In the latter half of the 20th century, the rapid development of molecular biology has greatly deepened people’s understanding of the nature of life and advanced the understanding of tumors to an unprecedented level. The flourishing research on oncogenes, anti-oncogenes, cycle-related genes and proteins, apoptosis-related genes and molecules, signaling systems, metastasis-related genes, drug resistance-related genes, and even the Human Genome Project have made it possible to observe and understand tumors from different aspects at the molecular level. The rapid development of informatics and network technology has made a mountain of literature available at the click of a mouse. However, despite this, the understanding of the nature of cancer and how to control this malady has not yet reached a qualitative leap, and several inferences are still hypothetical. The generally accepted explanation for this is that the development of technology and the understanding of molecular mutations in tumor cells have not yet reached the level they should be. The second explanation, which is not yet easily accepted, is that the direction of research has been biased. As D. Hanahan, an American oncologist, said, “Several people thought that for the first few decades of this century, our research on tumorigenesis and treatment would continue in the same way as in previous decades, and that increasingly complex scientific and technical literature would continue to pile up in an already extremely complex literature, but we were expecting a completely different way of research …… Admittedly, this change depends first and foremost on advances in technology, but the primary and most fundamental change also depends on a renewal of concepts.” [1] Although he does not specify what this “renewal of concepts” refers to, several findings in tumor molecular biology do suggest that the research thinking and mindset of the past decades may have been biased. Because of the conviction that tumorigenesis originates from cell-specific genetic alterations, that the mechanism of tumorigenesis must ultimately be explained at the genetic level, and that tumor control must ultimately be achieved through genetic intervention, most tumor research in the past decades has been devoted to the search for mutations in cancer cells or abnormalities in gene expression. Despite the increasingly widespread application of large-scale, high-throughput genetic analysis techniques, it is not practically easy to identify truly meaningful, tumor common but tumor-specific alterations from thousands of mutations due to the highly unstable genomic structure of tumor cells and the fact that these genetic mutations are always in time-dependent, space-dependent and individual-dependent variation. The surprise of each new discovery is often accompanied by the contradiction and confusion that follow. Einstein believed that an important sign of the correctness of a theory is its logical simplicity. The theory of genetic mutations has encountered inescapable contradictions in explaining the causes of tumors due to its increasingly prominent complexity and discordance. We strongly believe that there must be a concise mechanism of tumorigenesis with universal significance that explains the various biological phenomena of tumors, which need not be explained by cumbersome and variable genetic mutations, but in which genetic mutations can be incorporated. Importantly, this understanding implies the best way of thinking to solve the tumor problem. Just as Copernicus, if he had not proposed heliocentrism, people would still have to struggle to understand astronomy under the reign of Ptolemaic geocentrism; Einstein, if he had not proposed relativity, people would still have to struggle to understand space-time under the limitations of Newtonian classical mechanics, so the time has come for a conceptual change in oncology research. From the discovery of oncogenes in the 1960s to the discovery of anti-oncogenes through gene analysis and comparative analysis in the late 1970s; from the discovery of the Philadelphia chromosome in 1960 to the deepening of the understanding of chromosomal ectopic and fusion genes in the occurrence and classification of leukemia and lymphoma after the further improvement of chromosome banding technology; from relatively specific gene mutations in solid tumors to the deepening of the understanding of colorectal carcinogenesis. The deepening of the understanding of chromosomal ectopic and fusion genes in the occurrence and classification of leukemia and lymphoma; from relatively specific gene mutations in solid tumors to the analysis of sequence gene mutations in the process of colorectal carcinogenesis; from abnormal gene expression to alterations in gene amplification, gene methylation and other gene modifications, all of them give the impression that tumor is a molecular disease and the result of gene alterations. This conclusion has defined the mainstream of oncology research from the last century to the present, and people have been trying to find answers at the genetic level in both the study of tumorigenesis and treatment. This theory based on genetic alterations leading to tumor formation may be referred to as the mutation theory. Genetic alterations include abnormalities in chromosome number and structure (ectopic, loss, point mutation, amplification, microsatellite instability, etc.). This theory holds that: intracellular series of genetic mutations are the root cause of tumors, therefore tumors are monoclonal and their progeny cells can only be tumor cells after the malignant transformation