1. +
Introduction to
the Biology of
Functions and its
application to Cancer
By:
Jean Claude Lapraz, MD
Kamyar M. Hedayat, MD

2. +
Cancer: Introduction
 Cancer is a deregulation of cell growth
 Modern research has focused on the role of oncogenes and
proto-oncogenes in the etiology of tumors
 However, oncogenes and proto-oncogenes
 Require some type of stimulation (i.e. viral infections, environmental
toxins), thus the detection of oncogenes alone is not sufficient to
predict risk of cancer in all cases
 The degree and duration of their expression is managed by the
endocrine system and modulated by the immune and
neurovegetative systems and this cannot be determined by current
binary lab testing services

3. +
Presentation of Cancer
 Regardless of whether a cancer is slow or fast growing, there is
a time period in which there is dysplastic then dedifferentiated
cell growth before a diagnosis of cancer is made due to
 Palpation of a sufficient number of cancerous cells
 Mass effect from a space-occupying lesion
 Disruption of cellular metabolism
 By the time many cancers are detected by the above noted
methods, it is often in an advanced state
 The ability to detect a cancer in a less advanced state would be
invaluable

4. +
Cancer: Screening Tests
 The efficacy of common screening tests to diagnosis metastatic
cancers, such as yearly mammograms and PSA testing have
come in to question due to
 Detection and biopsy of benign masses1,2
 Treatment of tumors which may have spontaneously regressed3
 Inability to anticipate aggressive tumors which grow in a short period
of time1,2
1. Esserman L, Shieh Y, Thompson I. Rethinking screening for breast cancer and prostate
cancer. JAMA. Oct 21 2009;302(15):1685-1692.
2. Woolf SH. The accuracy and effectiveness of routine population screening with
mammography, prostate-specific antigen, and prenatal ultrasound: a review of published
scientific evidence. Int J Technol Assess Health Care. Summer 2001;17(3):275-304.
3. Zahl PH, Maehlen J, Welch HG. The natural history of invasive breast cancers detected by
screening mammography. Arch Intern Med. Nov 24 2008;168(21):2311-2316.

5. +
Cancer: Prevention and Risk
Assessment
 Large scale nutritional interventions aimed at preventing cancer
have been equivocal, or, even showed an increased rates of
cancer
 Diets rich in fruits and vegetables: equivocal1
 High doses of antioxidants: increased incidence of lung cancer2
 The short-coming in these studies was two
 Inappropriate or lack of stratification of subjects based on metabolic
type: catabolic vs. anabolic vs. mixed
 Inappropriate understanding of the quality and types of supplements
1. Hung HC, Joshipura KJ, Jiang R, et al. Fruit and vegetable intake and risk of major chronic
disease. J Natl Cancer Inst. Nov 3 2004;96(21):1577-1584.
2. The effect of vitamin E and beta carotene on the incidence of lung cancer and other cancers
in male smokers. The Alpha-Tocopherol, Beta Carotene Cancer Prevention Study Group. N
Engl J Med. Apr 14 1994;330(15):1029-1

6. +
Short comings in Cancer research
 Modern cancer research has been impressive in elucidating the
genetic, cellular, and sub-cellular mechanisms of cancer,
however, two issues continue to hamper cancer treatment
 The ability to account for individual metabolic, endocrine and
genetic factors in cancer risk assessment and treatment
 The ability to account for multiple risk factors simultaneously in a
dynamic, quantitative and qualitative manner in order to differentiate
 What is needed is a functional, dynamic testing system to both
anticipate, determine the causes of, and witness the efficacy of
treatment of cancers

7. +
Laboratory studies
• Classical lab data is based on binary considerations:
• disease vs. no disease
• normal vs. abnormal value
• In many instances, patients have normal lab values but exhibit
symptoms or physiological irregularities consistent with a sub-
optimal state of health.
• Binary considerations cannot be applied with any real
assurance of its functional relevance to a system as complex as
the human body.

