My book Neoplasms: principles of development and diversity was published last week. The full table of contents is available.
In the next few blogs, I will provide some short excerpts from the book. In Chapter 1,I review the properties of neoplasms.
Excerpt:
Cancer cells do not create new biological properties. They use the same properties that normal cells use, only they tie them all together in a package that nobody wants to receive. Let us examine the normal tissues that have properties of cancer cells.
You can think of the body as a collection of two types of cells: those that grow persistently and those that grow intermittently or never. The most numerous persistently growing cells line the outside and the inside surfaces of the body: squamous cells of the skin’s epidermis and enterocytes of the gastrointestinal tract (the gut). The growing cells of skin and gut exactly balance a second population of cells that are actively dying. The reason that the skin epidermis and the gut mucosa maintain a constant thickness is that the dead skin cells are sloughed into the air (as dust specks) and the dead enterocytes are sloughed into the fecal stream. Otherwise, both the epidermis and the gut would double in size every few weeks, a rate of normal growth that easily exceeds the growth rate of neoplasms.
Epithelial tissues (the tissues that line surfaces and populate most solid organs and glands) contain a subpopulation of growing (dividing) cells. Each division of a dividing cell yields two cells: one cell that performs the normal functions of the tissue, and another cell that is capable of dividing. The cell that performs the normal functions of the organ is referred to as a differentiated cell, because it has completed the developmental process and has attained a distinct morphologic appearance. Most differentiated epithelial cells are incapable of dividing and will eventually die. The precise balance of cell growth and cell death yields a zero net growth in normal adult tissues.
Some organs, like the liver, are composed of epithelial cells that cease to divide or divide only rarely. The liver of an elderly man may contain many of the same, hard-working hepatocytes (liver cells) it had when the man was a youth. In the event of a liver injury, the other-wise quiescent hepatocytes quickly divide, enlarging individual acini (i.e., microscopic liver glands), quickly restoring the liver. In the rat, the full weight of the liver is restored a week after surgically removing two thirds of the liver. The remarkable regrowth of the liver after partial hepatectomy appears in the myth of Prometheus, whose liver is eaten by eagles each night and restored the next day.
Some nonepithelial tissues lose the ability to divide at about the time that the human body has reached its adult size. Many of the diseases of aging are actually just the consequences of wear and tear in populations of cells that cannot renew themselves. Osteoarthritis is a joint disease that results from damage, over time, to articular cartilage. Cartilage cells (chondrocytes), in contrast to liver cells, have only limited ability to divide. When cartilage is damaged, it usually stays damaged, and this may cause a chronic inflammatory disease involving the damaged joint cartilage and the underlying bone (osteoarthritis). The dementia that accompanies aging is due, in part, to the limited ability of senescent neurons to renew themselves through division. You can think of the degenerative diseases of aging as the medical opposite of neoplasia. Aging results from accumulated damage in cells that cannot divide. Neoplasia is the result of accumulated damage in cells that must divide. (to be continued)
Chapter 1 Table of Contents:
1 What Properties Are Shared by All Cancers? 3
1.1 Background 3
1.2 Are There Any Properties of Neoplasms that Are Not Found in Normal Cells? 4
1.3 Persistent Growth in Normal Cells 4
1.4 Invasion by Normal Cells 5
1.5 Metastasis by Normal Cells 5
1.6 Is There a Common Temporal Sequence Leading to the Development of Cancer? 7
1.7 Why Is It Important to Treat Cancers Early? 7
1.8 Cancer Morphology 8
1.9 General Rules for Naming Neoplasms 8
1.10 What Is a Cytologic Diagnosis? 9
1.11 Morphology of Malignant Cells 10
1.12 Cancerous Atypia and Reactive Atypia 12
1.13 How Can You Distinguish Reactive Atypia from Cancerous Atypia? 13
1.14 Dysplastic Cells and How They Differ from Cancer Cells 14
1.15 Nuclear Atypia in Cancer Cells 15
1.16 Why Are the Nuclei of Malignant Cells Different from Nuclei of Normal Cells? 15
1.17 Tumor Monoclonality 15
1.18 Monoclonal Proliferative Lesions 16
1.19 Clonal Expansion in Paroxysmal Nocturnal Hemoglobinuria 17
1.20 Clonal Expansions of Normal Cells that May Not Lead to Cancer 18
1.21 Polyclonal Expansions that May Lead to Monoclonal Cancer 18
1.22 Tumor Growth Regulation and Tumor Autonomy 18
1.23 Limits on Tumor Autonomy 19
Summary 19
The full table of contents is available. In the next few days, I will continue to discuss content from Neoplasms in my blogs.
