Charles Rowlatt SIGLogo(t)

System Diseases - Learning from Neoplasia
Synopsis of selected publications by Charles Rowlatt

Sometimes you see only what you have, when you lose it: lessons for health and disease. The structure of the system integration will appear when it falls apart.

 

Introduction

New Growth, neoplasia, reminds us of the existence of general principles underlying the self-replication of our body. When the biological organization of the body becomes disturbing, are cells (functional units) to their primary functions. Therefore they function at a substantially different way than the environment. This helps understand why other forms of healing be necessary, operating according to different understanding of the organization and cohesion of our body. There is therefore understandable why the junction with the environment then disturbed again. In a vicious circle can lead to the collapse of the biological organization of large parts of the system. Charles Rowlatt presents a vision of cancer in terms of disruption of the system.

(The explanation in the text makes explicit how the integration system is involved.)

 

The consistency of our bodies is determined by a dynamic form of organization. Neoplasia (cancer) is not a new phase III study, only symptom of a systemic problem at the level of biological organization. Fall into different levels of development to be recognized. The fall in the previous levels of functional organization to recognize patterns that we describe in the diagnosis of disease. In a more comprehensive vision, we can, instead of watching typical patterns of loss of organization, looking at the underlying system of biological organization (integration).

 

Growth and Neoplasia

 

The description of neoplasia has changed from a clinical picture in our body, to that of an analytical model in the laboratory. The scientific interpretation, however, remains based on clinical assessment. The following gives a hypothesis, based on systematic observation, in which both can be used. This requires common definitions, and generalized terms, but does so it is already possible to better understand neoplasia. This makes it possible to better describe themselves neoplasia. While we get more fundamental understanding of the overall coherence of our body.

 

 

 

 

 

Figure 1 A comparison of embryonic growth and new growth

 

Diagnostics

 

Diagnosis is meant to provide clarity for policy. Also in neoplasia is about understanding the disease process, including the stages capable of being completed. This is subject to variation. "Assessment" includes medical knowledge, clinical training, research, expert advice from the clinic and the laboratory, and experience. The understanding of each practitioner is part of the established paradigm, plus my own experience. In sickness policy is a tricky interplay between clinical pathological laboratory experience and theoretical models.

 

Clinical versus scientific

 

The current understanding of neoplasia arose in the 19th century (Triolo, 1964). followed by animal studies (Foulds, 1969, 1975), with very recent analysis of mechanisms (Pitot, 1986: Sirica, 1989, Hodges & Rowlatt, 1994). Doctors, epidemiologists and pathologists base their general models still on the standard diagnostic methods of the 19th century. The models and hypotheses concerning the determining mechanisms are formulated for subsequent mechanistic models, such as those in physics were developed. Each is a reflection of the concept and technology of that time (Rowlatt, 1994a). Neoplasia is that mechanistic models is not easy to describe, and laboratory models are based on typical cases. More than a century of research shows that there is no single cause of neoplasia.

 

Current vision

 

Neoplasia is considered an irreversible condition, with area (s) of loss of tissue organization. These can be based on functional and morphological characteristics are recognized. "Growth," "Progression" (further loss of organization) and "Metastasis" (more sites of disorganization), "Malignant (clinically poor prognosis) and" benign "(good clinical expectation) are the terms used. They are often ambiguous terms . The prognosis depends on the organ of origin, and epithelial tissue containing the least predictable. It describes the disease to organ (eg breast), type (eg adenocarcinoma), extension (Stage class) and loss of cell organization (degree). These groups add very different processes and business development together. It does not distinguish between differences in growth and outcome. "Stage 4", for example, makes no distinction between points of remote metastasis, intercellular organization, organization of cytoplasm in the cell nucleus, or criteria of cell growth. The prognosis for the important distinction between growth and malignancy is lost.

It is more logical to design a classification system to which the meaning of the practice is based on typical cases, substantiated by experiments. Findings and practical laboratory experience are in it together.

 

Principles

 

Neoplasia can be seen as a disruption of normal growth, loss of normal biological context (Smithers, 1962; Rubin, 1990; Rowlatt, 1998, 1990, 1994a, b). This applies to all defects. Each lesion represents a derailment of the normal biological organization. This means that one or more of the control mechanism stops working. Limitations of our research to limit how far we can recognize. It is necessary to know the passage of time. This leads to the concept of relative malignancy "for research. The term "malignant" remains reserved for clinical use, to inform the patent on the result.

 

The schedule of Smithers (1962) is still significant:

 

1) Cancer is a disease of organization.

2) The word cancer describes only the most advanced form of loss of coherence in the succession of undeveloped, distorted, metaplastic, hyperplastic, de-differentiation, neoplasia, to disintegration.