8. +
Laboratory studies
• Biological systems, like social interactions are complex, multi-
tiered, dynamic interrelated and integrated systems
Yeast Protein Interaction Network
Bader and Hogue (2002) Nature
Pattern of cellular phone calls
between friends

9. +
Integrated systems
• Objective quantitative data (laboratory values) are required to
assess the organism
• However, the true utility of binary values is when they are able
to provide functional descriptions of quantitative and qualitative
activity:
• Within a particular unit of activity
• Of one unit to another,
• Of the system as a whole
• Only then can a truly dynamic and individualized assessment of
the patient occur

10. +
Laboratory studies
• The endocrine system, as the manager of the metabolic activity of the
body is the ideal object of evaluation
• Serum levels of hormones only reflect quantitative organ output, not
functional activity, which can be affected by:
• Hormone receptor binding1
• Intracellular messenger activity1
• Epigenetic changes2
• Heavy metal toxicity3, etc.
• Moreover, serum levels of hormones do not reflect the degree of
stimulation needed or the metabolic costs incurred in producing a
particular hormone
1) Raison CL, Miller AH. When not enough is too much: the role of insufficient
glucocorticoid signaling in the pathophysiology of stress-related disorders. Am J
Psychiatry. Sep 2003;160(9):1554-1565
2) Chiam K, Tilley WD, Butler LM, Bianco-Miotto T. The dynamic and static modification of
the epigenome by hormones: A role in the developmental origin of hormone related
cancers. Biochim Biophys Acta. Apr 2009;1795(2):104-109.
3) Gerhard I, Waibel S, Daniel V, Runnebaum B. Impact of heavy metals on hormonal and
immunological factors in women with repeated miscarriages. Hum Reprod Update. May-
Jun 1998;4(3):301-309.

11. +
Laboratory studies
• The ideal system of measurement of biological processes thus
should examine the metabolic products of hormonal
management of cellular activity
• In conclusion, the ideal laboratory system must
• Reflect the complex, integrated and dynamic nature of biological
systems
• Describe the functionality of the system in its
• Qualitative function
• Quantitative function
• Individual unit, relative to other units and as a whole
• Assess the organism at the metabolic and interstitial level

12. +
Biology of functions
• Biology of Functions (BoF) quantifies functional abilities of
the organism, before, during and after theeffects of
adaptation to stressors. Because functionality is dynamic, a
dynamic, integrated and evolutionary methodology must be
used instead of static lab values
• BoF is based on a number of specific indices defined by
mathematical relations between commonly used blood
analysis data
• The algorithms that permit the calculation of these indices
are based on the physiological relations that exist between
the direct or indirect products of hormonal activity:
cells, hormones or enzymes (eosinophils, monocytes, lactate
dehydrogenase, for example).

13. +
Biology of functions
• These relations allow one to visualize the functioning of the
organism at every level:
• maintenance of homeostasis
• Adaptation to stressors
• Recovery after aggression
• Immunity, etc.
• Each function is quantified by an index, specified by a level of
activity. The index expresses the actual activity of that function,
both in and of itself and in relation to the metabolic and tissue
needs of the organism.
• The whole set of indices gives an evolutionary assessment of
an individual body’s functionality, system by system, organ by
organ.

14. +
Biology of Functions and Cancer
 With respect to cancer, the BoF accounts for individual factors
that contribute to dedifferentiated cell growth:
 Endocrine: TRH, Estrogen, Testosterone, Insulin, etc.
 Neurovegetative: Norepinephrine, histamine, serotonin, etc.
 Immunologic: Interleukins, inflammatory activity
 As well as cumulative effects of these factors on
 Metabolism: Active and passive membrane permeability,
mitochondria strain, Redox status, etc.
 Cellular function: nucleocytoplasmic cytopathogenecity, membrane
fracture, membrane expansion, apoptosis, necrosis

15. +
Biology of Functions and Cancer
 By assessing the current, functional activity of the
organism, the Biology of Functions is able to assess multiple
risk factors in relationship to each other
 Carcinogenesis Index: The degree of dysplastic activity
 Cancerous Index: The relative degree of endocrino-metabolic
factors which are propitious to cancerous activity
 Expansiveness index no.2: the relative risk of anarchic cellular
development due to adaptive phenomenon
 Active Carcinogenesis: The actual functional rate of cancer cell
growth after assessing for the rate of pathological cell death from
apoptosis or necrosis
 Active effective carcinogenesis: Witnesses the insufficiency of
the organism’s defenses in the face of cancer over activity
 Carcinogenesis expansion: the degree and speed of a cancer’s
evolution