of normal cells into tumor cells; tumors arise based on defects in the control mechanisms of cell proliferation and apoptosis at the genetic level, and specific genetic mutations cause a paradoxical imbalance between the pair of proliferation and apoptosis, signaling and cycle-related genes, apoptosis Mutations in signal transduction and cycle-related genes and apoptosis-related genes are the key to the problem; almost all characteristics of tumor cells, including hypodifferentiated state, autonomous proliferation, invasive metastasis and multidrug resistance, can be attributed to abnormalities in specific genes; almost all carcinogenic factors (physical, chemical, biological) act on specific genes and act by inducing mutations; the most promising pathway to control cancer is genetic intervention –correcting mutated genes or introducing suicide genes. The gene mutation theory does have several incongruities and unavoidable contradictions in explaining the genesis of tumors. The genome of tumor cells exhibits extreme instability, changing continuously over time and space [2, 3]. Although certain genetic alterations are representative, such as relatively specific chromosomal ectopics and mutations in the K-ras and P53 genes in leukemias and lymphomas, tumors of the same organ exhibit a different spectrum of mutations in different groups and even in different individuals of the same group; different cancer cells within the same tumor tissue also present different cytogenetic and molecular genetic phenotypes [3]. Although it is possible to attribute this instability to malfunctioning surveillance mechanisms and to introduce the concept of mutator genes such as the mutated P53 gene [4], we have found in solid tumors that most mutators are actually present at progressive or advanced stages of tumorigenesis. Animal experiments have shown that transplantation of teratocarcinoma cells into early animal embryos can produce chimeric mice with normal development, suggesting that cancer cells can participate in the development of normal individuals. Similarly, transplantation of tumor cells into normal adult animals can produce no tumors, and the tumor cells were found to be involved in the composition of normal organs. Intervention of the extracellular matrix of tumor cells can also lead to reversal of the malignant phenotype of tumor cells, and both in vitro and in vivo experiments have shown that differentiation of malignant cells to normal cells can be induced by chemical intervention. In contrast, intraperitoneal transplantation of genotypically normal embryonic stem cells into homozygous mice can produce extremely malignant tumors, and transplantation of normal epithelial cells into an abnormal microenvironment or modification of the cell’s microenvironment can also lead to the production of tumors that can be malignant without any genetic alteration. Moreover, almost all “malignant” characteristics of malignant cells, such as invasive metastasis and induction of angiogenesis, are not unique to tumor cells, but are also present in normal cells at specific stages of individual development and even in adulthood, and they do not require genetic mutations to explain them. In addition, many physicochemical factors with clear carcinogenic effects do not act by acting on genes; the interstitial components of cells are the targets of their actions. The history of medical development has taught us that the explanation of disease can be reached at different levels, including the population, individual, organ, tissue, cellular, subcellular and molecular levels. For example, infectious diseases can be explained at the organ and tissue level, mitochondrial myopathies need to be at the subcellular level, whereas sickle cell anemia needs to go down to the molecular level. The evidence obtained so far suggests that tumors actually arise from abnormalities at the tissue and cellular levels, and that the nature of tumors is an abnormal tissue structure disease, and that genetic changes may only be an accompanying condition. No matter how misorganized the tumor is, since tumor is also a kind of tissue, in order to properly understand how tumor arises, it is necessary to first understand the natural process of tissue generation in human body. It is known from embryonic development that normal tissue generation is a very orderly process. The extent to which cells in a tissue need to proliferate and in what direction they need to differentiate depends on the constant exchange of information between the cells and their surroundings. Each differentiated or partially differentiated cell induces or inhibits the proliferation and direction of differentiation of other cells by producing some kind of messenger, and is influenced by other cells or interstitial structures. In other words, in the “tissue morphogenetic field”, cells gradually exchange information by “reading” and “being read” through a constant exchange of In other words, in the “tissue morphogenetic field”, cells gradually acquire the morphology and function of their differentiated state by constantly exchanging information and “reading” and “being read” specific signal molecules to form and maintain a complete tissue structure. Although the differentiation of tissues is manifested by the orderly expression and shutdown of genes, the orderly expression and shutdown of genes do not arise spontaneously, but are facilitated by the information exchange between cells and cells, and cells and the environment. For mature individuals, frequent regeneration and repair of tissue cells are required due to uninterrupted aging