-Jules Berman
Key words: tumors, tumour, neoplasms, neoplasia, carcinogenesis, tumor development, cancer research, neoplastic development, precancer preneoplasia, preneoplastic
Tuesday, September 30, 2008
Monday, September 29, 2008
Neoplasms: Classification and Eradication
As I've noted yesterday, my book Neoplasms: principles of development and diversity was published last week.
The full table of contents is available. As indicated yesterday, the book is divided into three parts: tumor speciation, tumor classification, and tumor eradication. By tackling these three major areas, we can start answering long-held questions of tumor biology.
Yesterday, we discussed tumor speciation. Today we'll continue a discusion of Neoplasms by describing Part 2 (Classification) and Part 3 (Eradication).
After the neoplasms of humans are assigned species, the next step is to divide the species of neoplasms into broad classes. Creating a neoplasm classification is a difficult scientific problem. Lessons learned through the millennia from naturalists such as Aristotle, Discorides, Ray, Linnaeus, Darwin, and Mayr have direct bearing on the classification of neoplasms. Modern classifications serve several purposes
1. To seek universal truths that pertain to all neoplasms
2. To simplify our understanding of an otherwise disconnected list of thousands of neoplasms
3. To serve as a conceptual framework on which hypotheses about the relationships among the different neoplasms, and about the properties of neoplasms in general, can be asked and answered
4. To serve as an information key to which data can be sensibly stored and retrieved
5. To provide a rational basis for developing class-targeted preventions, modifications, and treatments based on biological properties and pathways shared by the members of a class
Distinguishing the many different species of neoplasms and grouping them into a classification is a pointless exercise if it does not lead to a reduction in the number of human deaths caused by cancer. In Part III, we will learn that the agents that cause cancer, the measures we use to prevent cancer, the steps in carcinogenesis, the biological properties of cancers, and the treatment of cancers are all class-dependent. Treatments that may be effective in one class of tumors may not be effective in tumors from other classes. Much more importantly, we can hope that agents that can cure one type of cancer may be effective against all of the other types of cancers that share the same class.
At first glance, cancer cells seem to be characterized by a hopelessly complex set of abnormalities involving every cellular process. If we do not make the intellectual effort to speciate and classify neoplasms, new and effective approaches to eradicating cancer will not be forthcoming. In Part III, we examine a variety of research approaches that can contribute to the eradication of cancer.
In the next few days, I will continue to discuss content from Neoplasms in my blogs.
-Jules Berman
Key words: tumors, tumour, neoplasms, neoplasia, carcinogenesis, tumor development, cancer research, neoplastic development, precancer preneoplasia, preneoplastic
The full table of contents is available. As indicated yesterday, the book is divided into three parts: tumor speciation, tumor classification, and tumor eradication. By tackling these three major areas, we can start answering long-held questions of tumor biology.
Yesterday, we discussed tumor speciation. Today we'll continue a discusion of Neoplasms by describing Part 2 (Classification) and Part 3 (Eradication).
After the neoplasms of humans are assigned species, the next step is to divide the species of neoplasms into broad classes. Creating a neoplasm classification is a difficult scientific problem. Lessons learned through the millennia from naturalists such as Aristotle, Discorides, Ray, Linnaeus, Darwin, and Mayr have direct bearing on the classification of neoplasms. Modern classifications serve several purposes
1. To seek universal truths that pertain to all neoplasms
2. To simplify our understanding of an otherwise disconnected list of thousands of neoplasms
3. To serve as a conceptual framework on which hypotheses about the relationships among the different neoplasms, and about the properties of neoplasms in general, can be asked and answered
4. To serve as an information key to which data can be sensibly stored and retrieved
5. To provide a rational basis for developing class-targeted preventions, modifications, and treatments based on biological properties and pathways shared by the members of a class
Distinguishing the many different species of neoplasms and grouping them into a classification is a pointless exercise if it does not lead to a reduction in the number of human deaths caused by cancer. In Part III, we will learn that the agents that cause cancer, the measures we use to prevent cancer, the steps in carcinogenesis, the biological properties of cancers, and the treatment of cancers are all class-dependent. Treatments that may be effective in one class of tumors may not be effective in tumors from other classes. Much more importantly, we can hope that agents that can cure one type of cancer may be effective against all of the other types of cancers that share the same class.
