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| A back-calculation of the growth of Bernofsky's tumor suggests that his malignancy arose during the height of his chairman's unrelenting campaign of harassment. His oncologist agreed. |
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Dates Associated with Bernofsky's Disability Claim* | |
| Termination from Tulane(1) | |
| First self-observation of tumors | |
| Medical examination by Dr. Stephen S.
Cheng (Ochsner Clinic) |
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| Medical examination by Dr. Edward B.
Staudinger (Memorial Medical Center) |
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| Surgical removal of tumors by Dr. Staudinger | |
| Cancer treatment protocol outlined by Dr. Milton W. Seiler (Memorial Medical Center) | |
| End of annual employment contract with Tulane(2) | |
*Tulane made certain that Bernofsky would never collect a benefit from the disability insurance policy he had carried with TIAA for nearly 20 years. |
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Determinining The Onset of Disability
According to the Surgical Pathology Report on Bernofsky's tumors,(3) the larger of the two masses removed from his groin area measured 8 x 5 x 3.5 cm, or 140 cm3 in volume. From knowledge that a typical lymphoblastoid cell has a mean cell diameter of 12.4 µm [1] and cell volume of 1,000 µm3 [2], and employing the conversion factor of 1 µm = 10-4 cm, it follows that 1 cm3 contains 109 cells and that the tumor contained approximately 140 x 109 cells. Assuming that 100% of the tumor progeny had remained reproductively viable, one can calculate from the following formula [3] the number of cell doublings (n) required to obtain 140 x 109 cells.
| Thus: | 2n = 140 x 109 |
| Converting to logarithms: | n log 2 = log 140 + 9 log 10 |
| Solving for n: | n = 37.03 |
From this calculation, approximately 37 doublings of the lymphatic cell that underwent neoplastic transformation were required to produce the lymphoma mass that had been excised. Tumor cells can double every 1 to 5 days or more, and from this knowledge it is possible to estimate the developmental time of the excised tumor as illustrated in the following table.
Days Needed to Double
Cell PopulationExcised Tumor Estimated Total Tumor Days Needed
for
37 Doublings@ 100% viability
Days Needed
for
37 Doublings@ 50% viability
Days Needed
for
74 Doublings@ 100% viability
Days Needed
for
74 Doublings@ 50% viability
1 37 74 74 148 2 74 148 148 296 2.2* 81 163 163 326 3 111 222 222 444 4 148 296 296 592 5 185 370 370 740 *Doubling time for lymphoma as determined by Goldfeder [4]. Dr. Edward B. Staudinger, the surgeon who operated on Bernofsky, observed that in addition to the two tumor masses he was able to remove, the tumor had spread throughout the lymphatic chain of the lower abdomen and right thigh, giving rise to malignant foci too numerous and small to be surgically removed.(4) Eliminating the remaining tumor burden was the objective of the aggressive chemotherapy and radiation treatment that Bernofsky subsequently received. On the reasonable assumption that the disseminated tumor remaining after surgery was equal in mass to the unified tumor that could be removed, the estimated overall time frame of tumor development would be double that based on the excised tumor alone. Thus, development of the total tumor mass would require 74 doublings, as indicated in the table above. Because of uncertainty in the doubling time and the rate at which unstable tumor cells became reproductively moribund, one can only state with assurance that the onset of tumorigenesis occurred within the time frame of 5 to 20 months prior to observation, and most likely closer to a year. Additional information is needed to more accurately derive the time to reach a fixed tumor size. For example, lag times (periods of induction of cell growth) would increase the time needed for 74 doublings, while the rate of cell death (unknown), which would also increase the time needed for 74 doublings, should be subtracted from the rate of proliferation. In lieu of such data, a crude approximation of the increased time needed to reach the measured tumor size is given in the above table under the heading, "50% viability." The presence of necrotic (dead) cells in Bernofsky's tumor was documented in the Surgical Pathology Addendum Report.(5) If one does not allow for the presence of necrotic cells or the plateau [5] of tumor growth,(6) then the closest time of tumor inception would be 163 days prior to June 5, 1995, the date the tumor was excised and measured. However, because of the significant presence of necrotic cells, tumor inception must have occurred long before then and most likely about a year prior to June 5, 1995. For more than a year prior to his termination, Bernofsky found the need to engage in less physically demanding activities, which required more flexibility with regard to his work schedule. During this period, he reviewed research and wrote papers and grant applications. Bernofsky was the only faculty member in the Department who had been denied computer equipment for his Tulane office and had to rely on personal computer equipment in his home office. His chairman, Dr. Jim D. Karam, made an issue of this and reprimanded Dr. Bernofsky for taking time off to work at home. Bernofsky also suffered from chronic fatigue and needed afternoon rest, but he kept this fact from Karam, not wishing to give him the satisfaction of knowing that he was succumbing to his unrelenting harassment. At the time, Bernofsky did not realize his fatigue was the result of a growing tumor, and attributed it to stress arising from his chairman's persecution. In summary, Bernofsky suffered latent disability during the development of his malignancy even though his only physical symptom was fatigue, which he attributed to chronic stress and mental anguish. In any event, it is clear that tumor inception corresponded to that period that was characterized by his department chairman's hostility, interference with his research program, dismissal of his research coworkers, convening of a fault-finding committee, threats of termination, and the refusal to recognize his latest source of grant support from the Air Force. During that protracted interval of maltreatment and abuse, Bernofsky endured continual frustration and emotional distress, culminating in despondency over the loss of a life-long career dedicated to science and grief over the loss of a body of unfinished work. The weakening of a person's immune defenses — which are involved in the surveillance of malignancy [6-11] — and the vulnerability of tumor-suppression mechanisms in response to stress [12-14] are well-known medical phenomena [15-18] that undoubtedly contributed to Dr. Bernofsky's malignant disease.(7) Carl Bernofsky