and death of mature somatic cells, coupled with unexpected diseases and injuries. The overall and local factors of the organism play an important role in maintaining cell regeneration and tissue repair. At this time, the integrity of the “tissue organization field” (tissue field) still depends on the continuous exchange of information between cells and the external microenvironment. If non-physiological tissue damage and cell loss occur repeatedly, such as chronic hepatitis, chronic gastritis, enteritis, chronic tracheobronchitis, etc., the outcome of continuous tissue damage and regeneration is often accompanied by the destruction of tissue structure and the production of abnormal tissue structures such as hepatosclerosis, glandular epithelial atrophy or hyperplasia, chemosis, etc. Thus, most of the tumors seen are accompanied by chronic tissue damage and tissue transformation. The altered tissue structure provides an unfavorable microenvironment for the proliferation and differentiation of cells within the tissue. In the abnormal microenvironment, the proliferation level and differentiation direction of regenerated cells are still subject to the instructions of external information. Due to the disruption of the microenvironmental structure, the signaling molecules that induce cell maturation and differentiation may no longer be produced, or the amount produced may be reduced, or the signaling molecules may not reach the target cells; or the presence of oncogenic factors (such as various oncogenic compounds) interferes with the key steps of signaling, from ligand inactivation and receptor closure to interference with intracellular signaling pathways, at which time the organism has a functioning cell due to the inability of proliferating cells to differentiate and mature The paradoxical existence of this paradox allows the body to continuously generate stimulating proliferative signals, thus keeping the immaturely differentiated cells in a proliferative state. In this case, malignant proliferation is inevitable. Therefore, abnormal tissue microstructure and/or the presence of carcinogens interfering with the normal communication between cells in the tissue and their microenvironment is one of the prerequisites for tumorigenesis. This is somewhat similar to the “tissue structural field theory” of carcinogenesis proposed by C. Sonnenschein [5]. It explains the carcinogenesis by emphasizing the alteration of tissue microstructure and cellular microenvironment, and the extracellular mesenchymal component is the first target of various carcinogenic factors. To emphasize and re-understand the hypodifferentiated state of tumor tissues Another important feature of tumor cells, besides malignant proliferation and invasive metastasis, is their hypodifferentiated state. Regardless of the tissue origin of the tumor, the tumor always exhibits a lower degree of differentiation than its counterpart tissue, ranging from an undifferentiated state to a highly differentiated state. In short, a tumor is a tissue formed by cells in a partially differentiated state. Differentiation, like proliferation, is one of the universal characteristics of tumor tissues. However, since the malignant proliferation and invasive metastasis of tumors are relatively more prominent, more efforts have been focused on the study of proliferation- and apoptosis-related genes. Several differential genes of tumor cells obtained by comparative analysis techniques are actually differentiated genes corresponding to tumor cells at a specific level of differentiation, only that they are treated as potential oncogenes because they are not expressed or expressed in low amounts in normal tissues. Given that most of the malignant characteristics of tumor cells are actually also characteristics possessed by normal cells in a hypodifferentiated state, the question of how to properly understand the hypodifferentiation of tumor cells is precisely implied by the understanding of the nature of tumors. According to the viewpoint of developmental biology, there are only two sources of tumor cells: de-differentiation of mature differentiated cells (de-differentiation), and cessation of differentiation or dys-differentiation of stem cells already existing in the body or tissues at a specific level of differentiation (dys-differentiation). From the structural and biochemical characteristics of the tissues, probably due to the similarity of tumor tissues to their primary tissues and the mutation theory that the nature of tumors is the result of genetic mutations in somatic cells, it is taken for granted that tumor cells are the result of de-differentiation of mature somatic cells in the process of malignant transformation. However, there are indeed some clues that give us reason to believe that tumors may originate from the deregulation of stem cells rather than the dedifferentiation of mature cells. First, according to the mutation theory, after the action of carcinogenic factors on target tissues, sensitive cells acquire proliferative activity and/or anti-apoptotic properties by undergoing genetic alterations and enter a positive expansion state. However, theory and experience tell us that mature cells, such as hepatocytes, do not need to return to a hypodifferentiated state (i.e., dedifferentiated) to enter an exuberant proliferation stimulated by proliferative signals, nor do they need to regain telomerase activity sufficient to destroy the host within their limited capacity to divide; cells without telomerase activity can still proliferate for 50 generations. That is, if only the genetic effects on proliferation