3) There are no cancer cells - cells that only behave in a manner that is arbitrary defined as cancer.

4) absence of cancer cells, could also not a cause of cancer found.

5) Organization is to measure the degree of information in the system. Entropy is a measure of disruption. Entropy increases gradually increased, there is no sudden malignancy.

6) Disruption of organization leads to loss of growth regulation coupled with cell division leading to tissue that is no longer part of the overall co-ordination.

7) Organization can be more or less corrupt behavior of tumors which deteriorated or improved.

8) Abnormal (stem) cell, a specific stem cell clones can produce an abnormal response to the environment and thus promote disorganization.

9) Environmental stress can affect the behavior of a cell disrupting influence within a region (local or general) depending on the type and nature of the cells.

10. There are many organic causes of disorganization, it is necessary to understand tissue interactions and cooperation. That is complex, dynamic and not predictable.

Although most cancer research focuses on malignant cells, the major developments from understanding normal cellular organization.

 

Biological organization

 

Biological organization is complex, dynamic, interactive and self-replicating (Foulds, 1969) (Table 1). These characteristics are not, until disrupted. The distortions are typical for characterizing neoplasia, it shows that there is an underlying coherence plays a role. In summary, heterogeneity is based on complexity, growth (deviation) is the result of dynamics (disturbance), the type of deviation reflects the level in the hierarchy of growth development, complementarity of properties on either side of a system boundary are reflected in contrasting deviation between adjacent areas and differences in self-replication based on the meaning abnormal (cell) behavior.

 

Characterization of the defect Practical consideration

complex heterogeneity uniqueness

* dynamic growth rhythm disturbance

hierarchy relative malignancy level of observation

interactive polar development extrapolation

self-replication behavior only / multiplication

* Time dynamics is determined, which in the analysis of a structure / function confusion.

 

Table 1 Main features of normal and abnormal biological organization in neoplasia. (The differences in dynamics requires different models. Ed.)

 

Research Limitations

 

Each of the features of Table 1 presents a problem for research (Elsasser, 1981, Gelding, 1985, Albrecht-Buehler, 1990).

Heterogeneity means that a lesion in the first approach is considered unique (instead of a process).

Momentum can only be considered as part of an ongoing process (rather than as timing in a moment). The doctor looks at the growth of a tumor, the pathologist a fixed specimen under the microscope.

Biological hierarchy in the lab describes a loss of coherence of a sample (instead of in relation to the context, the body.)

Forecasts based on the model of the lab differs from the cell development in the body (where each process is interactive).

Self-replication concerns the coherence of the entire body (instead of a specific area). Is the behavior local / instantaneous, or it expands in time and space?

 

 

Level Loss Control Model diagnostic signs

cells, cell-cell interaction uiteenval, metastasis Cell culture

tissue invasion by tissue-tissue interactions associated tissue organ culture

* * organs mass unit associated tumor in vivo

surrounding illness experience life

 

* "Functional Unit" is the defining concept.

Table 2 Supra-cellular system organization and hierarchy of relative malignancy in neoplasia. (The differences in interactions (logic) requires different approaches medicine. Ed.)

 

Simultaneity

 

These properties are typical, inseparable, characteristics of living tissue. Each is to study, but their qualitative differences loses the detailed description of one level, the understanding of the existence and consistency with the other levels. Dynamics and self-replication can only be studied in living systems. In fixed samples, they only distract. Interaction hierarchy and can be regarded as structural coordinates of the lesion, for which a larger development / context to understand. Central to the overall biological process and its inherent coordination / organization. Complexity characterizes the placement of the coordinates in this larger context, thus indicating a basis for understanding differences in similar lesions. It provides a multi-dimensional matrix to indicate an understanding of system organization.

 

In this vision, growth and development, must be regarded as a matrix. Disturbances in growth is to stand as a change of level in this organization matrix, or loss of boundaries and a level of development. Based on this matrix organization (dynamic context), we neoplasia (growth disturbance) in four ways. Each lets see more of the child - usually invisible - natural process of growth and organization.

 

Characteristics of neoplasia

 

We can consider four development tracks:

1) the relative nature of malignancy at a time when

2) the origin of neoplasia in functional units

3) the difference between growth and malignancy

4) Changes in time

Later it will review the different meanings of these for the diagnosis.

 

1) the relative nature of malignancy at a moment in time

 

For normal growth shows the basic developmental biology interactive development lation layers (hierarchy) in biological organization (Gilbert, 1991).

Well known, the successive stages of single cell by multiple cells, tissue selection, organ formation, the formation of the integral body. It is also known that cell differentiation by cell division, depends on the interaction between complementary components in the different development levels in the body.

