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Posts Tagged ‘New England Journal of Medicine’

NEW ENGLAND JOURNAL OF MEDICINE: A single “precursor” cancer cell may be responsible for the spread of prostate cancer and eventual death of the patient, according to a paper in the latest Journal.

A recent study by Liu and colleagues has shown that metastases in prostate cancer have a common origin — that is, they originate from the same clone.

If the single lesion harboring this metastatic clone could be accurately identified and then targeted, it seems likely that the side effects of treatment for prostate cancer would be reduced.

The key question thus remains: Does the index lesion harbour the single precursor cell that gives rise to progression, metastases, and death?

Even if the index lesion is not the culprit, researchers must now focus on identifying the one  that does harbor the metastatic clone.

Once a means of identification can be determined, clinical trials will be warranted to investigate the effect of ablating that single lesion.

A positive result would have important implications for men with prostate cancer who currently endure much treatment-related harm.

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NEW ENGLAND JOURNAL OF MEDICINE: Some 350 cancer genes have so far been identified by researchers, but there may be as many as 2000, says Dr James R Downing, Memphis, in an analysis of cancer genome research. READ MORE>

…although the landscape of cancer genes will get substantially more complex, clinically relevant diagnostic, prognostic, and predictive markers and therapeutic targets will emerge long before our understanding of the cancer genome is complete.

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NEW ENGLAND JOURNAL OF MEDICINE: A new drug just approved by the FDA for high risk prostate cancer patients suffering bone loss has performed well in a trial.

Denosumab was associated with increased bone mineral density at all sites and a reduction in the incidence of new vertebral fractures among men receiving androgen-deprivation therapy for non-metastatic prostate cancer.

Background: Androgen-deprivation therapy is well-established for treating prostate cancer but is associated with bone loss and an increased risk of fracture.

We investigated the effects of denosumab, a fully human monoclonal antibody against receptor activator of nuclear factor-{kappa}B ligand, on bone mineral density and fractures in men receiving androgen-deprivation therapy for nonmetastatic prostate cancer.

Methods: In this double-blind, multicenter study, we randomly assigned patients to receive denosumab at a dose of 60 mg subcutaneously every 6 months or placebo (734 patients in each group).

The primary end point was percent change in bone mineral density at the lumbar spine at 24 months. Key secondary end points included percent change in bone mineral densities at the femoral neck and total hip at 24 months and at all three sites at 36 months, as well as incidence of new vertebral fractures.

Results: At 24 months, bone mineral density of the lumbar spine had increased by 5.6% in the denosumab group as compared with a loss of 1.0% in the placebo group (P<0.001); significant differences between the two groups were seen at as early as 1 month and sustained through 36 months.

Denosumab therapy was also associated with significant increases in bone mineral density at the total hip, femoral neck, and distal third of the radius at all time points.

Patients who received denosumab had a decreased incidence of new vertebral fractures at 36 months (1.5%, vs. 3.9% with placebo) (relative risk, 0.38; 95% confidence interval, 0.19 to 0.78; P=0.006). Rates of adverse events were similar between the two groups.

Researchers: Matthew R. Smith, M.D., Ph.D., Blair Egerdie, M.D., Narciso Hernández Toriz, M.D., Robert Feldman, M.D., Teuvo L.J. Tammela, M.D., Fred Saad, M.D., Jiri Heracek, M.D., Ph.D., Maciej Szwedowski, M.D., Chunlei Ke, Ph.D., Amy Kupic, M.A., Benjamin Z. Leder, M.D., Carsten Goessl, M.D., for the Denosumab HALT Prostate Cancer Study Group.

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NEW PROSTATE CANCER INFOLINK: New data published in the New England Journal of Medicine clearly suggests that bone-loss drug denosumab has a significant effect compared to placebo in men with prostate cancer. READ MORE>

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JULY 12: NEW ENGLAND JOURNAL OF MEDICINE: Letters to the editor have been flooding into the New England Journal of Medicine since it published the results of the two big randomised prostate cancer screening trials (March). READ MORE>

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JULY 3: PROSTABLOG NZ: In what seems to be exquisite timing, NZ’s parliamentary select committee on health is starting an inquiry into prostate cancer screening – just as some of the best recent analysis of screening emerges in the US.

The latest informative discussion comes from Mike Scott at the New Prostate Cancer Infolink website, one of the leading American aggregators of up-to-date information.

As global debate hots up following recent publication in a medical journal called CA: A Cancer Journal for Clinicians of an article about screening and an accompanying editorial, Scott today makes some interesting points:

  • Media reporting of this latest look at the two large randomised studies is well wide of the mark.
  • What the article actually makes clear is we just do not know how best to use the tools currently available to test an individual man so as to ascertain with accuracy his real risk for clinically significant prostate cancer.
  • So — surprise, surprise — we need better tests, as America’s Prostate Cancer Organizations have already clearly stated.
  • A critical element, covered in the article, is the importance of taking account of the patient’s age, life expectancy, family history, race/ethnicity, and other personal health factors in making the decision whether testing for prostate cancer is appropriate or not.
  • The article does not discuss, at all, the potential merits of  “baseline” PSA testing (at any specific age).
  • The journal’s accompanying editorial uses some “loaded” language in making the correct recommendation that regular, mass, population-based screening is not currently justified based on the available evidence. That “loaded” language is centered around the use of the terms “over-diagnosis” and “over-treatment.”
  • There is excellent evidence today that “mass, population-based screening” using mammograms to look for breast cancer is no more justified that prostate cancer screening, on any good statistical basis. Some 2,970 women must be screened once to find 27 cancers and save one life (in women aged between 40 and 65 years of age). The editorial repeats the finding of the European trial that it would be necessary to screen 1,410 men and find an additional 48 cancers to prevent one prostate cancer-specific death.
  • There are simple answers to the issue of “over-reaction” (to screening findings from doctors and patients), and they start with greater honesty — among the clinical community and among the survivor community — about what we really do and don’t know.
  • Over the past 30 years, prostate cancer deaths have dropped 20% in the US, but…”We still can’t tell [which patients are at real risk] beforehand, and so fear and  ‘standard practice’  tell us that we should proceed with treatment ‘to be on the safe side’. We need to do better. And it doesn’t help to demonize the problem with terms like ‘over-diagnosis’ and ‘over-treatment’.”
  • In all truth, we do not have good enough information to allow us to know the best thing to do for the vast majority of men who are at only a statistical (as opposed to a clinically evident) risk for prostate cancer.

It’s to be hoped someone draws the Health Select Committee‘s attention to this latest development in the debate, which has rumbled along since late March, when the results of the long-awaited studies were published in the New England Journal of Medicine – and failed to resolve anything.

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JUNE 27: NEW PROSTATE CANCER INFOLINK: A report in this week’s issue of the New England Journal of Medicine provides more early, and interesting, evidence of the future potential of so-called PARP (poly(ADP-ribose) polymerase) inhibitors in cancer therapy. READ MORE>

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