and apoptosis are considered, malignant cells do not need to dedifferentiate and acquire telomerase activity. Second, although not very common, mixed tumors are seen in various tissues and organs such as the liver, lung, colon, uterus, blood and nervous system. Hybrid tumors are tumor tissues with more than one tumor cell component, such as epithelial and mesenchymal carcinosarcoma, epithelial and epithelial mixed cell carcinoma of the liver, adenosquamous carcinoma of the lung, and mesenchymal and mesenchymal erythroleukemia. According to the mutation theory, different tumor cells are malignant and mixed from different cellular components and are polyclonal. However, recent studies suggest that the majority of mixed tumors are also monoclonal, with different cellular components actually derived from the same cancer progenitor cells [6], as a result of differential differentiation of stem cells in an abnormal microenvironment. This phenomenon is difficult to explain by dedifferentiation. Third, malignant tumors of various tissues and organs have a differentiation series from hypodifferentiated to highly differentiated, often even within the same tumor, and they are actually manifestations of stem cells that are blocked in differentiation at different levels of differentiation, and it is difficult to understand that “undifferentiated carcinomas” can be generated by dedifferentiation of mature cells. Fourth, embryo-associated antigens are differentiation antigens that are expressed by specific cells at specific stages of embryonic development, i.e., immature stages of tissue formation. Mature somatic cells do not express embryo-associated antigens, while some tissues regain the ability to express them after malignant transformation. For many years this ability was thought to be associated with the development of carcinogenesis and was also the result of cellular dedifferentiation after malignant transformation. These AFP-expressing non-cancerous cells, like AFP-expressing cancer cells in cancerous tissues, are in fact partially differentiated stem cells that play a compensatory proliferative role. The difference is that AFP-expressing stem cells in non-cancerous liver tissues can still be induced to differentiate by their microenvironment, whereas AFP stem cells in cancerous tissues have their differentiation blocked in their microenvironment. A similar situation may be found with carcinoembryonic antigen (CEA), prostate-specific antigen (PSA), and fetal gastric sulfur glycoprotein. Fifth, the most representative are various leukemias. Different types of leukemia manifest as differentiation blockage of hematopoietic stem cells at different developmental stages, and these leukemic cells proliferate exuberantly at different levels of differentiation, which is also difficult to understand using the theory of dedifferentiation. Similarly, chemical interventions on leukemic cells have confirmed in vitro and in vivo experiments that they can be induced to differentiate toward maturity, with the disappearance of characteristically marked chromosomes after differentiation and a tendency for the heteroploid karyotype to convert to a normal karyotype, and with a transition state during differentiation, i.e., between naïve and mature morphologically, manifested in cell surface markers as both naïve cell differentiation antigens and mature cell The differentiation antigens are expressed on the cell surface, while only the mature cell differentiation antigens are expressed after the completion of induced differentiation. Sixthly, the increasing theoretical and experimental studies on stem cells suggest that stem cells with multidirectional differentiation potential exist in adult individuals. For example, bone marrow mesenchymal stem cells and hematopoietic stem cells can differentiate into tissues of various germ layers, hepatocytes can be derived from bone marrow stem cells, and bone marrow stem cells can also be derived from neural stem cells [7, 8, 9]. In chronic pathological states, stem cells may be blocked at a particular differentiation state when the microenvironment is not induced due to disruption and modification of tissue structure (e.g., chronic inflammation), combined with the induction of carcinogens. Since immature differentiated cells cannot perform normal functions, the body continues to send strong proliferative signals in the absence of organ function, and partially differentiated stem cells continue to proliferate, at which point cancer actually arises. Partially differentiated stem cell clones can mimic normal tissue structures (hyperdifferentiated) or form abnormally differentiated disorganized tissue structures (hypo-differentiated), depending on which differentiation state the stem cells are blocked in. However, they have the following common features. The cells have cell surface markers and biochemical characteristics similar to those of normal stem cells; high proliferation rate and telomerase positivity; and proliferation that is accompanied by induction of angiogenesis. Importantly, the angiogenic cells themselves may also be derived from stem cells, at which point the tumor cells become inducers. During tumor formation, tumor stem cells themselves may also be involved in the composition of the vessel wall [10]. In situations where the microenvironment is unfavorable for proliferation, such as hypoxia and metabolite toxicity, stem cells can undergo their own apoptosis, which is clinically manifested by extremely high levels of apoptosis in malignant tissues, but overall apoptosis levels are lower than proliferation levels. Due