At first glance, cancer cells seem to be characterized by a hopelessly complex set of abnormalities involving every cellular process. If we do not make the intellectual effort to speciate and classify neoplasms, new and effective approaches to eradicating cancer will not be forthcoming. In Part III, we examine a variety of research approaches that can contribute to the eradication of cancer.
In the next few days, I will continue to discuss content from Neoplasms in my blogs.
-Jules Berman
Key words: tumors, tumour, neoplasms, neoplasia, carcinogenesis, tumor development, cancer research, neoplastic development, precancer preneoplasia, preneoplastic
Sunday, September 28, 2008
Neoplasms: More on Tumor Speciation
As I've noted yesterday, my book Neoplasms: principles of development and diversity was published last week.
The full table of contents is available. As indicated yesterday, the book is divided into three parts: tumor speciation, tumor classification, and tumor eradication. By tackling these three major areas, we can start answering long-held questions of tumor biology.
Tumor Speciation is the process that restrains neoplastic development to a finite set of biological types. We are taught that neoplasms are caused by mutations that lead to uncontrolled growth and genetic instability. We are also taught that the genetic instability in cancer cells leads to the progressive accumulation of additional mutations. If this is the fundamental mechanism of carcinogenesis, would you not expect a near-infinite number of cancers resulting from all of the possible different combinations of observed mutations?
The harsh realm of neoplasms is much like the realm of living terrestrial organisms. The world is composed of unique, individual life forms. Somehow, every unique life form belongs to one species from among a finite number of species. The squirrels in your backyard may all look alike, at first glance, but each squirrel has a unique genome and a unique personality. Each squirrel is a life form that has never before appeared on earth and that will never appear on earth again; nevertheless, each squirrel is an unmistakable member of the squirrel species. Every squirrel shares features in common with other squirrels and lacks features that are found in other animal species. Every neoplasm is unique, with a unique set of genomic and epigenomic variations that can distinguish one tumor from every other tumor. Why do we encounter certain types of tumors with the same morphology, occurring in different people? The shared morphologic and biological features among types of tumors allows us to examine any unique tumor under a microscope and say with complete certainty that the tumor is a testicular seminoma, or a Warthin tumor of salivary gland, or a pilomatrixoma of skin, or any one of the thousands of distinctive species of neoplasms? Why is it that even though humans are different from every other animal, tumors found in fish and rodents may look and behave very much like specific types of tumors found in humans?
Before we can start thinking about how to classify tumors, we need to understand why every unique tumor must belong to one of several thousand species of tumor. This topic is discussed in Part I of Neoplasms.
In the next few days, I will continue to discuss content from Neoplasms in my blogs.
-Jules Berman
Key words: tumors, tumour, neoplasms, neoplasia, carcinogenesis, tumor development, cancer research, neoplastic development, precancer preneoplasia, preneoplastic
The full table of contents is available. As indicated yesterday, the book is divided into three parts: tumor speciation, tumor classification, and tumor eradication. By tackling these three major areas, we can start answering long-held questions of tumor biology.
Tumor Speciation is the process that restrains neoplastic development to a finite set of biological types. We are taught that neoplasms are caused by mutations that lead to uncontrolled growth and genetic instability. We are also taught that the genetic instability in cancer cells leads to the progressive accumulation of additional mutations. If this is the fundamental mechanism of carcinogenesis, would you not expect a near-infinite number of cancers resulting from all of the possible different combinations of observed mutations?