In neoplasia, it has become clear from a comparison between clinical behavior and histopathology of cells for large groups of epitheliaalcellen to predict the outcome (Ewing, 1940, Nicholson, 1950, Willis, 1967). An outgrowth of a group of cells while maintaining its properties and cell type called benign. The situation is more serious when abnormal epithelial surfaces and grow into adjacent tissues. The situation is aggravated if the adult faces grow beyond their starting point and neoplastic cells or tissues are available remotely. It is clear that the normal control, the supra-cellular organization and provides consistency, disturbed. The cell-cell-, tissue-tissue interaction is disrupted, there is a disturbance in the organization of consistency between the functional units. The seriousness of the process is determined by the nature of the disturbance. We can deduce that the relative malignancy of neoplasia is determined by the level of supra-cellular organization (system connection) that the control still works.

 

This is an important fact: the loss of system control at the functional level, is the system - local / instantaneous - back to the underlying development phases, compare it to rebooting a computer. That are not successful reboot, the system remains partially on the underlying functional level work. The alignment with the environment there is different, because otherwise there is the cell function. The interactions therefore proceed differently, resulting in different interactions with nearby cells: growth disturbance in the form of growth disorders, new phase III study, by growth in the surrounding areas, or by growth from the cell group of origin.

 

This rule applies to epithelial neoplasia, adenomas and carcinomas. Not for mesenchymal-epithelial neoplasia, such as sarcomas, and the haemopoietic system is not so clear. This is the nature of the cells. Developmental Biology (Gilbert, 1991) and cytology (Alberts et al, 1994) show that epitheliaalweefsel usually consistent, and polar (self-limiting). Non-epitheliaalweefsel may occur as relatively isolated cells within the extracellular matrix, and have the ability to move freely in it, and respond to stimuli from the environment. In the body, we see two organizational principles: 1) local coherence determined on an interface, and 2) cells that are relatively free to move in their environment. If our assumption is that relative malignancy depends on the level of organization still operating (control), we can conclude that neoplasia mesenchymcellen no problem, even if they are dissociated and elsewhere, as the normal control but intact. Even if they would be the criteria for malignant epitheliaalcellen account. We can make the difference between carcinoma / sarcoma traced to an underlying complementarity between types of tissue (epithelial / mesenchymal).

 

The criteria for histopathological diagnosis based light microscope analysis of fixed tissue sections. However, this is a 2D image of a 3D situation, which always involves loss of information. Epithelial sheets are seen as strands, strands in the cross section seen as isolated cells and single cells are not seen as they are not in the coupe. Sectioned epithelial organs are recognizable by their supra-cellular organization into coherent epetheliaalvlakken or bags, surrounded by mesenchymal elements. Neoplastic variants of that structure can be recognized by the epithelial properties preserved. By contrast, sections of the supra-cellular organization mesenchymweefsels difficult to recognize, and it is virtually impossible to distinguish in the loss of control for epitheliaalcellen described. Histopathologen therefore made the agreement that the prognosis of neoplasia is described by organ, with different criteria for each organ. When they supra-cellular organization (clinical) can not see their diagnosis is determined by secondary signs such as new phase III study, instead of the relative malignancy, the actual parameter.

 

2) the origin of neoplasia in functional units

 

Behind the normal function hidden pathology. Behind carcinoma is to identify the healthy behavior (normal epithelial tissue whose coherence is lost). For a benign adenoma is less clear, we can only deduce that the functional unit is still basically healthy, but that local control is disrupted, increasing the number of functional units is increased neoplastic (Rowlatt, 1993).

A functional unit of an organ can be defined as the area of interactive cells, with their respective tribal lines, a (physiological) function provide. Each organ is a combination of Functional Units. The whole organism, analogous, composed Interactive Functional Units. Their collective role is that of the whole organism, providing some internal functional area, and other structural construction. This can be seen as the functional form of the integration system.

A Functional Unit is defined as a unit, they all have the same origin (Zygote), their functionality depends on the operation of other functional units in the system and their functions are partially overlapping. Nevertheless, the functional unit is a useful analytical tool. An epithelial component in a Functional Unit indicates the field is the associated mesenchymcellen, the support system (vessels, endocrine, etc.) that determines the differentiation and function, even though they are sometimes difficult to recognize. (In hormone-sensitive tissues can be seen that the decrease in tissue growth is proportional to the decrease of the respective hormones. The existence of Functional Units Mesenchymweefsel are indirect indications can be found in cytokine studies, even though it is not possible at this microscopic research to identify.)