16. +
Biology of functions
• SUMMARY: Biology of Functions allows one to determine:
• Pathogenic tendencies of the organism
• The stage of development and the degree of severity of a potential
pathology (i.e. cancer, cardiac disease, degenerative neurological
disease)
• Biology of functions can be used as a tool to track
• the natural development of pathology
• To derive a rational therapeutic treatment
• To evaluate the efficacy of the treatment over time

17. + CASE STUDY
GLIOBLASTOMA MULTIFORME
REFRACTORY TO RADIOTHERAPY
AND TEMOZOLOMIDE IN A 9 YEAR
OLD FEMALE

18. +
Case History
 9 year old female was diagnosed with a right thalamic tumor in
1/07. She underwent resection with post-operative morbidities
including intracerebral hemorrhage.
 Tumor size was noted to be increasing on a follow up MRI on
8/08
 A repeat MRI on 10/31/08 indicated continued growth of the
lesion.
 Partial resection was performed and a pathological assessment
determined the tumor to be a glioblastoma multiforme

19. +
Case History
 Patient underwent focal radiotherapy and daily Temozolomide
in early 2009, completed 3/09
 Follow up MRI 4/09 revealed progressive local disease in the
resection cavity, which was not considered to be resectable
 Patient sought a second opinion for assessment and treatment
using the endobiogenic system and the biology of functions
 Initial assessment performed 4/09, with subsequent follow up
on 10/09.
 Follow up MRI’s on 8/09 and 11/09 revealed stable tumor size
with no further growth or metastasis

20. +
Initial Assessment: 4/09
 The biology of functions revealed an encapsulated adenoid
type growth
 Fibrosis index: 9.82 (6-8)
 Adenoid index: 421 (10-30)
 The cancer was quite active, though the cancer was
characterized as a relatively slow-developing growth and not
extremely anarchic in its growth pattern and insufficient
apoptosis
 Active cancer index: 1,831 (0.01-4.8)
 Cancer expansion index: 0.004 (0.02-3.08)
 Expansivity index no.2: 6.47 (1-4)
 Apoptosis index: 0.15 (0.9-1.4)

21. +
Initial assessment:
Thyrotropic factors
 The hypothalamic-metabolic factors, namely TRH and cellular
metabolic factors were found to play the most important role in
the patient’s cancer growth.
 We have noted that in brain cancers in general, and pediatric
brain cancers in particular, that TRH plays a very important role
in the etiology and growth of the cancer
 TRH-influenced factors
 DNA fracture: 10.27 (0.5-1.5)
 Global TRH adaptation index: 18.6 (3-9)
 Pro-inflammatory index: 0.44 (0.1-0.4)

22. +
Initial Assessment:
Metabolic factors
 The cancer had a catabolic, acidic quality with a high degree of
intracellular communication:
 Active cellular permeability: 1,482 (6-9)
 With poor passive permeability, contributing to the high degree
of nucleocytoplasmic pathogenicity and toxin accumulation
within the cell, and excessive nutrient oxidation with free radical
accumulation
 Passive cellular permeability: 3.06 (4-9)
 Nucleocytoplasmic pathogenicity: 37 (0.8-1.5)
 Harmful free radical index: 122 (2-6)

23. +
Initial Assessment:
Other Factors
 There was a significant elevation in androgenic activity, as well
as an up-regulation of both peripheral androgen and estrogen
receptors
 Androgen index: 0.52 (0.05-0.09)
 Androgen index comparative: 0.31 (0.1-0.3)
 Quantitative estrogen organo-tissular yield: 23,635 (67-1006)
 Growth factors also played an important role
 Metabolic Growth Index: 16.53 (2-6)
 Membrane Expansion: 0.48 (0.08-0.16)

24. +
Initial Treatment
 Medicinal Plants:
 Prunusamygdalis(Sweet almond): reduces peripheral growth factors
 Quercuspedunculatus(English oak): Glucocorticoid activity to reduce
tumor size
 Tiliatomentosa (Silver linden): reduces TRH activity, anti-
inflammatory, neuro-calmative, liver regenerative
 Juglansregia(Black walnut): exo- and endocrine pancreatic activity,
reducing TRH and para-sympathetic stimulation of pancreas;
stimulates hepatic macrophages and plasmocytes
 Brassicanapus (Cabbage): blocks TSH stimulation of thyroxine
production and release, anti-inflammatory
 Ilex acquafolium(Holly tree):anti-fibrotic