New Orleans
December, 1998Footnotes
1. Memo of June 12, 1995 from Jim D. Karam to James J. Corrigan.
2. Letter of June 20, 1994 from James J. Corrigan to Carl Bernofsky.
3. Surgical Pathology Report SB-95-02445 from Mercy Baptist Medical Center, prepared June 6, 1995, Flora B. Shoaf, M.D., pathologist.
4. Personal communication from Edward Staudinger to Carl Bernofsky, June 5, 1995.
5. Surgical Pathology Addendum Report SB-95-02445 from Mercy Baptist Medical Center, prepared June 8, 1995, Flora B. Shoaf, M.D., pathologist.
6. Tumor growth rates tend to plateau with increasing size in response to limitations in nutrient supply, oxygen availability and the accumulation of necrotic cells.
7. Letter of October 11, 1995, from Bernofsky's treating physician, Milton W. Seiler, M.D., hematologist/oncologist.
References
Wintrobe, M.M., Clinical Hematology, 6th ed., Lea & Febiger, Philadelphia, 1967, p. 224.
Harris, M., Electronic enumeration and sizing of cells, in Tissue Culture: Methods and Applications, (Kruse, Jr., P.F., Patterson, Jr., M.K., eds.), Academic Press, New York, 1973, pp. 400-405.
Freshney, R.I., Culture of Animal Cells: A Manual of Basic Technique, Alan R. Liss, New York, 1983, p. 129.
Goldfeder, A., Cell kinetics, cell structure, and radiotherapy, Annals, N.Y. Acad. Sci., 397, 168-183 (1982).
Freshney, R.I., Culture of Animal Cells: A Manual of Basic Technique, Alan R. Liss, New York, 1983, pp. 126-128.
Monjan, A.A., Collector, M.I., Stress-induced modulation of the immune response, Science, 196, 307-308 (1977).
Riley, V., Psychoneuroendocrine influences on immunocompetence and neoplasia, Science, 212, 1100-1109 (1981).
Schleifer, S.J., Keller, S.E., Camerino, M., Thornton, J.C., Stein, M, Suppression of lymphocyte stimulation following bereavement, J. Am. Med. Assoc., 250, 372-377 (1983).
Callabrese, J.R., Kling, M.A., Gold, P.W., Alterations in immunocompetence during stress, bereavement, and depression: Focus on neuroendocrine regulation, Am. J. Psychiatry, 144, 1123-1134 (1987).
Evans, D.L., Leserman, J., Pedersen, C.A., Golden, R.N., Lewis, M.H., Folds, J.A., Ozer, H., Immune correlates of stress and depression, Psychopharmacol. Bull., 25, 319-324 (1989).
Friedman, E.M., Irwin, M.R., A role for CRH and the sympathetic nervous system in stress-related immunosuppression, Annals, N.Y. Acad. Sci., 771, 396-418 (1995).
Maxwell, S.A., Roth, J.A., Posttranslational regulation of p53 tumor suppressor protein function, Crit. Rev. Oncology, 5, 23-57 (1994).
Licinio, J., Gold, P.W., Wong, M.L., A molecular mechanism for stress-induced alterations in susceptibility to disease, Lancet, 346, 104-106 (1995).
Yu, C., Yap, N., Chen, D., Cheng, S., Modulation of hormone-dependent transcriptional activity of the glucocorticoid receptor by the tumor suppressor p53, Cancer Lett., 116, 191-196 (1997).
Bahnson, C.B., Stress and cancer: the state of the art, Psychosomatics, 21, 975-981 (1980).
Sklar, L.S., Anisman, H., Stress and cancer, Psychol. Bull., 89, 369-406 (1981).
Baltrusch, H.J.F., Waltz, M., Cancer from a biobehavioural and social epidemiological perspective, Soc. Sci. Med., 20, 789-794 (1985).
Huffer, K., Karin's Story, Fraud on the Court [Blog, 2007], http://www.fraudonthecourt.blogspot.com/..., accessed 02/16/08.
Web site created November, 1998 This section last modified February, 2001
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