If cells exist by virtue of their functions in the Functional Unit, it is the place where neoplasia will emerge. Specific genetic or epi-genetic regulation system can locally disrupt, but that does not mean the whole functionality disappears. The behavior of the new growth (neoplasia) is determined by the cells alive and the properties they represent, regardless of organizational level they still have. Example: single malignant cells may have characteristics of the higher system level, but they come from - the loss of biological organization - no longer functioning. Therefore, the light microscope still the research tool of choice, precisely because neoplasia is a deviation from the supra-cellular organization (functional unit).

 

3) the difference between growth and malignancy

 

Growth and malignancy are often viewed as related. Growth is the net increase in organic mass with time, malignancy is a feature of neoplasia, with fatal outcome. Growth is a normal feature of development. Cells produce more cells, tissues produce more of the same tissues, organs develop new functional units. Neoplastic growth was a loss of normal homeostasis regulation (control), which can be seen at all levels of organization. The number of signs for a fatal outcome has been so numerous and diverse that the term "malignant", without further explanation, almost meaningless for scientific comparison of neoplastic tissue. In the clinic, the term meaning in advising the patient. The term "Relative malignancy" is used here to describe the severity of disorder in the supra-cellular organization at the time of observation.

Growth can be assessed histologically on the basis of previous growth (mass), and cell division (mitotic values). The relative malignancy of the functional unit can be related to the level of organization for which the regulation is still intact. For epithelial tissues are neoplastic tissue invasion and collapse of tissue a strong tendency to spread, samples that show remotely. Each level of organization has a different cytological control system. The Markers vescrhillen that data can be used to identify differences in relative malignancy of a tissue sample to show. The standard stage classification provides a rough estimate of relative low malignancy. Typing, based on standard signs of malignancy, combines evidence of loss of tissue organization, parameters of accelerated cell replication with evidence of impaired cell replication. Loss of body in space, time and structure are in it together.

 

Level * Level of development Organisational Activeit in Regulating Embryo Expected impact of Failure in the Adult Diagnostic Indicator System Disruption of disorganization Diagnosis of Glandular neoplasia (relative malignancy) *

Division I Division without growth failure in copying the program: genetic afwijkinggen Bioaccumulation of neoplastic errors: Undifferentiated carcinoma heterogeneous structure (+ + + +)

Gastrulation II germ layers form and travel connection failure in tissue: cell dissociation Dissociation: metastasis of neoplastic cells dissociated carcinoma (+ + +)

III Organ formation Formation of rudimentary organs by tissue interaction balance in failure in tissue interaction: growth of / in organs Invasion: by cohesive neoplastic tissue invasive adenocarcinoma (+ +)

IV Cell differentiation and growth Maturation of Functional Units with replication to the required mass organ failure of interaction of Fundamental Units: Expansion proliferation: excessive number of functional units neoplastic adenoma (+)

* Level of organization, specified by random numbers. This corresponds to the boundary interaction: 1) nucleus, 2) the boundary as a compound, 3) the boundary as separation, 4) the super-cell (integration) system

 

Table 3. A comparison of the four stages of embryonic development - building organization - with the possible effects of regulation loss of the corresponding integration activity in the adult, with the supposed effects of loss of control for different levels of organization, in terms of diagnosis of malignancy of epithelial neoplasms by the pathologist

 

4) changes in time

 

Neoplasia is recognized and classified on the basis of the behavior over time, including apparent onrembare growth and / or risk growth. These are just generalizations, and by no means inevitable. It is important that these processes over time to understand in detail, with a breakdown in the underlying phenomena (Table 4).

 

Class Meaning

no change maintaining the status quo

 

Change is:

reversible change in the status quo

- Depending on circumstances

- Normalizes under appropriate conditions

irreversible determination (as in an embryo) mutation

and change:

simply the status quo is different

 

successive sequential changes in the status quo:

questionable selection:

- Changed relative malignancy

- Improvement of properties *

 

continued loss of status quo

for quick selection:

- The lowest common denominator,

"Former cell"

- Improvement of properties *

 

* Examples of improved features are: neovascularization, metastatic phenotypes and metabolic changes. etc.

 

Table 4 Summary of time-related changes in biological self-replication.

(The levels of the integration system operating in different time systems. Ed.)

 

 

Biological systems are determined by the reversibility in time. The normal form of an organ reflects its physiological and biochemical activity in the current phase of development from conception to aging on the Functional Unit. The smooth transition in the normal functional expression, over time, shows how the control systems of all these levels are interconnected.

 

This is an important observation: it's not about the regulatory system to look at the level of healthy bodies, but as a complex interplay of all systeemregulaties, all functional units, throughout the growth development of the body.

