Cancer and Immune Profile Test

The most highly calibrated Cancer-Profile and lmmune-Spectrurn Blood Test

simple questions, concrete answers by Dietmar Schildwaechter, M.D., Ph.D.

Chief Medical Investigator

How can I know for sure if I have cancer? 

How will I know if I am improving during treatment?

“Is there a reliable  scientific test that tells me whether  I have no cancer  risk right now and can this test tell me whether  I am out of danger?•

Yes, this is one of the features of this test.  If anyone in your family had or has cancer, statistically increasing cancer risk, all relatives can benefit from this test.

“What about the cancer  patient  who was diagnosed some time ago,  had perhaps  Surgery  or Chemotherapy or Radiation, or any combination and was told that he is free of cancer.   Is he  really ok?•

They may be, but no Scan, or MRI, or X-ray can tell for sure.  These tests measure a “status quo” at the time they were taken. They never really tell of all important functional dynamics and whether an individual still has existing primary cancer activity, new flare-up or metastatic activity and tendency for cancer to spread to other organs until a recurrence is finally determined by a doctor.

“Can this test tell me the real situation,  whether I am out of danger, or whether  there still is activity so I can do something about bringing it under control?

Absolutely. This is yet another feature of this highly calibrated test.

“My doctor  told me I am in remission. What does this mean?•

An individual with cancer, regardless at what stage of disease, is in remission when there is no primary and no metastatic activity and definitely no more progression of disease.  This test profile with its sophisticated calibration can ascertain when you are in remission and out of danger.

“I am and/or  was treated  with toxic therapies that severely  depressed my immune-system. Can this test tell me what the status of my immune-system is at this time?•

Yes. Your immune-profile is a very important part of this test.  We are now aware of the importance of our immune-system and the role it plays in protecting us from disease.

The interpretation of your test results will tell you where you stand with your immune-defense  situation at this time.

“If I do have a risk to develop cancer  within a period of one to two years can I reverse  this risk?

Yes, if your immune system is low, we can recommend the necessary steps to strengthen it.  In 1977 scientists established with statistically significant correlation that cancer is a preventable disease.

“Why  was this important finding suppressed?•

The answer may lie in the documentable fact that cancer is one of the highest profit-makers for pharmaceutical giants and institutional medicine.

Dietmar Schildwaechter, M.D., Ph.D., of Sovereign Consultants, International and Chief Medical Investigator of this project, brings thirty-six years of knowledge and expertise in preventive medicine, early cancer detection, therapy response and guidance to the individual interpretation of each test result.


In order to establish a baseline of health and to track progress through the treatment process, a blood test is available which will indicate the presence of primary and metastatic cancer activity, liver function and immune function.

This blood test identifies and quantifies in a highly calibrated, manually conducted test five significant markers, the HCG (human chorionic gonadotropic hormone) by the HCG-beta­ chain test, PHI (phosphohexose  isomerase), the key enzyme in glycolisis which is greatly increased in cancer cell lines, GGTP for liver function, CEA (carcinoembryonic antigen) and DHEA-S.

The FDA requires an adequate means to monitor and track progression or regression during clinical use of an unapproved substance within the scope of the Institutional Review Board.  Beyond these requirements the test allows the following:

  1. For Prevention of disease:
  2. Establish an individual’s health baseline.
  3. Determine an individual’s immune defense status.
  4. In established disease:
  5. Determine activity status, such as primary and secondary in malignant diseases not possible with status quo type scans or MRis, thus allowing:

2. Exact monitoring of response to whatever treatment chosen by treating physician and/or patron, conventional as well as unconventional.

  1. permits exact and scientific determination of remission in a patron.
  2. Establishes cures over longer period interval testing.
  3. Thus preventing recurrence or relapse of disease. C. For Scientific Clinical Studies and Trials
  4. Eliminates double blind etc., studies with high degree of inaccuracies (certainlyfrom a true epidemiological scrutiny).
  5. Eliminates randomized trials.
  6. Provides early risk factors for malignancies as a true prevention, therefore, complements cancer-search at too late a (clinical) stage with reduced survival chances (Mammography, Colonoscopy, etc.).
  7. Provides exact clinical-biochemical parameter results for effectiveness of new substances.
  8. In conjunction with unconventional medical practices.
  9. Complements Gaston Naessens’ Somatoscopic diagnosis
  10. Monitors effect of Cell-Milieu-Medicine, fetal tissue therapy, bio-electronic and homeopathic approaches.

DHEA-S  (De-Hydro-Epi-Androsteron)

Dr. Nieper compares the immune system with the army (which calls out the reserves when there is danger), and the anti cancer surveillance system with the police whose strength is essentially fixed.

The latter system includes mechanisms for gene repair, and certain steroids such as turnosteron and DHEA.  Approximately 60% of all people have sufficient DHEA in their blood to be protected from cancer.  Of the remaining 40% about half will develop hidden cancer but not die from it while the rest (20%) will die of diagnosed cancer.

A lack of DHEA has been correlated with peculiarities of the person’s character– non aggressive, amiable, easily depressed and indecisive.