The harsh realm of neoplasms is much like the realm of living terrestrial organisms. The world is composed of unique, individual life forms. Somehow, every unique life form belongs to one species from among a finite number of species. The squirrels in your backyard may all look alike, at first glance, but each squirrel has a unique genome and a unique personality. Each squirrel is a life form that has never before appeared on earth and that will never appear on earth again; nevertheless, each squirrel is an unmistakable member of the squirrel species. Every squirrel shares features in common with other squirrels and lacks features that are found in other animal species. Every neoplasm is unique, with a unique set of genomic and epigenomic variations that can distinguish one tumor from every other tumor. Why do we encounter certain types of tumors with the same morphology, occurring in different people? The shared morphologic and biological features among types of tumors allows us to examine any unique tumor under a microscope and say with complete certainty that the tumor is a testicular seminoma, or a Warthin tumor of salivary gland, or a pilomatrixoma of skin, or any one of the thousands of distinctive species of neoplasms? Why is it that even though humans are different from every other animal, tumors found in fish and rodents may look and behave very much like specific types of tumors found in humans?
Before we can start thinking about how to classify tumors, we need to understand why every unique tumor must belong to one of several thousand species of tumor. This topic is discussed in Part I of Neoplasms.
In the next few days, I will continue to discuss content from Neoplasms in my blogs.
-Jules Berman
Key words: tumors, tumour, neoplasms, neoplasia, carcinogenesis, tumor development, cancer research, neoplastic development, precancer preneoplasia, preneoplastic
Saturday, September 27, 2008
Neoplasms: Short excerpt from Preface
As I've noted yesterday, my book Neoplasms: principles of development and diversity was published last week.
The full table of contents is available. As indicated yesterday, the book is divided into three parts: tumor speciation, tumor classification, and tumor eradication. By tackling these three major areas, we can start answering long-held questions of tumor biology.
In the book's Preface, I list some of the questions addressed in the text. Here's an excerpt:
What intrinsic cellular properties are common to all cancers?
Are there properties of neoplasms that are not found in normal cells?
How can we stop the progression of a normal cell into a cancer cell?
How can we kill cancer cells without harming normal cells?
Can we reverse the cancer process and transform cancer cells into normal cells?
How have studies on rare tumors led to new cures for common tumors?
What are the inherited tumors, and how do they differ from non-inherited tumors?
What is the relationship between inherited cancers and inherited malformations?
Why do chemical carcinogens need to be activated by cells in our bodies before they can causecancer?
Are there some carcinogens that cause only benign tumors and others that cause only malignant tumors?
What carcinogens are responsible for the majority of tumors that occur in man?
Can tumors occur spontaneously, without any external cause?
Is a single gene alteration sufficient to cause a cancer?
What is the smallest dose of a carcinogen sufficient to produce a cancer?
Are animal tumors good models for human tumors?
Are childhood tumors fundamentally different from tumors that occur in adults?
Why aren’t the same characteristic genetic changes seen in all tumors of a specific
type?
Why do tumors that arise from the ectoderm and endoderm (embryonic layers) account for more than 95% of the tumor burden of humans?
What is a stem cell tumor?
How do germ cell tumors differ from all other tumors of humans?
Why are there different kinds of tumors and how many kinds of tumor are there?
How might a tumor classification be used to guide the development of new chemotherapeutic agents?
Is cancer prevention more important than cancer treatment?
How can our understanding of precancers lead to the eradication of all human cancers?
In the next few days, I will continue to include short excerpts from Neoplasms in my blogs.
-Jules Berman
Key words: tumors, tumour, neoplasms, neoplasia, carcinogenesis, tumor development, cancer research, neoplastic development, precancer preneoplasia, preneoplastic
The full table of contents is available. As indicated yesterday, the book is divided into three parts: tumor speciation, tumor classification, and tumor eradication. By tackling these three major areas, we can start answering long-held questions of tumor biology.
In the book's Preface, I list some of the questions addressed in the text. Here's an excerpt:
What intrinsic cellular properties are common to all cancers?
Are there properties of neoplasms that are not found in normal cells?
How can we stop the progression of a normal cell into a cancer cell?
How can we kill cancer cells without harming normal cells?
Can we reverse the cancer process and transform cancer cells into normal cells?
How have studies on rare tumors led to new cures for common tumors?
What are the inherited tumors, and how do they differ from non-inherited tumors?
What is the relationship between inherited cancers and inherited malformations?
Why do chemical carcinogens need to be activated by cells in our bodies before they can causecancer?
Are there some carcinogens that cause only benign tumors and others that cause only malignant tumors?
What carcinogens are responsible for the majority of tumors that occur in man?
Can tumors occur spontaneously, without any external cause?