 

Neoplatische development may be reversible when the normal biological functions are expressed differently in changed circumstances, restoring the conditions leads to restoration of normal function. Where several factors determine the disturbance, will each of these disturbances disturbed regulation. Restoration of normal organization, then restore the system takes control at each of these factors, the normal organization system restore. If the regulation can not recover functional unit falls back on an underlying level of development, and thus operates within a more primary control function. When the downturn in the organism is not to integrate, "the system falls apart." The supra-cellular organization is unable to different functional units as a domain to regulate. This is referred to irreversible disruption of the organization. an irreversible change can manifest itself as change in the physiological determination of the cell line, or a change in the self-replication (a mutation), causing a new phenotype develops. In both cases it is a local attempt to adapt the organism to a changed environment, but at the expense of the overall coherence of the overall organism.

Where a single change would lead to a full adjustment of the phenotype, successive changes lead to variations in the phenotype. If this regulation systems at a low level of organization, then it is a gradual increase in relative malignancy expected, the development is "progressive" (Foulds, 1954). The more decisive forms of behavior are given priority by addressing a higher level of organization, rather than increased vitality. However it can also lead to a change in local regulation, which neovascularization, metastases or metabolic changes occur.

Continuous change means that the terugvan of regulatory systems are not limiting. One after another control system 'collapses'. The new growth (neoplasia) is less and less coherent, as the organization of the functional unit is missing. The cells degenerate to their most basic level, the lowest common denominator, with only the capacity for self-replication. Such cells are unable to adapt, as in much of the tumor transplant models shown. If those cells also have the ability to embed themselves in their environment, they can form a vascularization and, what is called "malignant".

 

Both clinical observation and the carcinogenesis experiments show Fould's (1954) 'step change to the worst outcome. " If in addition, separately, also disrupts the regulation system can be found all kinds of pattern distortions, which reversible and irreversible characteristics, simultaneously, to find. Previously it was assumed that neoplasia was irreversible, until research showed that modulation effect could have (Beatson, 1896, Pierce & Verney, 1961; Seiler-Aspang & Kratochwil, 1962,, Huggins, 1967).

 

The picture for terminal cancer is being explained by "genetic deviation". Neoplasia by failure to understand the regulation, the way is opened to see what dynamic factors inducing or influencing carcinogenesis (Rowlatt, 1993). If bodies and their functional units are organized at various levels, with private feedback systems, it is expected that gradually collapsing as its parameters exceed their critical values. Each functional unit can function autonomously. Within a common environment such as a body, will all Functional Units equivalent levels of relative malignancy develop, because the decline in that environment is shared. This is a known fact, and serves as a criterion for non-genotoxic carcinogenesis (Butterworth Will & Slaga, 1987). This also takes place at different levels of relative malignancy. For example, in the colon polyposis often begins around the age of 20 years. Change in cholesterol intake was found in animal studies to affect the malignancy of dimethylhydrazine-induced colon cancer (Cruse et al, 1984) In chronic ulcerative colitis dysplasia of the glands in the rectum indicator of preventing carcinoma (Morson & Pang, 1967).

 

Application of these insights for diagnosis

 

We previously described a number of important characteristics of biological organization, and characterizing the disturbances surrounding the observed changes in Neoplasia (new growth) can explain. Unfortunately, for practical applications, research methods sometimes distort the characteristics of the neoplasia. In research we want to match with the same compare the characteristics of the research material must match. A number of questions on biological properties, for the laboratory information for determining a biological profile (Table 5). As a result, better comparisons and generalizations of findings to fork away.

 

Interaction

1) Which of Functional Unity Orgniatie system is involved?

2) Which side of a tissue interaction, the cells are most common?

3) What degree of differentiation they?

 

Hierarchy

4) To what degree of organization is the control system failure?

 

Dynamics

5) Is there net growth?

6) Display of samples at different times were cut in relation to the normal biorithme?

 

Self-replication

7) Are there indications of behavior?

 

Complexity

8) How is this case different from apparently similar case?

 

Table 5 Questions to determine the biological profile of normal or neoplastic tissues, for comparative studies. (These questions test various aspects of the integration system.)

 

This is in detail, but a general answer is sufficient, and thus can be sufficient for a re-interpretation of the histological material. Over time, specific markers are also used, once it finds. In general, different features that the case of neoplasia, but these are the characteristics of intact normal behavior to maintain the exemption.

 

interaction. Questions 1 through 3 characterize the cell type and organ of origin better than in tumor diagnosis is common. Histopathology can only approximate a diagnosis, differentiation and development of new tests will help to better distinguish for research purposes. The answers to these questions illustrate the normal behavior of the tissue.