DHEA-S is produced in the adrenal glands and circulates in the body as DHEA sulfate. A special activation factor, (which possibly is produced in the pineal gland or the thymus gland or the small intestines) changes DHEA-S into free DHEA.

DHEA paralyzes an enzyme (glucose-g-phosphate dehydrogenase)  which is of primary importance to the action of cancer cells.  This drastically reduces the vitality of the cancer cell and makes it possible for lymphocytes and other white blood cells to overcome the cancer cell.

Dr. Nieper found that during the course of disease, there is a tendency for the DHEA level to gradually decrease, sometimes to values less than 0.1 (100 nano-grams per milliliter). The cancer patient then does not have sufficient starting material to form free DHEA.

There are a number of drugs whose side effects are to cause the level of DHEA-S to drop.  Most prominent are the clofibrates that are used to reduce lipid levels.  A correlation has been found between higher cholesterol levels in the blood and lower frequency of cancer–if accompanied by higher values of DHEA.

DHEA was isolated by the German Nobelist Butenandt in 1934 and analyzed by the German chemist and Nobelist Windaus.  However, the credit for having identified it as an important pillar of our anticancer surveillance system goes to Arthur Schwartz and his coworkers at Temple University in Philadelphia.

A summary of Dr. Hans Neiper’s discussion of DHEA  from “Revolution in Medicine and Health,” November 1958.

HCG  (Human Chorionic Gonadotropic hormone)

Radioimmunoassay for the HCG-Beta-chain allows the quantitation of minute amounts of human choironic gonadotropic hormone even in the presence of LH, FSH and TSH. The obvious value is the detection of pregnancy within 2-3 days after conception, detection of microabortion and detection and follow-up of HCG-secreting tumors.

Teratoma, hydatidiform mole and choriocarcinomas in the uterus, ovaries, testes, mediastinum, pineal and pituitary glands, stomach, lungs, esophagus and bladder have long been recognized as trophoblastic HCG-secreting tumors.  However, HCG-B has been found in patients with practically all types of malignancies where trophoblasts were not expected:

1) testicular, nontrophoblastic gastrointestinal:  carcinoid, colonic/rectal, gastric, pancreatic, small intestinal

2) hematopoietic:  leukemia, all types of lymphomas, multiple myeloma

3) sarcomas: fibrosarcoma, leiomyosarcoma, osteogenic sarcoma

4) miscellaneous tumors:  breast, thyroid, uterine, bladder, adrenal gland, insulinomia, pheochromocytoma

5) lung carcinoma

6) hepatoma/hepatoblastoma.

Indeed it seems that the HCG-secreting trophoblast may play an important role and it may be closely associated with not only embryogenesis but also carcinogenesis.  As more data is becoming available, utilizing the sensitive and specific HCG-B test, it becomes evident that the frequency and types of tumors associated with HCG production are much greater than it has been suspected.

Due to the extreme sensitivity of the test (0.0025 IU/ml or about 0.2 ng/ml) it is possible to detect, without localization, ongoing malignancies at a very early stage. Once a base level has been established, a patient’s response to therapy can be monitored.  The probability of detecting HCG in cancers of all types is, according to the literature surveyed, 10-100%.

The longest interval for elevated HCG-B before cancer diagnosis was 26 months.

PHI  (Phospho-Hexose Isomerase or glucose phosphate isomerase)

PHI is a key enzyme in glycolysis, i.e. the main anaerobic energy generating step of glucose metabolism.  Glycolysis has been observed to become greatly increased in cancer cell lines, hence the measuring of PHI became accepted as a valuable tool in the appraisal of neoplasias.

Elevated PHI levels were found in localized and metastasized cancers of the: bladder, bone, brain, breast, intestines, liver, lungs, lymphosarcoma, melanoma, mouth, head, neck, esophagus, pancreas, prostate, ovary, stomach, colon, rectum and uterus.

PHI has been shown to be elevated in more patients with neoplasia than other enzymes. However, it may not be elevated in the serum of some patients in an early state of neoplasia and indeed, it is not elevated in the serum of some patients with active diseased state. The detection of the enzyme at elevated levels may warrant a more thorough evaluation of the patient.

Once a base level has been established, PHI is a promising enzyme in following the effectiveness of therapy.  When, for instance, this enzyme was monitored during treatment of breast cancer, changes in activity followed progression or regression of tumor growth and antedated other laboratory evidence by days or weeks.

It was also found to be indicative of regressions induced by steroids, radio-therapy, oophorectomy, chemotherapy, and hypophysectomy.  In cases of confirmed malignancy any elevation or drop, even within the normal ranges, may be significant.

PHI may be elevated in heart, liver and skeletal muscle diseases.  Preliminary data indicates that PHI levels parallel CEA results (Personal communications, Miami Heart Institute and Worthington Biochemical Corporation), however, it does not seem to be affected by smoking and it seems to reflect upon a greater variety of diseases.  (The performance cost of PHI is about one-half of that of CEA.)

PHI is very abundant in the red blood cells: therefore it is imperative that the serum specimen is free from hemolysis.

