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New Techniques in Cervical Cancer Screening & Detection By Caroline Seydel

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  2. New Techniques in Cervical Cancer Screening & Detection By Caroline Seydel
  3. Cracking Drug-Resistant Pancreatic Cancer By Caroline Seydel

Anttila et al., pp. 1204–1212

Cantor et al., pp. 1151–1168

Introducing two new improvements to cervical cancer screening and detection procedures. The first is an automation-assisted cytological screening method, presented as a valid alternative to the conventional Pap smear. The second is an optical spectroscopy device, more effective for diagnosis than screening, which detects cervical cancers well or better than standard colposcopy.

In their study, Anttila et al. selected women from the Finnish cervical cancer screening program and randomly assigned them to receive either automated screening or conventional cytology. The women's conditions were followed up for a maximum of nine years. The authors observed no difference in cervical cancer rates between the automated and the conventional methods, suggesting that both work equally reliably in screening programs.

In another study, Cantor et al. tested the diagnostic capability of optical spectroscopy compared with conventional colposcopy. They found that, as an adjunct to colposcopy, optical spectroscopy works well for detection of cervical cancers. The spectroscopy device worked better for diagnosing patients who had been referred with abnormal Pap smears than for screening of patients with a history of normal Pap smears. The authors are currently developing another device, the multispectral digital colposcope, better suited to screening purposes.

HPV and Cervical Cancer By Gina Kirchweger

Merikukka et al., pp. 1114–1119

Chen et al., pp. 1192–1203

Virtually all cases of invasive cervical cancer are associated with human papillomavirus (HPV) infections but only 12 out of the more than 100 known genotypes of HPV have been classified as carcinogenic: HPV16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58 and 59. Since the two high-risk strains HPV16 and 18 alone account for around 70% of invasive cervical cancers worldwide, both vaccines currently on the market were designed to protect against these two genotypes. Barely explored geographic variations in the prevalence of individual genotypes might, however, render the available vaccines less effective in certain populations.

A large-scale community-based cohort study conducted by Chen et al. revealed that in Taiwan HPV16 (48.2%), 58 (25%), 52 (19.6%), 31 (8.9%), 33 (8.9%) and 18 (3.6%) are strongly associated with cervical neoplasia. They estimate that only 49% of cervical cancer cases in Taiwan could be prevented by eliminating HPV16 and 18 infections, a much lower percentage than in Europe or North America. An additional 40% of cases could be prevented by targeting HPV58, 52, 33 and 31.

To better understand how HPV vaccination could rapidly change the ecosystem of genital HPV types by diminishing the pool of individuals susceptible to infection with certain genotypes, Merikukka et al. evaluated competition among the seven most common HPV types in a population sample of unvaccinated Finnish women aged 15-49. Their findings suggest a competitive advantage for HPV33 over a number of other genital HPV types in the studied population.

Understanding epidemiological patterns of genotype-specific HPV infection is essential to estimate the likely impact of HPV screening and vaccine coverage on the prevention of cervical neoplasia.

Cracking Drug-Resistant Pancreatic Cancer By Caroline Seydel

  1. Top of page
  2. New Techniques in Cervical Cancer Screening & Detection By Caroline Seydel
  3. Cracking Drug-Resistant Pancreatic Cancer By Caroline Seydel

Banerjee et al., pp. 1240–1250

When a cancer becomes resistant to one drug, patients' lives depend on having a second line of treatment ready to go. Oxaliplatin, though it's been used as the second line against pancreatic cancer, doesn't work as well as had been hoped. In this paper, Banerjee et al. set out to determine whether treating cancer cells with a chemical found in soybeans could make them susceptible to death by oxaliplatin. They found that the chemical, called genistein, did make it easier for oxaliplatin to induce apoptosis, which could be good news in the fight against pancreatic cancer.

“…hitting the cells first with genistein, then with oxaliplatin, killed significantly more cells than either agent alone.”

Most people with pancreatic cancer die within the first year after diagnosis. After several cycles of chemotherapy, the cancer generally becomes drug-resistant. Oxaliplatin, which clinicians turn to as a second line of treatment, causes severe adverse side effects in high doses, but low doses don't do much against the disease. Banerjee et al. investigated whether these drug-resistance cancers could be made sensitive to oxaliplatin. They looked to a soy isoflavonoid called genistein, which has been shown to inhibit cell growth, limit tumor cell migration, and spur cell death.

The researchers treated the resistant cancer cells with genistein to find out whether that would open the door to destruction by oxaliplatin. They found that hitting the cells first with genistein, then with oxaliplatin, killed significantly more cells than either agent alone. Genistein paves the way for oxaliplatin by suppressing NF-kB, thus downregulating a variety of downstream anti-apoptotic genes, including Bcl-xL, BCL-2, survivin, and others. This could mean that genistein's ability to sensitize cancer cells might work in various tumor types. Genistein also selectively targets tumor cells, leaving normal pancreatic cells unharmed. Experiments in mice then showed that the combined treatment shrunk tumors, bolstering the cell culture results and marking genistein as a very interesting prospect for pancreatic cancer treatment. 1

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Illustration 1. Combining genistein and oxaliplatin dramatically reduced metastases

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