Hierarchy. Question four is about the relative malignancy of the neoplasia. In practice, the level at which the regulation is disturbed to recognize the (underlying) level of organization that is still intact. As tissue regulation qualitatively different for each level of biological organization, it is expected that loss of regulation characteristic is different to other marker molecules for each level of relative malignancy. The instructions to do so may be indirect, indicating reversible properties at an earlier stage, as well-differentiated metastases have a higher degree of organization than (uiteenval s) metastasis occurred.

Dynamics. Question 5 characterizes the growth. Histopathological evidence of net growth at any time in the growth of neoplastic tissue mass. The ratio of cells in mitosis, or the equivalent appropriate molecular markers, showing that excessive cell proliferation, ie growth. Self-replication requires a balanced proliferation at higher levels of biological organization, the underlying molecular markers such as in simple cell cultures are therefore still relevant to conduct better organized tissues. Question 6 researchers warn of possible problems in the sampling in dynamic systems where the characteristic parameters change over time.

Self-replication. Many neoplasien are remarkably homogeneous, with a similar pattern for the supra-cellular organization that repeats itself over large numbers of microscopic image fields. Histopathologen maintain their standard samples, in order thereby to distinguish a neoplasm or part of an old lesion, or new growth. This shows that the fall in the underlying regulatory system is in set patterns, so the typical patterns in the tissues can be identified. Change in the pattern (for which no explanation can be seen in the microenvironment of the cells) is evidence for changes in behavior (question 7). Evidence of possible behavior is seen in cytological signs of genetic instability, such as cytological variability, nuclear abnormalities and abnormal mitoses.

Complexity. Question 8 reminds the casual observer may note that deviations, and each lesion must be considered, regardless classificaie broad categories currently used. For research purposes, the biological subgroups of the standard classifications of cancer are used to determine new treatment strategies (Loizidou & Rowlatt, 1995).

 

Significance

 

Cancer is such a large area of multidisciplinary research cooperation is required. It follows that it is possible to find a common framework for the analysis of biological organization. Scientific research is usually confined its analysis of variables, and compares it with the same level. The proposed common classification framework distinguishes different than the usual categories, and thus includes not only a larger group of neoplastic phenomena, but also provides insight into the limitations of available methods in which to examine. Additional questions should enable specific scientific models to compare clinical findings of lesions. By the applicability to indicate the laboratory results more meaningful, also avoids the risk that unfounded generalizations actual effects in specific subsets mask. This is the communication between the researcher and physician benefits.

 

The assumption that each case is unique forces the researcher to look beyond function exception, because each of the successive steps in the regulatory system can be derailed. The better regulation loss of the stages are known in the laboratory, the greater the proof lies in practice. The wider the damage in carcinogenesis, the wider is the spectrum of lesions ar there to follow.

 

Most researchers regard cancer as a celziekte, despite the plea for a broader view (Smithers, 1962; Dilman, 1971, Rubin, 1985). Here, we make that neoplasia results from disturbances in the supra-cellular organization of functional units, which our body is built. Laboratory models must reflect the supra-cellular organization of the neoplastic lesions they represent. This concerns both the level of complexity of intercellular interactions - that characterizes the relative malignancy - even in March on the differentiation of cell types - which is typical for the prognosis, the possible behavior of the genotype will be expressed.

At all levels we see interaction with the complementary form, the yin-yang of biological organization. The difference between carcinoma and sarcoma is due to the respective tissue type. Contrast effect by imbalance is also the basis of other paradoxes, such as misplaced cytokine therapy, or control of neoplasia secondary sexual organs, by using complementary steroids.

The disadvantage of malignancy is usually in terms of time to the intended outcome. But unexpected contingent (reversible) neoplasia it is indistinguishable from irreversible change, and should be actively sought daarr (Beatson, 1896; Vernay & Pierce, 1961; Seilern-Aspang & Kratochwil, 1962, Huggins, 1967).

Recognizing the specific parameters in the biological profile helps overcome the effects of modulators of growth and relative malignancy to identify and follow. Each lesion is unique and sets out the parameters chosen to follow in time, irrespective of the overall picture. If withdrawal is possible, is to test reversibility. Practical objections to the great potential value of this theoretical approach is not in your way.

 

The coherence of functional units is determined by the Organic Organization. This is clearly composed of a regulatory system that operates on several levels. Each level has a different 'logic'. Loss of control in the system at one level, we see the body thereby functioning in other ways. These (local) 'fallback' to biological levels of previously developed control system succeeds a 'logic', so are the patterns of distortions as patterns. "Diagnostics" is based on this. The transition between these levels in case of illness, thus offers an insight into the structure and coherence of the Biological Organization System (the Integration System) in a manner not seen during normal growth and health. Then walk all changes "seamlessly" together. Neoplasia is a special form of disease, we see in it the principle of new growth within an area of organizational decline. It is like an attempt by the organism to begin anew, at a place where the 'lost the plot. "This play not only different levels of control system (organization) a role, but also the dynamic processes by which they are interconnected. This we see in the rhythms of our body.