to the excessive proliferation rate, their genomic structure tends to be unstable. The phagocytic capacity possessed by tumor stem cells may also allow tumor cells to acquire additional chromosomes. Abnormalities in karyotype or mutations in chromosomal microstructure may then arise. The outcome is twofold: either they trigger their own apoptosis or they further acquire an autonomous clonal dominance, when they may also show a vigorous proliferative and invasive metastatic capacity independent of growth factors. In normal blood and lymphatic system, hematopoietic stem cells need to undergo rearrangement and ectopic chromosome structure at a specific differentiation level, and if oncogenesis occurs at this differentiation level, then malignantly proliferating blood cells take on characteristic marker chromosomes, but after such cells are induced to differentiate, the characteristic chromosomes should disappear. The low expression of adhesion molecules on the cell surface of partially induced differentiated stem cells that have not yet participated in histogenesis leaves them in a relatively free state and more susceptible to dissemination through lymphatic fluid and blood. Stem cells that can grow in distant metastases still maintain their partially differentiated state and have structural and biochemical signatures similar to those of their tissue of origin. However, the ability to grow in metastatic target tissues still depends on the specific selection of environmental signaling molecules, i.e., whether they “settle” or not depends on the specific recognition of the target organ microenvironment, which is selective. In conclusion, from the perspective of normal tissue genesis, development and differentiation process, tumor generation is actually the process of immature differentiation of pre-existing stem cells in the body. The important prerequisite for this is the destruction or modification of tissue microenvironmental structure, the suppression of alternative proliferation of mature cells, and the interference of induction signals by the effect of various carcinogens, which makes immature differentiation of stem cells possible. Most of the malignant features possessed by tumor cells are actually the same features possessed by stem cells when they are immaturely differentiated, as manifested by either high or low expression of specific genes. Karyotypic alterations and genetic mutations may be concomitant phenomena in the process of tumor production. The essence of the differentiation status of a cancerous tissue is the external expression of the proportion of stem cells with different degrees of differentiation it contains. The highly differentiated form is due to the fact that most stem cells have undergone some degree of differentiation, whereas the hypodifferentiated form is due to the prominence of stem cells and their partially differentiated daughter cells compared to the differentiated component. Scavenging or Inducing Differentiation The history of human fight against cancer dates back to more than two thousand years of written history. In the last one or two centuries, surgical procedures have evolved with the application of anesthesia techniques. In particular, the development of microsurgery, minimally invasive surgery and transplantation surgery in recent decades has led to the increasing maturity of oncologic surgery from theory to practice. Radiotherapy also has a history of more than one hundred years. With the development of computer technology, radiotherapy technology has developed to three-dimensional display, stereotactic and hyper-segmentation radiotherapy. Half a century ago, the application and development of tumor chemotherapy drugs made the systemic treatment of tumors possible, and the survival of patients was significantly extended, and some solid tumors such as leukemia, lymphoma and choriocarcinoma were cured. These three traditional treatments, which represent the mainstream of contemporary tumor treatment, as well as immunotherapy, gene therapy, angiogenesis inhibitor therapy, interventional therapy and hematopoietic stem cell transplantation-supported chemotherapy established later, all share a common guiding principle: tumor tissues and tumor cells must be removed or killed to the maximum extent. However, due to the biological characteristics of tumor cells, the limitations of this guideline are obvious: incompleteness, not to mention the emphasis on local surgery and radiotherapy, even the emphasis on overall chemotherapy can hardly kill the tumor cells and their metastases completely; serious side effects, while killing the tumor cells, the normal proliferating cell population of the body also suffers serious injuries, not to mention some The problem of recurrence, chemotherapy resistance leading to residual cancer cells is one aspect, but new cancer foci can also appear at any time under the continuous action of carcinogenic factors, such as primary hepatocellular carcinoma; new technological approaches including guidance therapy, immunotherapy, gene therapy, angiogenesis inhibitors and new target-based telomerase inhibitor and farnesyl protein transferase inhibitor therapy seem It is also difficult to escape from such paradox. The reasons are simple: tumor antigens are not sufficiently specific; tumor stem cells are often components that have been present at specific stages of embryogenesis and thus the body is inherently tolerant to tumor cells; and every tumor-specific target one envisions is present in normal tissues and is required to exercise its function when necessary. The reason for this limitation