25. +
Initial Treatment
 Supplements:
 Vitamin C 6gm/d + Vitamin K 2, K3: anti-tumoral activity in conjunction
with Vitamin C1
 Melatonin2 10 gm qHS to reduce estrogen receptors2, Leutinizing
hormone3 and for its anti-tumoral activity4
 Exocrine digestive enzymes: to reduce parasympathetic activity
 Diet: Dietary changes aimed to reduce the degree of highly
assimilable nitrogenous proteins and parasympathetic and insulin
activity: Low-glycemic, dairy and gluten-free vegetarian diet with
whey protein supplements
1. Verrax J, Taper H, Calderon P. Targeting cancer cells by an oxidant-based therapy. Current
Molecular Pharmacology. 2008;1:80-92.
2. del Rio B, Garcia Pedrero JM, Martinez-Campa C, Zuazua P, Lazo PS, Ramos S.
Melatonin, an endogenous-specific inhibitor of estrogen receptor alpha via calmodulin. J Biol
Chem. Sep 10 2004;279(37):38294-38302.
3. Kripke DF, Kline LE, Shadan FF, Dawson A, Poceta JS, Elliott JA. Melatonin effects on
luteinizing hormone in postmenopausal women: a pilot clinical trial NCT00288262. BMC
Womens Health. 2006;6:8.
4. Lissoni P, Barni S, Ardizzoia A, et al. A randomized study with the pineal hormone melatonin
versus supportive care alone in patients with brain metastases due to solid neoplasms.
Cancer 1994;73:699-701.

26. +
Follow Up Assessment: 11/09
Laboratory Chemistries
Chemistry 4/09 11/09 Comment
LDH 300 194 Reduction in chronic metabolic strain
CPK 137 90 Reduction in acute metabolic strain
CEA 0.7 <0.5 Cell adhesion molecule
CA 15-3 34 23 Associated with gonadotropic activity and
thyroid’s role in hyperplasia and inflammation1,2
CA 19-9 40 34 Associated with abdominal cancers; repre-sents
metabolic role of thyro-somatotropic activity

27. +
Follow Up Assessment: 11/09
Laboratory Chemistries
Chemistry 4/09 11/09 Comment
Osteocalcin 17.8 42 Serum levels are inversely related cellular
metabolic activity as inducers of anabolism, as
it stimulates insulin release1
BUN/Cr 29 15 Elevated BUN/Cr ratio can be associated with
a hyper-catabolic state
Na 155 138
ALT 96 38
Hg 9.5 10.7 Improvement in anemia
1. Atkinson SA. Vitamin D status and bone biomarkers in childhood cancer.
Pediatr Blood Cancer. Feb 2008;50(2 Suppl):479-482; discussion 486.

28. + Follow up assessment: Biology of Functions:
APOPTOSIS INDEX: Global rate of apoptosis relative to
the rate of dysfunctional apoptosis during adaptation (nl
0.3-0.7)
04/27/05 11/01/05
index d'apoptose (0,3 à 0,7) 0.15 0.86
0.00
0.10
0.20
0.30
0.40
0.50
0.60
0.70
0.80
0.90

29. + Follow up assessment: BoF
DNA FRACTURE: Degree of nuclear fragility and its risk of
rupture, and by extension, of transcription errors (nl: 0.5-
1.5)
04/27/05 11/01/05
index de fracture adn (0,5 à 1,5) 10.27 5.55
0.00
2.00
4.00
6.00
8.00
10.00
12.00