References for HCG:

B.D. Weintraub and S.W. Rosen, Ectopic Production of HCS (and HGB) by Nontrophoblastic Cancers.  J. Clin. Endocr., 32, 94, 1971.

  1. Civantos and A.M. Rywlin, Carcinomas with Trophoblastic Differentiation and Secretion of

Chorionic Gonadotropins.  Cancer. 29. 789, 1972.

G.D. Braunstein, et al., Ectopic Production of ‘HCG by Neoplasms.  Annals Int. Med.. 78, 39, 1973.

A.S. Rabson et al., Production of HCG in vitro by a Cell Line Derived from a Carcinoma of the Lung.  J. Natl. Cancer lnst., 50, 669, 1973.

W.S. Floyd and S.L. Cohn, Gonadotropin Producing Hepatoma.  Obst. Gyn, 41, 665, 1973. D.W. Gold et al., Gonadotropin-Secreting  Renal Carcinoma.  Cancer. 33. 1048, 1974.

D.P. Goldstein et al., The clinical Application of Specific RIA for HCG in Trophoblastic and

Nontrophoblastic tumors.  Surg. Gynec. Obst.. 138, 747, 1974.

D.C. Torney et al., Biological Markers in Breast Carcinoma.  Cancer. 35. 1095, 1975.

R.R. Williams et al., Tumor-Associated Antigen Levels Antedating the Diagnosis of Cancer in the

Framingham Study.  J. Natl. Cancer lnst.. 58. 1547, 1977.

References for PHI:

  1. Bodansky, Serum PHI in Cancer: II. As an Index of Tumor Growth in M:etastatic Carcinoma of the Breast.  Cancer, 7, 1191, 1954.0. Bodansky, Serum PHI in Cancer:  Ill.  As an Index of Tumor Growth in Metastatic Carcinoma of the Prostate.  Cancer. 8. 1087, 1955.

M.M. Griffith and J.C. Beck, The Value of Serum PHI as an Index of Metastatic Breast Carcinoma Activity.  Cancer. 16. 1032, 1963/

M.H. Gault et al., Serum Enzymes in Patients with Carcinoma of the Lung.  Canada Med. Assoc. J .. 96. 87, 1967.

C.R. Ratliff et al., Serum LDH, PHI and Serological Evidence of Malignant Diseases.  .Q1io…Chern., 16. 527, 1970.

C.R. Ratliff, Serum PHI: A glycolytic Enzyme for Appraising Neoplasia.  4th Ann. So. Calif. Lab. Conference, Anaheim, March 6, 1973.

Worthington Biochemical Corporation, In Case of Malignancy–PHI Monitors Therapy, 1974.

Letter from Dietmar Schildwaechter, M.D.  Ph.D. to Ms. Jeanne O’Hara, Medicare regarding reimbursement for Cancer-immune profile test .

Ms. Jeanne O’Hara

MEDICARE General Delivery

Department of Benefits – Physician’s Services

P.O. Box 890089

Camphill, PA 17089-0089

Re: CA Profile and Immune -Profile clinical-biochemical parameter testing (according to Schandl and Nieper) for Us patients.

Dear Ms. O’Hara,

Pursuant to our telephone discussion yesterday, April 19, 1994, I am herewith attaching to this letter a 1 page copy of my testimony at N.I.H., since it describes in a concise way the features of this test.

The problem appears to be an unwillingness, of even first class laboratories, to go into the required, highly scientific calibration of our markers, so they become meaningful differential diagnostic values.

In today’s automated systems, clinical pathologists who indicated an interest to work with us, after learning the extent of required, qualified personnel, time and financial involvement etc., remarked “This is impractical for us” and perhaps questionable in its financial reward.

Since Dr. Emile K. Schandl, Ph.D., pioneered this profile in combining (biostatistically) overlapping markers to achieve an unsurpassed accuracy in 1977 (duly published and presented at scientific meetings), it has become the only reliable and constantly upgraded functional monitoring test.

Our high-cost (certainly for insurance carriers) Scans, MRis, or tornograms, etc. are strictly “status quo• examinations, not giving us any clue as to the functional ‘dynamics of primary or metastatic activity, when patients are truly in •remission• how their immune-defense situation is, etc. Recent (MAYO-clinic initial source) negative criticism about the value of CEA-markers* as a single monitoring test for Colon Cancer patients is a confirmation of our experience that it is very limited as a SINGLE marker!

In regard to insurance re-imbursement  and payments for these profile tests, let me state that there apparently has been no problem (except with KAISER or HMO).  All tests have the basic Blue Cross code number.  Even European socialized medical insurance systems do re-imburse patients.  Most tests are ordered by their physicians.

Samples from the U.S. and Canada are shipped daily to Germany by international air carriers.  The results are being faxed to us and accordingly interpreted.  The interpretation for all tests regardless from what country and whether for patients directly, referring physicians, clinics or hospitals, are done by me.

The German laboratory is one of the leading fully licensed and high caliber laboratories in Europe. My association goes back to the early seventies (70s) while I was Medical Director of the newest Cancer Rehabilitation Hospital within the German Government’s social medical system.   I am still a licensed physician within the European community, but retired from the practice of medicine in the United States.  Sovereign Consultants International was founded thereafter and is a Loudoun County, Virginia licensed and registered firm.