Is a single gene alteration sufficient to cause a cancer?
What is the smallest dose of a carcinogen sufficient to produce a cancer?
Are animal tumors good models for human tumors?
Are childhood tumors fundamentally different from tumors that occur in adults?
Why aren’t the same characteristic genetic changes seen in all tumors of a specific
type?
Why do tumors that arise from the ectoderm and endoderm (embryonic layers) account for more than 95% of the tumor burden of humans?
What is a stem cell tumor?
How do germ cell tumors differ from all other tumors of humans?
Why are there different kinds of tumors and how many kinds of tumor are there?
How might a tumor classification be used to guide the development of new chemotherapeutic agents?
Is cancer prevention more important than cancer treatment?
How can our understanding of precancers lead to the eradication of all human cancers?
In the next few days, I will continue to include short excerpts from Neoplasms in my blogs.
-Jules Berman
Key words: tumors, tumour, neoplasms, neoplasia, carcinogenesis, tumor development, cancer research, neoplastic development, precancer preneoplasia, preneoplastic
Friday, September 26, 2008
Tumor Speciation in Neoplasms book
My latest book, Neoplasms: Principles of Development and Diversity, has just been published and is available from the Publisher's (Jones & Bartlett) web site.
The two categories of fundamental questions discussed in Neoplasms are:
1. Is cancer a single disease process that is manifested in many different types of tumors, or is cancer many different diseases, all related by excessive cell growth? If all cancer can be characterized by a single disease process, why haven't we isolated the process and cured cancer? If cancer is thousands of different diseases, how can we ever hope to cure all of the different kinds of cancer?
2. If cancer is characterized by the progressive accumulation of genetic abnormalities, and if every tumor specimen is genetically unique and distinct from every other tumor specimen, why do tumors fit into precisely named types? Worded another way, why does every unique tumor fall into one of the diagnostic entities (e.g., Warthin tumor, melanoma, lobular carcinoma of breast, and so on) that pathologists are taught to recognize?
Believe it or not, by tackling these two questions, it is possible to develop a practical strategy to eradicate cancer. Though there are thousands of distinct named neoplasms, all neoplasms can be sensibly grouped into biological classes, and these biological classes can be characterized by shared developmental pathways (including precancer/cancer transitions), shared functional pathways (including genetic and epigenetic features), and shared restraints (determined by the cell lineage of the neoplasm).
The book is divided into three major parts. The first part, Speciation, covers the causes of cancer, and why we see the kinds of restricted cancers that occur in man and animals. The concept of tumor speciation is key to building a classification of cancer, and it has been a constant wonder to me that the people who write cancer textbooks always accept the extant species of cancer as a "given" condition that does not require any deep thought or explanation. It is very important to understand why we see the species of tumors that we see. We cannot start thinking about how to classify cancers until we understand tumor speciation. The lack of any serious attention to the subject manifests itself in the popular classifications of cancer, which are basically just lists of tumors that occur in an anatomic region (e.g. tumors of head and neck).
The second part of the book is Classification. This section describes the different ways that cancers can be classified. In this section, I used a variety of informatics methods to build a classification of neoplasms. The classification can be downloaded by readers as an ontology (in RDF format), or as a plain-text file, or as an XML file. The supplementary materials are available.
None of this effort (i.e., understanding tumor speciation and constructing a neoplasm classification) has any value if it does not lead to the reduction of deaths from cancer. The last part of the book explains how a biologically relevant classification reduces the perceived complexity of cancer by assigning each tumor to one of several dozen classes of tumors that may be amenable to class-specific prevention, diagnosis, and treatment. This is the most important part of the book, because it suggests practical ways of eradicating cancer by applying pre-existing approaches (designed for individual cancers) to classes of cancer, using an available neoplasm classification.
The complete Table of Contents of Neoplasms: Principles of Development and Diversity is now available for review.
-© 2008 Jules Berman
The two categories of fundamental questions discussed in Neoplasms are:
1. Is cancer a single disease process that is manifested in many different types of tumors, or is cancer many different diseases, all related by excessive cell growth? If all cancer can be characterized by a single disease process, why haven't we isolated the process and cured cancer? If cancer is thousands of different diseases, how can we ever hope to cure all of the different kinds of cancer?