 

Rhythms play an important role in our body. Franz Halberg (Cornelissen et al, 1989) described the chronobiology, an important research area for the future. The structure of rhythms in biology has led to a description of the functional dynamics. Circadian rhythm, rhythms week, month and year rhythms in our body rhythms are all available, along with many infrastructure diane rhythms, less than one day. For the physiology means that measurements of multiple frequencies, in conjunction, the usual time measurements must be replaced. For the role of steroids, peptides and their biological indolaminen time measurements already done. The disruption of control systems, is due to the disruption of time rhythms. In the time measurement is therefore more likely on the relationship of biological organization system. The significance of this is great for the diagnosis and prognosis of many chronic diseases, including cancer. Halberg has over 40 years studied. One of his findings is that development of breast cancer associated with relocation of circatrigintaan to circaseptaan rhythms in the body (a shift from 3 to 7 daily rhythm, Simpson et al, 1989).

 

This means that the regulation of tissue homeostasis and dynamic quality is determined from the coherence of biological organization system. It is composed of several layers, corresponding to cell development from Zygote. Between all those levels of development is a dynamic interplay in which the control system can also fall back to previous levels and the associated - typically other - processes. The histological interpretation of a coupe should also be understood within this context, it is important when applying the research to specify the time factors.

 

Conclusion

 

Through the scheme described the behavioral disturbance in neoplasia can be traced to loss of biological organization. by biological organization as a yardstick to use is the gap between technology and to bridge differences in disciplines. Researchers who work with this schedule, to give profile to a biological tissue, so their findings in this context to interpret, think a level of precision of their choice. A reader from another discipline can compare their results and materials.

 

Literature

Alberts B, Bray D, Lewis J, Raff M, Roberts K, Watson JD (1994): Molecular Biology of the Cell (3rd ed), New York: Garland Publishing Inc.

Albrecht-Buehler G (1990): In Defense of "nonmolecular" Cell Biology International Rev. of Cytology 120:191 -241

Beatson GT (1896): On the treatment of inoperable cases of carcinoma of the mamma: suggestions for a new method of treatment, with illustrative cases, Lancet ii: 104-107,162-165

Butterwoth BE, Slaga TJ (eds) (1987): Mechanisms in Nongenotoxic Carcmogensis. Cold Spring Harbor: Cold Spring Harbor Laboratory.

Cornelissen G, Halberg E, Halberg F, Sampson M, Hillman D, Nelson W, Sanchez de la Pena S, Wu J, Delmore P, Marques MD, Fernandez Jr., "Hermida RC, Guillaume F, Cara Dente F (1989): Chronobiology : a frontier in biology and medicine. Chronobiologia 16-383-408

Cotran RS, Kumar V, Robbins SL (1994): Robbins' pathology Basis of Disease (5th ed). Philadelphia: WB Saunders Company

JO Cruse, MR Lewin, CG Clark (1984): An Investigation into the mechanism of co-carcmogenesis or dietary cholesterol consistently the induction of colon cancer to rats by l 2dimethylhydrazine. Clin Oncology 10'213-230

Dilman VM (1971): Age-associated elevation of hypothalamic threshold to feedback control and Its role in development, aging and disease. Lancet i :1211-1219

Elsasser WM (1981): Principles of a new biological theory: a summary. J Theorectical Biology 89:132-150

Foulds L (1954): The experimental study of tumor progression: a review. Cancer Res 14:327-339

Foulds L (1969): Neoplastic Development 1. London: Academic Press

Foulds L (1975): Neoplastic Development 2. London: Academic Press

Gatter KC (1992): Morphology of neoplasms. In: JO McGee, PG Isaacson and NA Wright (eds.), Oxford Textbook of Pathology (vol. 1 Principles of Pathology, pp. 577-589). Oxford: Oxford University Press

Gilbert SF (1991): Developmental Biology (3rd ed). Sunderland, MA: Sinauer Associates Inc.

Hodges GM, Rowlatt C (eds.) (1994): Developmental Biology and Cancer. Boca Ratton, FL: CRC Press Inc..

Huggins C (1967): Endocrine-induced regression of cancers. Science 156:1050-1054

Kuhn TS (1972): The Structure of Scientific Revoluations (2nd ed). Chicago: University of Chicago Press

Morson BC, Pang L (1967): Rectal biopsy as an aid to diagnosis in ulcerative colitis. Gut 8:423-434

GWDP Nicholson (1950): Studies on Tumour Formation. London: Butterworth & Co..