Laboratory super-bills are similar to the one’s used for procedures previously.  They reflect the higher cost for sophisticated calibration methods required for accuracy and meaningful interpretation.

I hope this letter will help to establish a baseline for–at least partial re-imbursement for patients like Mrs. Thank you for your courtesy and cooperation.

Very truly yours,

Dietmar Schildwaechter, Ph.D., M.D.

Enzyme Therapy of Cancer by Max Wolf, M.D. (circa 1936).

Enzyme Therapy of Cancer by Max Wolf, M.D.

Proteolytic enzymes in the treatment of malignant tumors have been used in historical times already.  Long before the discovery of America by Columbus, medicine men of the Indians applied fruits and leaves of the papaya plant to malignant tumors, they used local enzyme therapy empirically.  It was known that fresh papaya fruits favorably influenced inflammations and edemas, that wounds, burns, bruises or infections healed faster and pains subsided sooner, also that malignant tumors responded sometimes to this therapy.

About the  year 1820, Physick  in Philadelphia was the first to use proteolytic enzymes in the form of stomach juice for surface cancer with good results.  In 1836 Schwann  isolated pepsin from stomach juice, in 1871 Purden and in 1888 Douglass  applied the enzyme pepsin to ulcerated cancerous lesions.  At the end of the 19th century the first attempts were made to give pepsin intramuscular and trypsin intravenous.

In the year 1902 the enzyme therapy of cancer received a decided impulse when John Beard  began cancer treatment with enzyme extracts of the pancreas.  His therapeutic successes caused great excitement.

By 1906 he had used trypsin, amylopsin and other unknown enzymes of the pancreas in treating different cancers.  His comprehensive book: The Enzyme treatment of Cancer  stirred up great interest among many scientists and clinicians who soon went about to develop further this therapy and to use it extensively.

Beard, the leading embryologist of his time, concluded from his studies for many years of the embryonal development of animals that during the progressive differentiation of the developing organs undifferentiated polyvalent “sex” cells wander from the trophoblast mainly through the mesoderm within the embryo to their goal of destination, the gonads.

Countless cells of them get stuck on this voyage between somatic cell aggregates. These everywhere dispersed embryonal trophoblast isles remain dormant, according to Beard , and do not multiply during the entire life span of the individual.

However, the one or the other cell can by specific irritants (cancerogens)  start a cell division and thus form a functionless tissue island, a tumor. Indeed, American scientists, like Hayflick, during recent years were able to identify in tissue cultures of the different organs sucr1 scattered cells, about 0.25 to 0.5% of the total, the least number in heart tissues.

They differ morphologically from the other cells by absorbing more dyestuff, but without mutagenic or cancerogenic irritations they remain dormant.  When their mitosis starts, they stain darker than the somatic cells, also typical characteristics of tumor cells appear.  Compared with normal cells, they are potentially immortal, i.e. they multiply without any restraint through hundreds of subcultures while all somatic cells in the cultures age, they lose their ability to further divide and die after not more than 50 mitoses.

Soon physicians all over the world were interested in the theoretical as well as the excellent therapeutic results.  The preparations used consisted mainly of freshly prepared pancreatic extracts (Campbell, Goeth, Duprey, Curtfield, Marsden, Meggit, Cleaves, Shaw­ McKenzie, Little, Bainbridge)

Hald, Pusey  and Blumenthal  reported before that intra-tumoral injections of trypsin would bring about a relatively fast softening of the tumor, with aseptic liquefaction.  However besides the therapeutic successes also side effects of a pyrogenic and toxic nature appeared.

Finally they began to produce pancreas extract industrially for a longer shelf life of the product.  But it was unknown at that time that after a few hours of storing at room temperature the enzyme activity of the liquid extracts was lost.  Their use resulted in a deterioration of therapeutic results obtained and led finally to the fact that the enzyme therapy of cancer was forgotten, or rather fell into hibernation.

Only much later the factors were recognized which ruined the confidence in Beard’s therapeutic development: the instability of the enzyme products, their antigenicity and the impurity of the extracts used that time as well as their contents of pyrogens and toxic admixtures.

When much later it became possible to produce crystalline and pure enzymes, the therapeutic application could be resumed again in larger amounts.  Sumner  crystallized in 1926

Urease, Northrop  in 1930 Pepsin, Northrop  and Kunitz, Trypsin.  Thus it became possible to stabilize the enzymes and to eliminate pyrogens and other toxic substances.

In 1934 in Vienna Freund discovered that in the serum of people or animals free of cancer chemical substances existed which were able to dissolve cancer cells, while the blood of cancer patients was lacking this ability.

Besides that, the Freund- Kaminer  team also found that the serum and urine of cancer patients not only was lacking in cancerolytic property but that cancer cells were even protected by it against dissolution by normal serum and produce a cancer-protection substance in the serum.

If, for instance, to normal serum half the amount of cancer serum is added, the former loses its proteolytic capacity against cancer cells.  Freund  isolated this water-soluble, thermolabile substance from the serum and urine of men and horses free of cancer; he called it “Normal Substance” and used it with partly good results as parenteral therapy on inoperable cancer cases.

