Proto-Oncogenes and Oncogenes|
Tumor suppressor genes and proto-oncogenes regulate cell division. Tumor suppressor genes slow down or stop cell division for repair of DNA damage and promote apoptosis. A mutated tumor suppressor gene results in uncontrolled cell growth, which can be associated with the HPV-related carcinogenisis of cervical cancer. Proto-oncogenes promote cell division, initiate DNA synthesis, and inhibit apoptosis. Mutations occurring in proto-oncogenes convert them to oncogenes which can cause malignancy; this can also play a role in HPV-related malignancies.
|Conditions Associated with Hyposegmented Neutrophils|
The presence of hyposegmented neutrophils can be an acquired phenomenon, as a result of severe infection, burns, malignancy, chemotherapy or other drugs such as sulfonamides. When the causative agent is removed, the cells will return to normal. Percentages of neutrophils affected will vary in this condition. Hyposegmented neutrophils as an aquired phenomenon are known as pseudo-Pelger-Huet cells.