A New Vision of Cancer
Questions and Mysteries of Cancer

“Advances are made by answering questions; discoveries are made by questioning answers” (Bernhard Haisch 1975)

Cancer and Microorganisms

According to the American Cancer Society, up to 20% of cancers worldwide have been related to infectious agents. The pathogenetic relationship between different types of cancer and many viruses such as papillomavirus, hepatitis B virus, and Epstein-Barr virus has previously been well documented .Viruses can integrate into the human genome and they seem to directly initiate tumourigenesis, such as human papillomavirus (HPV) in cervical cancer and herpesvirus in Kaposi’s sarcoma.

Concerning bacteria,certain of them are frequently found in cancerous lesions.The most widely known of these bacteria would be H. pylori which is the strongest known risk factor for gastric cancer . However only a small minority of those infected develop gastric cancer or precancerous gastric lesions .

If the connection of the above viruses and bacteria with cancer was undeniably causative, then their presence and their effect in the initiation and promotion of the neoplasmatic lesions of the relevant clinical cases would comply with the Koch principles about the criteria for a microorganism to be accepted as the cause of a disease. So,in each one cancer type a specific microbe should be isolated and, when injected into the organism,it should produce a specific cancer type, scenario not at all consistent with the vast majority of the relevant research and clinical data.

One of most common microbes found in malignancy are mycoplasmas. Mycoplasmas were first thought to be viruses due to their minute genome and size and the total lack of a cell wall covering their cytoplasmic membrane. They are really microbes, the smallest self-replicating microbes,but undeniably they share certain characteristics with viruses. Despite multiple studies suggesting that mycoplasmas are involved in a malignancy potential and demonstrating their prevalence in patients with different types of cancer, the pathological role of mycoplasmas in carcinogenesis is still unknown.

Besides,recent studies have shown that many healthy individuals are often colonized by mycoplasmas without any obvious clinical effects. Also,Mycoplasma “contamination” in cultured cells is common and a major problem in bio-laboratory work.

Moreover, certain acute infections of cancer patients have been observed to lead to cancer regression.William Coley, the “father of immunotherapy”, identified the presence of S. pyogenes in soft tissue sarcoma, and was one of the first to characterise concomitant infection of tumours and how this could lead to remission of incurable neoplastic malignancy . In recent years there have been a number of studies that show a correlation between bacterial infection and tumour regression. It has been found that patients who developed empyema after lung cancer had a significantly improved survival rate after 5 years compared with uninfected patients (50% v’s 18%) . Furthermore, two patients with malignant CNS tumours unexpectedly regressed after an infection.

WHY microbes, especially the virus-like microbes, the mycoplasmas, are commonly involved in the pathogenesis ,the promotion and the outcome of cancer of many important organs of the body, while it is obvious that they do not cause cancer in the conventional, at least, sense?

WHY certain serious acute infections lead to cancer regression in certain cases , while it would be expected that they would seriously and negatively affect the whole economy and prognosis of the cancer patient?

Blood Coagulation and Cancer

Malignancy affects the hemostatic system and the hemostatic system affects malignancy. In cancer patients there are a number of coagulation abnormalities which provide the background for an increased tendency of these patients to both thrombosis and hemorrhage,since cancer cells are able to activate the coagulation system. But the reverse process, the facilitation of cancer initiation and promotion when blood has increased coagulability is not at all easily explainable.Tumors also seem to activate procoagulatory factors and inhibit fibrinolytic factors, leading to the development of thrombosis, a major complication in cancer patients . Indeed, thromboembolism is estimated to be the second most common cause of cancer-related mortality

WHAT is the reason for this curious interconnection in cancer pathogenesis? None of the mainstream cancer theories can correlate with evidence the pathogenesis of cancer with blood coagulability ; no mutational genome or tissue imbalance can be identified in the mechanisms predisposing or following an increased blood coagulability. ARE there anymore important connections of the organs who produce blood constituents

Strange new blood vessels within the cancerous tissue

As tumours develop, they promote the construction of new blood vessels (neo-angiogenesis). However, these newly formed vessels are highly disorganized with incomplete endothelial linings and blind ends, resulting in ‘leaky’ blood vessels and slow blood flow. It has been supported that this leaky tumour vasculature may allow circulating bacteria to enter tumour tissue, and embed locally.
COULD these new vessels facilitate blood-borne metastases,since their construction is especially primitive,with blind ends , blood flow too slow and, consequently,they may function too inadequately ?If they could not, what is their meaning in the local tissue economy?