Furthermore, this phenomenon  led to the development of the Freund-Kaminer  reaction. This test indicated that the serum of cancer-free people and animals dissolves a large percentage of cancer cells in a fresh cancer suspension {later he used for this test heat-killed necrotic cells) or it changed them markedly.

However, cancer serum hardly affected them, it even protected them against disintegration by normal serum.  Kretz  and Benda  could verify these facts, also Klein  and Lustig. Freund  had found 30 years earlier that cancer serum possesses  these cancer­ protective qualities which are derived from abnormal fatty acids found in the intestinal tract.

His directions to fight the cancer disease by diet {total elimination of animal fats afermentative foods and by elimination, as much as possible, of the abnormal {acid-fast) colibacteria, which live in the colon of cancer patients, by intestinal antiseptics like menthol, or by enemas) are based upon these investigations.

Freund and Lustig showed in 1993 on tar cancers of mice that a cancerophile diet hastens the tumor development and the animals died earlier, while a cancerophobe diet protects 50% of the mice.

On account of the beginning World War, Freund  and Kaminer  were forced to discontinue their activity in Vienna and therefore hadno chance anymore to identify chemically the isolated Normal Substance.  By Christiani  in Vienna it was later identified as a cytolytic enzyme and, independently shortly before, by us (Wolf) as a proteolytic-lypolytic enzyme.

Christiani  worked on the problem of closer examination of the cancerolytic enzymes and could demonstrate that the “normal substance” is in fact a hydrolytic enzyme which he called “solving enzyme”.  He proved 1938 that this solving enzyme is bound to the albumin fractions and is thermolabile.

It is present in the serum and urine of healthy people and animals (horses), but absent in the serum and urine of cancer patients.  Later on Christiani  found in the serum of cancer patients some of the inhibitors of the solving enzyme.

They protect cancer cells against the solving enzyme and are produced by the cancer cells.  Also Freund  knew about such inhibitors which were named “protective substances”. Cholesterol esters, e.g. cholesterol-butyrate or cholesterol-succinate have this protective action and indeed are identical with those formed by the cancer cells.

Christiani  also could show that inhibitors, identified by him, could themselves be inactivated by a number of substances, like oxydation products of ergosterol or the?­ dehydrocholesterol.   Such substances have acidic character.  He called them deactivators. In vitro they were able to prevent the attachment of the inhibitor-the protection of the cancer cell-to the solving enzyme, as well as to free again an already blocked enzyme.

Further investigations proved that the de-activator present in healthy people is bound to the globulin fraction of the serum.  The de-activator is synthesized from ?-dehydrocholesterol by means of the enzyme ergosteroloxydase, which cannot be demonstrated in cancer tissues.

Since then numerous scientists were able to prove that the serum of healthy men and animals is rich in proteolytic, lypolytic and amylolytic enzymes.  Patients with more or less active inflammations or infections have in general a lower enzyme potential, but by far the lowest enzyme content as a rule is found in cancer cases (32,33).

Since in precancerous  and in earliest stages of beginning cancers the enzyme niveau in the serum appears very reduced, it seems most probable that low enzyme values represent a predisposition or condition for the malignant process.  Sometimes the low level is inherited, in some cases it may be caused by chronic infections, damage to the pancreas or other diseases, possibly also faulty nutrition.

Gaschler  et al. determined the proteolytic activity in the serum of a great number of people.  They found that healthy men in general have a high protease index, while this was reduced with sick people, particularly patients with chronic inflammations or infections, also in old age.  The serum of cancer patients, of those with precanceroses and patients who later developed malignancies  showed a significantly decreased proteolytic enzyme level.

The Gaschler  test is very simple.  It is not dependable, but in our experience with over 1000 tests, it gave some valuable information, particularly as a negative exclusion test for malignancies.

It was clinically applied that time to cancer patients with tumors of all different types, even in advanced stages.  With the oral application of his enzyme mixture Gaschler could accomplish only some slight local beneficial effects.  Therefore he confined his therapy exclusively to parenteral application.

In several clinics of the Charita  in Berlin, encouraging results were accomplished. Elevation of general well-being, improved appetite, gain in weight and other subjective improvements were registered.  With a number of patients regressions could be determined.

All these results were taken in consideration during our own developments and experiments.  We developed in numerous animal experiments and trials at the Biological Research Institute in N.Y. individual enzymes and enzyme combinations with and without activators which had selectively a lytic action on cancer cells.

In the experimental groups, on the other hand, the following events could be observed: first the cancer cel s.grew without restraint into all directions, fastest in the direction against the normal tissue.  Almost suddenly the cancer cells stopped growing further.

They changed partly into a spindle shape, also ball-like form, some shriveled, became enucleated and finally dissolved, while the normal tissues showed hardly any influence by the enzymes added to the cultures.  They rather pushed back the front rows of the tumor cells. The cell damages were much more pronounced than those seen in damage to normal tissues observed in the controls.