2. If cancer is characterized by the progressive accumulation of genetic abnormalities, and if every tumor specimen is genetically unique and distinct from every other tumor specimen, why do tumors fit into precisely named types? Worded another way, why does every unique tumor fall into one of the diagnostic entities (e.g., Warthin tumor, melanoma, lobular carcinoma of breast, and so on) that pathologists are taught to recognize?
Believe it or not, by tackling these two questions, it is possible to develop a practical strategy to eradicate cancer. Though there are thousands of distinct named neoplasms, all neoplasms can be sensibly grouped into biological classes, and these biological classes can be characterized by shared developmental pathways (including precancer/cancer transitions), shared functional pathways (including genetic and epigenetic features), and shared restraints (determined by the cell lineage of the neoplasm).
The book is divided into three major parts. The first part, Speciation, covers the causes of cancer, and why we see the kinds of restricted cancers that occur in man and animals. The concept of tumor speciation is key to building a classification of cancer, and it has been a constant wonder to me that the people who write cancer textbooks always accept the extant species of cancer as a "given" condition that does not require any deep thought or explanation. It is very important to understand why we see the species of tumors that we see. We cannot start thinking about how to classify cancers until we understand tumor speciation. The lack of any serious attention to the subject manifests itself in the popular classifications of cancer, which are basically just lists of tumors that occur in an anatomic region (e.g. tumors of head and neck).
The second part of the book is Classification. This section describes the different ways that cancers can be classified. In this section, I used a variety of informatics methods to build a classification of neoplasms. The classification can be downloaded by readers as an ontology (in RDF format), or as a plain-text file, or as an XML file. The supplementary materials are available.
None of this effort (i.e., understanding tumor speciation and constructing a neoplasm classification) has any value if it does not lead to the reduction of deaths from cancer. The last part of the book explains how a biologically relevant classification reduces the perceived complexity of cancer by assigning each tumor to one of several dozen classes of tumors that may be amenable to class-specific prevention, diagnosis, and treatment. This is the most important part of the book, because it suggests practical ways of eradicating cancer by applying pre-existing approaches (designed for individual cancers) to classes of cancer, using an available neoplasm classification.
The complete Table of Contents of Neoplasms: Principles of Development and Diversity is now available for review.
-© 2008 Jules Berman
Wednesday, September 3, 2008
Journal articles on the Developmental Lineage Classification and Taxonomy of Neoplasms
In the past few blog entries, I've announced the most recent version of the developmental lineage neoplasm classification, which is available for download.
The classification and taxonomy contains about 6,000 classified types of neoplasms and over 130,000 neoplasm names. The Classification is an open source computer-parsable data set that can be used to organize, collect, merge, share, analyze, understand, develop hypotheses, test hypotheses, and discover new information related to neoplasia. The classification is used extensively in software projects linked from my home page. It is the largest cancer nomenclature in existence and has been described in several journal articles:
Berman JJ. Tumor classification: molecular analysis meets Aristotle. BMC Cancer, BMC Cancer 2004, 4:10.Download manuscript
This article is among the all-time most-viewed articles in BMC Cancer, and, as of September 2008, has been downloaded about 15,000 times from BiomedCentral. Statistics Page
Berman JJ. Tumor taxonomy for the developmental lineage classification of neoplasms. BMC Cancer. 2004 Nov 30;4(1):88. Download manuscript
Berman JJ. Modern classification of neoplasms: reconciling
differences between morphologic and molecular approaches.
BMC Cancer 2005, 5:100. Download manuscript
-Jules Berman
key words: ontology, neoplasia, classification, medical terminology, medical terminologies,
The classification and taxonomy contains about 6,000 classified types of neoplasms and over 130,000 neoplasm names. The Classification is an open source computer-parsable data set that can be used to organize, collect, merge, share, analyze, understand, develop hypotheses, test hypotheses, and discover new information related to neoplasia. The classification is used extensively in software projects linked from my home page. It is the largest cancer nomenclature in existence and has been described in several journal articles:
Berman JJ. Tumor classification: molecular analysis meets Aristotle. BMC Cancer, BMC Cancer 2004, 4:10.Download manuscript
This article is among the all-time most-viewed articles in BMC Cancer, and, as of September 2008, has been downloaded about 15,000 times from BiomedCentral. Statistics Page
Berman JJ. Tumor taxonomy for the developmental lineage classification of neoplasms. BMC Cancer. 2004 Nov 30;4(1):88. Download manuscript
Berman JJ. Modern classification of neoplasms: reconciling
differences between morphologic and molecular approaches.