30. + Follow up assessment: BoF:
Carcinogenesis index: Rate of dysplastic activity
(nl: 1-3)
1.00
10.00
100.00
1000.00
04/2
7/05
04/2
9/05
05/0
1/05
05/0
3/05
05/0
5/05
05/0
7/05
05/0
9/05
05/1
1/05
05/1
3/05
05/1
5/05
05/1
7/05
05/1
9/05
05/2
1/05
05/2
3/05
05/2
5/05
05/2
7/05
05/2
9/05
05/3
1/05
06/0
2/05
06/0
4/05
06/0
6/05
06/0
8/05
06/1
0/05
06/1
2/05
06/1
4/05
06/1
6/05
06/1
8/05
06/2
0/05
06/2
2/05
06/2
4/05
06/2
6/05
06/2
8/05
06/3
0/05
07/0
2/05
07/0
4/05
07/0
6/05
07/0
8/05
07/1
0/05
07/1
2/05
07/1
4/05
07/1
6/05
07/1
8/05
07/2
0/05
07/2
2/05
07/2
4/05
07/2
6/05
07/2
8/05
07/3
0/05
08/0
1/05
08/0
3/05
08/0
5/05
08/0
7/05
08/0
9/05
08/1
1/05
08/1
3/05
08/1
5/05
08/1
7/05
08/1
9/05
08/2
1/05
08/2
3/05
08/2
5/05
08/2
7/05
08/2
9/05
08/3
1/05
09/0
2/05
09/0
4/05
09/0
6/05
09/0
8/05
09/1
0/05
09/1
2/05
09/1
4/05
09/1
6/05
09/1
8/05
09/2
0/05
09/2
2/05
09/2
4/05
09/2
6/05
09/2
8/05
09/3
0/05
10/0
2/05
10/0
4/05
10/0
6/05
10/0
8/05
10/1
0/05
10/1
2/05
10/1
4/05
10/1
6/05
10/1
8/05
10/2
0/05
10/2
2/05
10/2
4/05
10/2
6/05
10/2
8/05
10/3
0/05
11/0
1/05
index de carcinogenèse (1 à 3)

31. + Follow up assessment: BoF:
Cancer index: : The relative degree of endocrino-metabolic
factors which are propitious to cancerous activity (nl: 6-10)
0.00
0.01
0.10
1.00
10.00
04/27/
05
04/29/
05
05/01/
05
05/03/
05
05/05/
05
05/07/
05
05/09/
05
05/11/
05
05/13/
05
05/15/
05
05/17/
05
05/19/
05
05/21/
05
05/23/
05
05/25/
05
05/27/
05
05/29/
05
05/31/
05
06/02/
05
06/04/
05
06/06/
05
06/08/
05
06/10/
05
06/12/
05
06/14/
05
06/16/
05
06/18/
05
06/20/
05
06/22/
05
06/24/
05
06/26/
05
06/28/
05
06/30/
05
07/02/
05
07/04/
05
07/06/
05
07/08/
05
07/10/
05
07/12/
05
07/14/
05
07/16/
05
07/18/
05
07/20/
05
07/22/
05
07/24/
05
07/26/
05
07/28/
05
07/30/
05
08/01/
05
08/03/
05
08/05/
05
08/07/
05
08/09/
05
08/11/
05
08/13/
05
08/15/
05
08/17/
05
08/19/
05
08/21/
05
08/23/
05
08/25/
05
08/27/
05
08/29/
05
08/31/
05
09/02/
05
09/04/
05
09/06/
05
09/08/
05
09/10/
05
09/12/
05
09/14/
05
09/16/
05
09/18/
05
09/20/
05
09/22/
05
09/24/
05
09/26/
05
09/28/
05
09/30/
05
10/02/
05
10/04/
05
10/06/
05
10/08/
05
10/10/
05
10/12/
05
10/14/
05
10/16/
05
10/18/
05
10/20/
05
10/22/
05
10/24/
05
10/26/
05
10/28/
05
10/30/
05
11/01/
05
04/27/05 11/01/05
index de cancérose (6 à 10) 1.13 0.00
index de cancérose (6 à 10)