These characteristic pictures of cell cultures show the reaction of normal and malignant cells under influence by proteolytic enzymes.  While fibroblasts remain uninfluenced, cancer tissue undergoes lysis after a short period of time.

The enzymes tested in these experimental groups were solutions of trypsin, chymotrypsin, plasmin, kathepsin, pepsin, liver catalase, papain, ficin, bromelin, and enzyme extracts of lens esculenta, pisum sativum, aspergillus oryzae, spleen, thymus (mainly nucleases), liver and primarily the enzyme combination finally determined by us as optimal.*

During our investigation it was necessary to develop new tests for assaying the proteolytic and fibrinolytic activity in body fluids.  The specificity and sensibility of the plate tests were not high enough (methods after Astrup and Mullertz ).

In extensive animal experiments on rats we tested the proteolytic activity of the serum after taking the proteolytic enzymes mixture.  It was given to the animals in gradually increasing amounts orally, intramuscular, intraperitoneal or by rectum.  After 90 minutes the proteolytic activity of the serum was determined by the plate method mentioned.  A significant relation between the proteolytic potential and the concentration of the enzyme mixture given was shown.

Some authors discuss the importance of general membrane defects in cancer. (Hoelzi-Wallach ).  They distinguish between:

  1. plasma membrane (cell contact, cell surface, immunological changes),
  2. mitochondrial membrane (protein and lipid synthesis),
  3. lysosomal membrane,
  4. nuclear membrane and
  5. the endoplasmatic reticulum, responsible for enzymatic changes and enzyme biosynthesis

It concluded that the membrane hypothesis of tumors postulates that an oncogenic agent acts to introduce an inappropriate protein into or through cell membranes-either in replacement of or in addition to normal components.

*Proteolytic enzymes of fractionated hydrolysates of beef pancreas, calf thymus, pisum sativum, lens esculenta, papayotin, mannit.

Sagiroglu  could show in his experiments that in stained malignant tissues many epitheloid cancer cells show smaller or larger membrane defects near the nucleus. Through these tears the cytoplasma leaked out producing the picture of a “nucleus halo” after staining. Such damages of the cell membrane of malignant cells could give a natural explanation for their selective destruction by enzymes.

Exact observations of the cancer cells made it probable  that their cell membrane, in contrast  to that of fibroblasts and other normal cells, is permeable for the proteolytic and lypolytic enzymes in our mixture. Thus the catabolic  enzymes penetrate into the inner cell and are able to dissolve the cytoplasma.

The fact that normal cells are more protected against lysis than cancer cells through enzyme inhibitors certainly also plays a part. But since the enzyme mixture used by us contains also lipolytic enzymes against which no inhibitors have been found so far, the cancer cell membrane seems to be insufficiently protected against these enzymes; a factor which therapeutically is very important.

All cell membranes consist mainly of phospholipids and mucopolysaccharides.  They cannot normally be attacked by the specific enzymes present in small concentration in the blood, since no sufficiently wide pores exist which would allow the entrance of the macromolecules of the enzyme.

The protective cell wall becomes, however, penetrable for lytic enzymes when marked irritations lead to cell damages or to necrobiotic or necrotic processes.  In such cases the penetration succeeds easily, also enzymes are set free from the lysosomes, thus bringing about an endogenous lysis.

Electron microscopic and isotopic investigations showed that catabolic  enzymes penetrate also through membranes  of malignant cells.  Possibly this is brought about by the fact that the cell membrane  shows defects and that it is incomplete during the rapid mitosis.

In further comprehensive experiments we investigated the effects of the enzyme combination besides in vitro tests, upon the different tumor implants, in rats and mice on chemically induced rat tumors and on spontaneous mamma carcinomas of dogs. The preparation Carzodelan®  of Gaschler was part of in the investigations.

In both cases definite significant damages of the cancer cells could be demonstrated without influencing normal tissues.

The de-activator is present in all tissues except the thymus.  With cancer patients this de­ activator is not found in the tumor and in tumor-bearing organs, but in tumor-free organs in the form of a lactone.  In this form it cannot de-activate the applied protective substance (inhibitor); it is biologically inert.

In the solid Ehrlich- carcinoma of the mouse, after intratumoral injection of Carzodelan® or of our mixtures, statistically significant tumor regression took place.  The tumors partly ulcerated or necrotized, in other cases a partial shrinking in size appeared.  Later on the disease process lead to death but the prolongation of life was significant

During the examination of calf pancreas extract it was found that pure trypsin and chymotrypsin are to a great extent inhibited by the cancer serum, but their inhibition is blocked or is absent if amylases and lipase, but also certain other substances of the pancreas extraction are present.

The cytolytic  effect of our enzyme  mixture was demonstrated by animal experiments of several investigators. The enzymes administered via various  routes to hamsters  with cheek pouches of hetero-transplantable human tumors showed this anti tumor effect (Goldenberg , personal communications).

One interesting model for the selective  effect of proteolytic  enzymes  upon tumor cells is the spontaneous mamma  adenoma of the sprague-Dawly rat.  In all female animals of this certain strain a spontaneous fibroadenoma resp. adenofibroma develops in advancing age. These tumors develop  subcutaneously and can grow into all regions  of the body.