BMC Cancer 2005, 5:100. Download manuscript
-Jules Berman
key words: ontology, neoplasia, classification, medical terminology, medical terminologies,
Tuesday, September 2, 2008
Sample pages for formatted versions of Neoplasm Classification
As announced in a recent blog, the newest version of the free, open source, Developmental Lineage Classification and Taxonomy of Neoplasms has been released. This Classification contains about 135,000 different names of neoplasms classified under about 6,000 neoplasm concepts. It is the largest neoplasm nomenclature in existence.
The classification can be downloaded from:: http://www.julesberman.info/devclass.htm
The Classification is available in several different formats: XML, RDF and flat-file.
I have prepared three web pages that display short excerpts of each document style, so that you can quickly assess the different formats.
The excerpts are available at:
Flat-file: http://www.julesberman.info/plaintxt.htm
XML: http://www.julesberman.info/plainxml.htm
RDF (Resource Description Format): http://www.julesberman.info/plainrdf.htm
A search engine that permits look-ups of neoplasm names, retrieving synonyms and related terms from the Developmental Classificaiton, is available at: http://www.julesberman.info/neoget.htm
-Jules Berman
key words: ontology, classification, medical terminology, medical nomenclature, neoplasms, tumors, tumours, pathology
In June, 2014, my book, entitled Rare Diseases and Orphan Drugs: Keys to Understanding and Treating the Common Diseases was published by Elsevier. The book builds the argument that our best chance of curing the common diseases will come from studying and curing the rare diseases.
I urge you to read more about my book. There's a generous preview of the book at the Google Books site. If you like the book, please request your librarian to purchase a copy of this book for your library or reading room.
The classification can be downloaded from:: http://www.julesberman.info/devclass.htm
The Classification is available in several different formats: XML, RDF and flat-file.
I have prepared three web pages that display short excerpts of each document style, so that you can quickly assess the different formats.
The excerpts are available at:
Flat-file: http://www.julesberman.info/plaintxt.htm
XML: http://www.julesberman.info/plainxml.htm
RDF (Resource Description Format): http://www.julesberman.info/plainrdf.htm
A search engine that permits look-ups of neoplasm names, retrieving synonyms and related terms from the Developmental Classificaiton, is available at: http://www.julesberman.info/neoget.htm
-Jules Berman
key words: ontology, classification, medical terminology, medical nomenclature, neoplasms, tumors, tumours, pathology
In June, 2014, my book, entitled Rare Diseases and Orphan Drugs: Keys to Understanding and Treating the Common Diseases was published by Elsevier. The book builds the argument that our best chance of curing the common diseases will come from studying and curing the rare diseases.
I urge you to read more about my book. There's a generous preview of the book at the Google Books site. If you like the book, please request your librarian to purchase a copy of this book for your library or reading room.
Monday, September 1, 2008
New version of Precancer nomenclature now available
The precancer nomenclature has been described previously:
Berman JJ, Henson DE. Classifying the Precancers: A Meta Data Approach. BMC Medical Informatics and Decision Making 3:8, 2003.
The precancer nomenclature has been incorporated into the latest version of the Developmental Lineage Classification and Taxonomy of Neoplasms.
A search-engine for precancer terms is now available at the site that had served the precancer nomenclature:
http://www.julesberman.info/presum.htm
-Jules Berman
key words: nomenclature, medical nomenclature, classification, ontology, terminology, neoplasms, neoplasia, precancerous conditions, open source, free
Berman JJ, Henson DE. Classifying the Precancers: A Meta Data Approach. BMC Medical Informatics and Decision Making 3:8, 2003.
The precancer nomenclature has been incorporated into the latest version of the Developmental Lineage Classification and Taxonomy of Neoplasms.
A search-engine for precancer terms is now available at the site that had served the precancer nomenclature:
http://www.julesberman.info/presum.htm
-Jules Berman
key words: nomenclature, medical nomenclature, classification, ontology, terminology, neoplasms, neoplasia, precancerous conditions, open source, free
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