Pierce GB, Verney EL (1961): An in vitro and in vivo study of differentiation in teratocarcinomas. Cancer 14:1017-1029

Pitot HC (1986): Fundamentals of Oncology (3rd ed). New York: Dekker

Rowlatt C (1989): Defining neoplasms. The Cancer Journal, 2 (ll) :363-368

Rowlatt C, Cruse JP, Hodges GM (1990): The tissue disorganisation as neoplasms: an hypothesis or neoplasia. The Cancer Journal 3 (5) :283-287

Rowlatt C (1993): Some Consequences of Defining the focal neoplasms as self-perpetuating tissue disorganisation. In: OH Inverson (ed.), New Frontiers in the Irish Cancer causation: Proceedings of the Second International Conference on Theories of Carcinogenesis (pp. 45-58). Washington DC: Taylor and Francis

Rowlatt C (1994a): Relative ontogeny and malignancy. In: Hodges GM, Rowlatt C (ed.), Developmental Biology and Cancer (pp. 29-60). Boca Raton, FL: CRC Press Inc.

Rowlatt C (1994b): Applying molecular biology to neoplasia. The Cancer Journal 7:99-102

Rowlatt C, Loizidou M (1995): Biological subsets within-Conventional diagnostic categories of cancer. The Cancer Journal 8:32 Assessing neoplasia

Rubin H (1985): Cancers a dynamic developmental disorder. Cancer Res 45:2935-2942

Rubin H (1990): On the nature of enduring modifications induced in cells and organisms. American Journal of Physiology 258: L19-L24

Salomon JC (1987): Cancer Classification. The Cancer Journal l (6) :286-289

Seilern Aspang-F, Kratochwil K (1962): Induction and differentiation of an epithelial tumor in the newt (Triturus cristatus). Morphology experim Embryol 10:337-356

Simpson HW, Pauson A, Wilson DW (1989): The chrono-bra: the "electrocardiogram" or the breast? Proc 2nd Ann IEEE Symp on Computer-Based Medical Systems (pp. 214-225). Minneapolis: Computer Society Press, Washington DC

Sirica AE (1989): Classification of neoplasms. In: AE Sirica (ed.), ThePathobiology or neoplasia (pp.25-38). New York: Plenum Press

Smithers DW (1962): Cancer: an attack on cytologism. Lancet i :493-499

Sporn MB (1991): Carcinogenesis and cancer: different perspectives of the Same Disease. Cancer Res 51:6215-6218

Triolo VA (1964): Nineteenth century cancer research: origins of experimental research. Cancer Res 24:4-27

Willis RA (1967): Pathology of Tumor (4th ed). London: Butterwoths

 

Summary

Living organisms have a dynamic organization. From conception through aging cells, tissues and organisms typical stages. The coherence is defined in the Organic Organization. Loss of coherence leads to relapse to earlier stages. This should be considered in terms of functional units (hairstyles of epithelial cells to diffuse mesen Chiem, with an accompanying vascularization and innervation). These functional units are all interconnected, and often only distinguishable when their relationship is disturbed. That disruption of coherence is seen in neoplasia: distorted new growth. Neoplasia is one clue to the biological organization of growth which would otherwise not be seen, a better understanding. The principle of relapse (a) previous development (s) - due to loss of biological organization - also helps understand why Functional Units other physiological characteristics, and so through other intervention models need to be understood.

 

Summary

Living Beings operate on the basis of dynamic Organization. Cells, tissues and Organisms initially develop through distinct Phases, from conception to old age. These internships are Determined in the Biological Organization. Loss of integration leads to a relapse to EARLIER Phases of development, as Functional Units. Functional units are inter-related groups or cells, with Usually Their Own capsule innervation and vascularisation. Their integrated interconnection When The integration Becomes visible decay, as can-be seen in neoplasms: derange new growth. Neoplasms thereby offering insight Into the stratification and interaction in biological organisatie. This helps understand why collapse of system integration leads to a fall-back failure Underlying functions, operating by a differential logic, or require different models for understanding and differential forms of health care for treatment.

 

Key Words

Growth, Neaoplasia, Biological Organization, Loss of Control, Organisational Dynamics

 

The Author

Charles Rowlatt, was a researcher at the Imperial Cancer Research Fund. Through his extensive experience in microscopic examination, he was able the connections between the cells he saw to examine and describe. The article is a translation of "Assessing neoplasia" in Kellen, JA (1996) Tamoxifen: Beyond the ani-estrogen, Woodbine, NJ. Schedule 1 and Table 2 are from Hodges, GM & D Rowlatt (1993) Developmental Biology and Cancer, CRC, Lodon, and Figure 1 is a poster presentation, CR June 10, 1993.

The author has been developing his retirement educational toys for children.

 

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