They may reach a size twice the size of the whole rat.  If the proteases  are injected intratumorally in these rats, necrosis resp. liquefication  of the tumor takes place till the entire tumor has disappeared.  With tumors  up to the size of a hens egg, these results are always reproducible, with tumors beyond the size of a man’s fist the success  is not always constant.

As an explanation it may be mentioned that the tumor necrotises rapidly in rats and the death of the rat is caused  by the overwhelming floodings  of the organism  with the catabolic products of the tumor.

It is remarkable that the enzyme activity stops causing  necroses  as soon as all tumor tissue is dissolved, the surrounding healthy tissues (connective and muscular  tissues) are not affected.  Also the necrotized skin over the tumor heals during enzyme therapy  without complications.  Mostly not even noticeable scar tissue remains  (Weigelt )

Especially  clearly the protective effect of the enzyme mixture  can be shown with the sarcoma  180 of the mouse.   Tl1is sarcoma  has a taking rate of over 95%.   But in mice which received  4 days before  and during transplantation 5 mg of the enzyme mixture, in only 20% of the animals  tumors  were formed.

John Bailar’s Righteous Attack on the “War on Cancer”



John Bailar’s Righteous Attack on the “War on Cancer” By putting forth this unpopular opinion, Bailar reminded us of the value of evidence-based decisions.

John Bailar challenged the war on cancer when doing so was almost sacrilege.

Melissa Bailar

When then-President Richard Nixon launched the “war on cancer” in 1971, there was no more admirable cause to support. The dreaded disease was the second leading cause of death that year for Americans, after heart disease, and has maintained that spot for decades. Yet John C. Bailar III, a physician and epidemiologist who died in September at age 83, persistently challenged the war—at a time when doing so was almost sacrilege.

In recent years, others have picked up Bailar’s points, such as the notion that early cancer detection may not save lives. And we’ve moved on to a new metaphor for cancer control: the “moonshot,” championed by Vice President Joe Biden. But, in an era in which even a cancer moonshot is likely to be politicized, it is worth remembering a critic like Bailar, who thoughtfully opposed quick fixes for a complicated disease. Bailar would have been the first to say that it is impossible to separate science and rhetoric, but as a scientist and an advocate, he always tried to focus on what he believed the data showed.

Bailar grew up in Illinois, the son of a chemist; he graduated from the Yale University School of Medicine in 1955. But a passion for mathematics led him to lay down his stethoscope in favor of a career in research. In 1962, after several other jobs, he wound up at the National Cancer Institute (NCI), eventually becoming its chief of demography. Meanwhile, Bailar earned his stripes, obtaining a Ph.D. in statistics from American University. By the mid-1970s, he was a prominent biostatistician and epidemiologist, serving as the NCI’s deputy associate director for cancer control. That meant he had a front row seat to the new war on cancer.


It was fairly shocking, then, when Bailar went public in January 1976 with his misgivings about a new NCI breast-cancer screening program that was technically under his auspices. In 1972, shortly after Nixon’s announcement, the NCI—working with the American Cancer Society (ACS)—had initiated the Breast Cancer Detection Demonstration Project (BCDDP). The goal was to screen 270,000 American women aged 35 to 74 for breast cancer, offering them free annual mammograms for five years. As with many cancer control strategies, mammography relied on the philosophy of early detection—that finding smaller and presumably more curable breast cancers necessarily saved lives.


Bailar’s salvo, “Mammography: A Contrary View,” appeared in the well-respected medical journal the Annals of Internal Medicine. In it, he registered several concerns, many of them drawing from his statistical background. First, he wrote, the benefits of screening mammography “have not been determined.” Although a research study then being run by the Health Insurance Plan of New York suggested its value for women over 50, no such data existed for younger women. “Not every lesion discovered by screening should be considered a success of the program,” Bailar wrote. This conclusion drew on the epidemiologic concepts of lead-time and length-time bias, which falsely elevate actual survival rates by focusing on the date of cancer detection rather than a patient’s actual outcome.


Second, according to Bailar, the risks of mammography “may be greater than are commonly understood.” Among his concerns was the worry that the radiation from repeated mammograms could actually cause breast cancer and that many of the machines being used in the BCDDP were using higher-than-necessary doses of radiation.

Bailar was most assuredly not a showman or publicity hound. When I interviewed him for a book on the history of breast-cancer control and asked him for a photograph, all he had was a wallet-sized image. Was he a whistleblower, intent on providing an insider’s exposé to the public? Some said yes, but in speaking to his daughter, Melissa Bailar, after his death, a different picture emerged. Her father, she said, “saw himself as a scientist, and the scientific questions and data drove his work, not any political motivation.” It helped, she added, that he did not care much for social conventions and what other people thought. Bailar’s wife Barbara, herself a statistician, termed her husband a lifelong “skeptic.”

Regardless of his motivations, the ramifications of what Bailar was charging were explosive. The uproar only increased when, in 1977, another researcher reported that 66 women who had undergone mastectomies as a result of BCDDP screening had not even had cancer. Through Freedom of Information Act requests, a series of journalists obtained internal documents cataloging the concerns of Bailar and other NCI staff. “There is more than a bit to be appalled about in the archives of the Breast Cancer Demonstration Project,” Daniel Greenberg wrote in the New England Journal of Medicine.

