Malignant Mesothelioma | Surviving Mesothelioma

Malignant Mesothelioma

Paul Kraus is not the only long-term survivor of malignant mesothelioma. There are others such as Rhio O’Connor, Ruth Phillips, and Gene Adoline.  In addition, there are many others we have heard about or spoken to over the years. What is fascinating is that many of these mesothelioma survivors have something in common – they have all taken steps to improve or enhance their immune system. Some used alternative or complimentary therapies (with guidance from licensed clinicians) while others participated in clinical trials of immune therapy.

This raises the question – does the immune system play a role in controlling malignant mesothelioma? Paul Kraus’ experience and those of other long-term mesothelioma survivors suggests that such a role may be possible. In fact, here’s an interesting question:

While scientists tell us that asbestos causes mesothelioma, why is it that only a small percentage of people exposed to asbestos are ever diagnosed with mesothelioma? Could there be another aspect that makes some people susceptible to the disease? Some doctors have contemplated that a patient’s immune status could play a role in the genesis of mesothelioma and other cancers. If this is true, it would explain why immune boosting modalities could help some patients control their disease.

In other sections of this website we present case histories of malignant mesothelioma survivors who were diagnosed with either pleural mesothelioma or peritoneal mesothelioma. In some of the pleural mesothelioma case histories, doctors discuss the role that the patient’s immune system may have played in their extremely long survival.

History of Malignant Mesothelioma and Immunity

In 1986, an article appeared in a medical journal that discussed this very issue of mesothelioma and immunity.(1)  This research focused on the immune responses of 118 healthy people compared to 20 patients with malignant mesothelioma and 375 long-term asbestos workers who were cancer-free.  The researchers wanted to know if there were any measurable differences in the immune responses of the mesothelioma patients.  Their findings demonstrated a relationship between the immune system and mesothelioma.  For example:

  • The number of total T (T11+) and T-helper (T4+) cells were normal in asbestos workers with cancer, but were significantly reduced in patients with mesothelioma.  T cells orchestrate, regulate and coordinate the overall immune response. This suggests that the immune systems of mesothelioma patients may be compromised by mesothelioma or perhaps a compromised immune system allowed the disease to advance.
  • Most patients with mesothelioma had a profound deficiency in Natural Killer cell (NK) activity which is suggestive of the role the immune system plays in the control of malignant mesothelioma.  NK cells are a type of lethal lymphocyte that target tumor cells and protect against a wide variety of infectious microbes.

In the discussion section of the report, the researchers stated:

“These findings led us to speculate that biological phenomena generally categorized as chronic immunosuppression associated with the presence of asbestos fibers in the exposed workers may have caused the eventual breakdown of the host’s surveillance system and the onset of neoplasm.”

In other words, the researchers are suggesting that mesothelioma may result from immune suppression.  If this is true it would provide the biological basis for the role that the immune system and immune boosting approaches may play in the management of mesothelioma.  For example, if a “breakdown” in a patient’s immune system helped lead to cancer then a corollary would be that strengthening the immune system would be beneficial in managing the disease. These are theories only and should be studied further. If you are interested in learning more about immune boosting modalities, speak to your doctor.


(1) Lew, F., et al., High Frequency of Immune Dysfunctions in Asbestos Workers and in Patients with Malignant Mesothelioma, Journal of Clinical Immunology; 1986, 6:3, 225-232.

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