32. +Follow up assessment: BoF:
Expansivity no. 2: Rate of anarchic cellular
development (Pink square) (nl: 1-4)
1.00
10.00
04/27/
05
04/29/
05
05/01/
05
05/03/
05
05/05/
05
05/07/
05
05/09/
05
05/11/
05
05/13/
05
05/15/
05
05/17/
05
05/19/
05
05/21/
05
05/23/
05
05/25/
05
05/27/
05
05/29/
05
05/31/
05
06/02/
05
06/04/
05
06/06/
05
06/08/
05
06/10/
05
06/12/
05
06/14/
05
06/16/
05
06/18/
05
06/20/
05
06/22/
05
06/24/
05
06/26/
05
06/28/
05
06/30/
05
07/02/
05
07/04/
05
07/06/
05
07/08/
05
07/10/
05
07/12/
05
07/14/
05
07/16/
05
07/18/
05
07/20/
05
07/22/
05
07/24/
05
07/26/
05
07/28/
05
07/30/
05
08/01/
05
08/03/
05
08/05/
05
08/07/
05
08/09/
05
08/11/
05
08/13/
05
08/15/
05
08/17/
05
08/19/
05
08/21/
05
08/23/
05
08/25/
05
08/27/
05
08/29/
05
08/31/
05
09/02/
05
09/04/
05
09/06/
05
09/08/
05
09/10/
05
09/12/
05
09/14/
05
09/16/
05
09/18/
05
09/20/
05
09/22/
05
09/24/
05
09/26/
05
09/28/
05
09/30/
05
10/02/
05
10/04/
05
10/06/
05
10/08/
05
10/10/
05
10/12/
05
10/14/
05
10/16/
05
10/18/
05
10/20/
05
10/22/
05
10/24/
05
10/26/
05
10/28/
05
10/30/
05
11/01/
05
04/27/05 11/01/05
index d'expansivité (0,06 à 2) 3.58 1.19
index d'expansivité bis (1 à 4) 6.47 1.17
index d'expansivité global (0,01 à 3,2) 7.62 4.62

33. + Follow up assessment: BoF:
Active Carcinogenesis: Current functional state of cancer activity
after accounting for cell death by apoptosis or necrosis (nl 0.01-
9.6)
1.00
10.00
100.00
1000.00
10000.00
04/27/
05
04/29/
05
05/01/
05
05/03/
05
05/05/
05
05/07/
05
05/09/
05
05/11/
05
05/13/
05
05/15/
05
05/17/
05
05/19/
05
05/21/
05
05/23/
05
05/25/
05
05/27/
05
05/29/
05
05/31/
05
06/02/
05
06/04/
05
06/06/
05
06/08/
05
06/10/
05
06/12/
05
06/14/
05
06/16/
05
06/18/
05
06/20/
05
06/22/
05
06/24/
05
06/26/
05
06/28/
05
06/30/
05
07/02/
05
07/04/
05
07/06/
05
07/08/
05
07/10/
05
07/12/
05
07/14/
05
07/16/
05
07/18/
05
07/20/
05
07/22/
05
07/24/
05
07/26/
05
07/28/
05
07/30/
05
08/01/
05
08/03/
05
08/05/
05
08/07/
05
08/09/
05
08/11/
05
08/13/
05
08/15/
05
08/17/
05
08/19/
05
08/21/
05
08/23/
05
08/25/
05
08/27/
05
08/29/
05
08/31/
05
09/02/
05
09/04/
05
09/06/
05
09/08/
05
09/10/
05
09/12/
05
09/14/
05
09/16/
05
09/18/
05
09/20/
05
09/22/
05
09/24/
05
09/26/
05
09/28/
05
09/30/
05
10/02/
05
10/04/
05
10/06/
05
10/08/
05
10/10/
05
10/12/
05
10/14/
05
10/16/
05
10/18/
05
10/20/
05
10/22/
05
10/24/
05
10/26/
05
10/28/
05
10/30/
05
11/01/
05
04/27/05 11/01/05
index de carcinogenèse active (0,01 à 9,6) 1831.81 198.22
index de carcinogenèse active comparée
(0,01 à 4,8) 42.64 13.92

34. + Follow up assessment: BoF:
Estrogen index: Endocrino-metabolic activity of estrogens
(nl, females: 0.2-0.4)
04/27/05 11/01/05
index oestrogénique (0,20 à 0,40 F)
(0,15 à 0,25 H)
0.36 0.20
0.00
0.05
0.10
0.15
0.20
0.25
0.30
0.35
0.40

35. + Follow up assessment:
BoF: Total Androgens (Blue diamond): total androgen
activity (nl, females: 0.2-0.25)
04/27/05 11/01/05
taux d'androgènes totaux (0,2 à
O,25 F) (0,2 à O,3 H)
0.44 0.26
taux d'androgènes cortico
surrénaliens (0,05 à 0,09)
0.08 0.04
taux d'androgènes génitaux (0,12 à
0,17 F) (0,18 à 0,22 H)
0.36 0.22
0.00
0.05
0.10
0.15
0.20
0.25
0.30
0.35
0.40
0.45
0.50

