Isolation of Mycoplasma From Leukemic and Nonleukemic Patients&lt;xref ref-type="fn" rid="FN2"&gt;2&lt;/xref&gt;

Murphy, William H.; Bullis, C.; Dabich, Lyubica; Heyn, Ruth; Zarafonetis, Chris J. D.

doi:10.1093/jnci/45.2.243

Cited by 21 publications

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“…Since the initial hints of an association between Mycoplasmas and oncogenesis, many studies have attempted to understand its oncogenic properties and its direct or indirect role in the onset of cancer or its progression ( 335 – 337 ). There is not much evidence to support current proposed mechanisms for Mycoplasma-induced oncogenesis.…”

Section: Chlamydia Trachomatismentioning

confidence: 99%

Bacteria-Mediated Oncogenesis and the Underlying Molecular Intricacies: What We Know So Far

et al. 2022

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Cancers are known to have multifactorial etiology. Certain bacteria and viruses are proven carcinogens. Lately, there has been in-depth research investigating carcinogenic capabilities of some bacteria. Reports indicate that chronic inflammation and harmful bacterial metabolites to be strong promoters of neoplasticity. Helicobacter pylori-induced gastric adenocarcinoma is the best illustration of the chronic inflammation paradigm of oncogenesis. Chronic inflammation, which produces excessive reactive oxygen species (ROS) is hypothesized to cause cancerous cell proliferation. Other possible bacteria-dependent mechanisms and virulence factors have also been suspected of playing a vital role in the bacteria-induced-cancer(s). Numerous attempts have been made to explore and establish the possible relationship between the two. With the growing concerns on anti-microbial resistance and over-dependence of mankind on antibiotics to treat bacterial infections, it must be deemed critical to understand and identify carcinogenic bacteria, to establish their role in causing cancer.

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Section: Chlamydia Trachomatismentioning

confidence: 99%

Bacteria-Mediated Oncogenesis and the Underlying Molecular Intricacies: What We Know So Far

et al. 2022

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SCE induction and harlequin staining in mycoplasma-contaminated Chinese hamster cells

White

Ockey

1985

Chromosoma

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Chinese hamster V79 and CHO cells infected with Mycoplasma hyorhinis show elevated sister-chromatid exchange (SCE) levels but normal cell proliferation and levels of chromosomal aberrations when compared with uninfected cells. Harlequin staining patterns differ from those seen with uninfected cells at similar levels of bromodeoxyuridine (BrdUrd), indicating that BrdUrd is rapidly depleted from the medium by the mycoplasmal uridine phosphorylase and therefore becomes unavailable over the two cell cycles necessary for harlequin staining. Continuous treatment with the antibiotic minocycline restores the SCE level and harlequin staining to that seen in uncontaminated cells. The results suggest that mycoplasma infection should be suspected if harlequin staining patterns indicate a sudden decrease in incorporation of BrdUrd in cells grown in normal levels of BrdUrd.

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Mycoplasmal infection of lymphocyte cell cultures: Infection withM. salivarium

1980

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Many conclusions concerning cell culture mycoplasmas are based on data from studies in fibroblast cultures. Some conclusions may not be valid in other types of differentiated cell cultures. M. salivarium was isolated from 35 human lymphocyte cultures (HLC), 34 from the same laboratory. The organism grew to more than 10(8) colony forming units (CFU) per ml of lymphocyte suspensions and was readily detectable by microbiological culture, uridine phosphorylase, and uridine/uracil assays. Direct mycoplasmal assays on HLC by DNA fluorochrome staining and scanning electron microscopy (SEM) yielded artifacts that interfered with diagnosis. For DNA and SEM of HLC, inoculation into indicator cell cultures is recommended. M. salivarium infection of HLC did not produce any immediate difference in growth rates; however, infected cultures eventually died 14 to 29 passages after infection in contrast to uninfected controls. The same organism in 3T6 fibroblasts effected a 60% decrease in growth rate. Although M. salivarium is a frequent isolate from the oral cavity, it is a rare cell culture isolate. M. salivarium was able to initiate growth over a wide pH range, grew as well in cell cultures as in cell-free media, and was resistant to 50 microgram per ml of gentamycin, tylocine, kanamycin, and erythromycin. By Cot1/2 analysis, M. salivarium had a genomic molecular weight of 4.2 X 10(6) daltons. M. salivarium did not increase chromosome aberrations in one HLC. Some of these results have application to infection of HLC by other mycoplasmal species.

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Isolation of Mycoplasma From Leukemic and Nonleukemic Patients<xref ref-type="fn" rid="FN2">2</xref>

Cited by 21 publications

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Bacteria-Mediated Oncogenesis and the Underlying Molecular Intricacies: What We Know So Far

Bacteria-Mediated Oncogenesis and the Underlying Molecular Intricacies: What We Know So Far

SCE induction and harlequin staining in mycoplasma-contaminated Chinese hamster cells

Mycoplasmal infection of lymphocyte cell cultures: Infection withM. salivarium

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