Bone Marrow and the Cancer niche

Βone marrow stem cells are found in many tissues,especially when a metastasis from a primary site follows after a “suitable niche” has been prepared for the installation of blood-borne cancer cells,as it is currently believed.The impression is that bone marrow stem cells travel from bone marrow to a site of an organ,which has been selected by the primary malignant tumor as a second home via the dispatch of specific messenger exosomes,which are directed with surprising exactness to find this predefined site after a vigorous travelling in the blood stream.

Besides,some times bone marrow stem cells are founded embedded within an epithelium,from which a malignant neoplasm arises.They are also believed to run to this site to encourage the initiation of a tumor.

If these bone marrow cells, being the quintessence for the production of the most important cells for the survival of the organism, are not really so maliciously and successfully activated to damage organs and tissues without any good reason, then
WHY are they found in various tissues of the body under the above circumstances of carcinogenesis at primary and secondary sites?

Moreover, in carcinomas,especially those arising in the breast,it has been observed that normal breast epithelial cells may be often found in the bone marrow from the stage of a primary mammary tumour with no metastases.
WHAT is ,then,the meaning of the presence of these cells in the bone marrow?

Finally,is it simply coincident that the bone marrow is wholly enclosed within the skeleton just like the central nervous system? If not,then
WHAT properties,processes and functions are mutually shared between the bone marrow and the brain? Is,perhaps, the bone marrow the alter ego of the brain ,complementing each other in health and disease,especially cancer?

The organ-selectivity of metastases

An aspect of metastasis which draws attention is the organ-selectivity of metastasis.It is well known that certain cancer types seem to have preferential sites to where they metastasize. For instance, if metastasis occurs in patients with primary breast tumors, metastases often form in lungs, liver, bone, and brain, whereas liver and lung are the most common sites of metastasis for patients with primary colorectal or pancreatic cancer .

WHY there is a remarkable organ-selectivity of metastasis, providing it is supported by the mainstream biomedicine that metastasis are created by blood-borne cancer cells, which, anyway, may reach any organ and site in the organism ,their distibution in the body is absolutely random ,not at all neglecting that and their survival chance in the blood is extremely low?


The mechanism of Metastasis

It is necessarily accepted that metastases are not at all explained accurately, and, more importantly, they are far from being successfully managed. Both epidemiologic and experimental evidence confirm the fact that metastases still remain an obscure subject .
It has to be emphasized ,first, that the ability for synchronous appearance of the same cell type in distant organs is not exclusive to cancer cells. For example, endometriosis, foci of normal endometrium ,having a similar histological pattern to that of normal endometrial mucosa, form in many distant from the uterus organs ,like the brain, the lung and the liver. .


From the very beginning of the establishment and expansion of a primary tumor, millions of cancer cells escape and enter the circulation, but most die . Upon arrival at a distant site, almost all disseminated tumor cells cannot colonize and form metastases. It is easily understood by simple reasoning that the chances for a cancer cell from the primary tumor to locally invade, intravasate into either the blood or lymphatic vessels, survive during a very long circulation under highly adverse conditions and without any kind of navigation, and successfully extravasate and colonize a distant site are extremely small if at all existing.Disseminated tumor cells usually undergo apoptosis or enter into an autophagy or senescence process or in a stage.

It seems that tumor dissemination from the primary site to the sites of metastasis involves tumor cell transport through the blood or lymph circulation systems.But,once the tumor cells enter the bloodstream, they encounter a new hostile microenvironment. The cells must withstand hemodynamic forces and overcome the effects of fluid shear. The cells are exposed to immunological signaling insults from leukocytes, to collisions with erythrocytes, and to interactions with platelets or macrophages. Finally, the cells need to attach to the blood vessel walls and extravasate to the surrounding stroma to form tumor metastases. Although only an extremely small fraction of invasive cells would be objectively able to complete the supposed metastatic process, most cancer-related deaths are the result of tumor metastasis.

Providing the above generally accepted mechanism is obvious that it is deprived of a sufficiently reasonable explanation by commonsense, simple reasoning and by a basic scientific foundation,
WHAT is the real mechanism for the creation of Metastases?

The Carcinogenesis-Embryogenesis Similarities


Carcinogenesis is characterized by a dramatic change in structure balance f in a model that is reminiscent of embryogenesis.It has been also described in the modern medical literature that cancer cells introduced into developing embryos can be committed to a complete reversion of their malignant characteristics.This return to embryogenesis patterns recalls the regeneration healing phenomena after a wound, so that certain researchers have used for cancer local phenomena the poetic ,but also objectively true, phrase “cancer, a wound that does not heal”, since wound healing and local cancer progression have striking similarities.