36. + Follow up assessment: BoF:
(Intracellular) Growth Index (nl 2-6)
04/27/05 11/01/05
index de croissance (2 à 6) 16.53 9.04
0.00
2.00
4.00
6.00
8.00
10.00
12.00
14.00
16.00
18.00

37. + Follow up assessment:
BoF: Membrane Expansion (Blue) (Nl: 0.08-0.16)
Structural Expansion (Pink) (nl 0.04-0.08)
0.01
0.10
1.00
04/27/
05
04/29/
05
05/01/
05
05/03/
05
05/05/
05
05/07/
05
05/09/
05
05/11/
05
05/13/
05
05/15/
05
05/17/
05
05/19/
05
05/21/
05
05/23/
05
05/25/
05
05/27/
05
05/29/
05
05/31/
05
06/02/
05
06/04/
05
06/06/
05
06/08/
05
06/10/
05
06/12/
05
06/14/
05
06/16/
05
06/18/
05
06/20/
05
06/22/
05
06/24/
05
06/26/
05
06/28/
05
06/30/
05
07/02/
05
07/04/
05
07/06/
05
07/08/
05
07/10/
05
07/12/
05
07/14/
05
07/16/
05
07/18/
05
07/20/
05
07/22/
05
07/24/
05
07/26/
05
07/28/
05
07/30/
05
08/01/
05
08/03/
05
08/05/
05
08/07/
05
08/09/
05
08/11/
05
08/13/
05
08/15/
05
08/17/
05
08/19/
05
08/21/
05
08/23/
05
08/25/
05
08/27/
05
08/29/
05
08/31/
05
09/02/
05
09/04/
05
09/06/
05
09/08/
05
09/10/
05
09/12/
05
09/14/
05
09/16/
05
09/18/
05
09/20/
05
09/22/
05
09/24/
05
09/26/
05
09/28/
05
09/30/
05
10/02/
05
10/04/
05
10/06/
05
10/08/
05
10/10/
05
10/12/
05
10/14/
05
10/16/
05
10/18/
05
10/20/
05
10/22/
05
10/24/
05
10/26/
05
10/28/
05
10/30/
05
11/01/
05
04/27/05 11/01/05
taux d'expansion membranaire (0,08 à
0,16) 0.24 0.07
taux d'expansion structurale (0,04 à 0,08) 0.04 0.06

38. + Follow up assessment: BoF:
Proinflammatory (Blue): endogenous potential for
inflammation (nl 0.1-0.4)
Inflammation index (Pink): Current functional state of
inflammation (nl 0.3-2.5)
04/27/05 11/01/05
index proinflammatoire (0,1 à 0,4) 0.44 0.22
index d'inflammation (0,3 à 2,5) 1.35 0.07
index d'inflammation comparée (0,2
à 2,5)
2.69 0.00
0.01
0.10
1.00
10.00

39. +
Conclusions
 The endobiogenic concept is an approach to integrative
physiology based on the management of the organism by the
endocrine system
 It is a whole model system, integrative in its approach to
understanding the functioning of the individual parts and their
relationship to the whole
 Cancer is a multifactor disorder of disregulated cell growth
 The endobiogenic system is well suited to analyze the causes
of cancer and its possible treatments because of its ability to
simultaneously assess multiple factors that influence cell
growth

40. +
Conclusions (cont.)
 The biology of functions is biological modeling software that is
able to assess the quantitative, qualitative and functional
activity of the organism
 The biology of functions is able to provide a rational basis of
treatment
 It provides for longitudinal assessment of the progression of a
patient’s tumor as well as their response to treatment

41. +
Contact
 For research in North and Central America, Middle East:
 Kamyar M. Hedayat, MD, International Society of Endobiogenic
Medicine and Experimental Physiology
 Email: acquamarine@mac.com
 Phone: 1-318-525-6311
 For research in Europe and North Africa:
 Jean Claude Lapraz, MD, President, International Society of
Endobiogenic Medicine and Experimental Physiology
 Email: sfpa@club-internet.fr
 Phone: 011 33 6 07 71 94 00