is also simple. Because of the disorganized karyotype and numerous genetic mutations in tumor cells, coupled with gene transfection techniques that convert non-tumor cells to malignant cells, it is taken for granted that the essence of a tumor is a genetic abnormality and that treatment can only be achieved by removing or killing tumor cells. If the essence of tumor is not the mutation of genes, the result of understanding the phenomenon as the essence will make people continue to increase the meaningless investment on one hand, but on the other hand, they are caught in the mire of fatalism in the face of the extremely large number of genetic mutations in tumor cells. Since cancer can originate from the abnormal differentiation of stem cells, then trying to induce or “manipulate” the differentiation of cancer cells to normal cells by altering the microenvironment can be the foothold and hope for cancer treatment. In the 1970s, K. Illmensee discovered that transplanting teratocarcinoma cells into the blastocysts of normal homologous animals resulted in chimeric mice that did not grow tumors, and in the 1980s, CG. Webb transplanted leukemia cells into early embryos of homologous animals and found that leukemia cells could participate in the development of the blood system of normal animals, and after the animals matured In the 1990s, WB. Coleman transplanted hepatocellular carcinoma cells into liver tissue of homozygous adult animals and found that cancer cells could participate in cell renewal in the normal liver; similarly, breast cancer cells could undergo reversal of the malignant phenotype by modifying the extracellular matrix microenvironment. A compounds have been shown to have good differentiation-inducing effects in human leukemia. Many laboratory and clinical experiences have also been accumulated for differentiation induction studies in solid tumors, confirming that tumor cells can be induced to differentiate by environmental interventions [11]. Most of the current studies on induced differentiation involve chemical interventions on tumor cells. The chemicals that can produce differentiation-inducing effects include vincristine, dimethyl sulfoxide, vitamin D and butyric acid. Some substances that have significant differentiation-inducing effects in vitro have limited their application because of their high toxicity to humans. In addition, relapse after induction and the development of tolerance after repeated use of inducers are also issues that need to be further explored, and the search for highly efficient and less toxic chemical inducers will be the direction of future research. Another area that has not yet been addressed is the search for substances in normal tissues that have the function of inducing stem cell differentiation. The maintenance of normal tissue structure depends on the strict spatial and temporal regulation of the organism, and the regeneration of liver tissue, the healing of fractures, and the repair of wounds are excellent examples of this. The possible presence of tissue morphology maintaining molecules (morphostats) [12] should have a directive role in the proliferation and differentiation of tumor stem cells. The most promising inducers of differentiation will probably be derived from embryonic tissues. During tissue development in the embryo, tissue morphogenetic molecules (morphogens), which determine the degree of cell proliferation and the direction of differentiation [12], can have a pronounced, normal-to-normal cell transformation effect on tumor cells. This has been demonstrated in animal experiments, and specific human embryonic tissue extracts have shown good results in some advanced malignancies. In the post-genomic era, with the intensive study of proteomics and protein microarray technologies, it may provide great possibility and convenience to search for molecules with specific differentiation-inducing effects in the histomorphogenetic field of embryonic tissues and in the histostructural field of adult tissues. Humanity has entered the 21st century. It is recognized by the medical community that the most fundamental aim of oncology research is to reduce morbidity and mortality. However, from the standpoint of the general public, this purpose must have a prerequisite – the huge medical costs must be greatly reduced while alleviating physical and mental pain. This depends on a qualitative leap in people’s understanding of cancer. No matter how complex the causes of cancer are, there must be a most universal mechanism behind it, so that the complex biological, physicochemical and genetic factors of cancer occurrence can all be united in the same way, and a leap in cancer treatment can be achieved under the guidance of this mechanism. The concept of cancer research must be renewed. It is the findings of modern molecular biology and cell biology research that make us realize that the understanding of cancer must be grasped from a new perspective. The combination of tissue microstructure theory and stem cell theory presents a logical explanation for the emergence of cancer and provides the basis for an in-depth study of the theory of induced differentiation, believing that an in-depth study of this field will lead us to the dawn of cancer treatment. Our ideal is as Hanahan said: the study of cancer biology and cancer therapy is still today a patchwork of cell biology, genetics, histopathology, biochemistry, immunology, and pharmacology. We expect that one day it will become a perfect science with a complete conceptual structure and logical coherence comparable to contemporary chemistry and physics [1].