Bailar’s concerns about whether mammography, especially in women under 50, causes more harm than good, inaugurated a debate that persists today. But he had bigger fish to fry. In 1986, on the 15th anniversary of Nixon’s war, Bailar and Elaine M. Smith coauthored an article in the prestigious New England Journal of Medicine titled “Progress against Cancer?” Citing data that overall cancer mortality had only declined by 5 percent since 1971, and that breast-cancer mortality had not budged at all, Bailar and Smith called the war a “qualified failure.” Indeed, data from the Centers for Disease Control indicated that death rates from cancer actually increased until 1991, when they finally peaked. As would be expected, the cancer establishment immediately challenged Bailar and Smith’s findings, calling them “erroneous” and even “reprehensible.” But other skeptics, such as San Diego oncologist Michael Shimkin, called the article a “public service.”


In 1997, Bailar was at it again, writing again in the New England Journal of Medicine with medical student Heather L. Gornik that “blind faith” in screening and treatment had left cancer “undefeated.” Lost in all the rhetoric and reliance on expensive and ineffective surgery, radiation, and chemotherapy—the authors argued—was a strategy for controlling cancer that was smarter than catching it early: preventing it in the first place.

To physicians, cancer survivors, activists, bureaucrats, and legislators waging the war, Bailar was a constant nuisance. In response to his criticisms of the BCDDP, the ACS and NCI had doubled down, arguing that women with conditions such as cystic breasts, early menstrual histories, no past pregnancies, and even simply a high fear of breast cancer should be considered “high risk.” In sum, this meant 80 percent of women were at high risk—a concept that the statistician Bailar labeled “mathematically absurd.”

Bailar particularly raised the ire of Arthur I. Holleb, the ACS medical director at the time of the BCDDP. As a clinician, Holleb remained wedded to the idea that finding breast cancers earlier necessarily led to a better prognosis, something we now know to be untrue. Playing the doctor card, Holleb memorably termed Bailar’s epidemiologic research “the practice of medicine without the tears.” Others were less veiled, suggesting that by interfering with screening, Bailar was in essence “murdering” women.

Despite this harsh criticism, Bailar’s career thrived. After his years at the NCI, Bailar moved to Harvard, McGill, and then the University of Chicago. He retired in 2000. Although he was too sick near the end of his life to comment on the moonshot, he remained a fervent proponent of cancer prevention, according to Melissa Bailar. Bailar’s work received validation from both inside and outside the medical profession. In 1990, he was named a MacArthur Fellow. Three years later, he was named to the prestigious Institute of Medicine.


So was Bailar “right”? It depends whom one asked. Critics reasonably argued that his use of cancer mortality as the primary marker for the war’s success was misleading. And they pointed to prevention programs, most notably with regard to cigarette smoking, that had produced genuine change. But it was hard to challenge his basic premise, which was that the war on cancer had been grossly oversold. The rhetoric that accompanied Nixon’s war had not been subtle: Nixon stated that the effort once used to split the atom and send a man to the moon now needed to be turned to cancer. One oncologist even predicted that the disease would be eradicated by the time of the American bicentennial in 1976. Yet overall mortality from the disease has declined by only about 10 percent since 1971. And while survival from certain cancers, such as breast and prostate, has gone up, deaths from liver, kidney, and pancreatic cancer have actually increased.*

To some degree, the language surrounding the moonshot appears less fanciful than that surrounding the war on cancer. Thanks in part to the funding generated after 1971, we now know much more about cancer, particularly the role played by genetic mutations. We also know that it makes less sense to focus on the organs in which tumors originate (lung cancer, ovarian cancer, etc.), and more sense to see cancer as many different diseases that differ from person to person. Biden himself has cautioned that the goal of new cancer treatments may not be so much to cure the disease but to control it.

Still, proponents of the moonshot, signed into law by President Obama on Dec. 13, 2016, are still using flowery language that may not jibe with the scientific reality. Biden, for example, has called for a “national commitment to end cancer as we know it,” and Obama hopes that the moonshot “make[s] America the country that cures cancer once and for all.” Scientists hope to have an “effective vaccine-based immunotherapy to combat cancer by 2020.”


Such promises may not be realistic. For one thing, the fact that cancer is so many diseases will make it harder to find cures that work for everyone. Second, a series of recent studies have documented high rates of serious side effects to the exact types of immunotherapies being touted as curative. Third, as Norwegian physician Jarle Breivik has argued, cancer is a disease of aging—and we have to die of something.

These are not reasons to stop trying to cure cancer. But they are reminders, like those of John Bailar, to focus on the actual science.


*Correction, Jan. 12, 2017: Due to an editing error, this story originally stated that survival rates from breast and prostate cancers have gone down. They have gone up. (Return.)

Barron H. Lerner, a professor in the divisions of medical ethics and general internal medicine at the NYU Langone Medical Center, is the author of The Breast Cancer Wars, and, most recently, The Good Doctor.


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