SETI bioastro: FW: SCIENCEWEEK EXPRESS June 15, 2001

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From: Larry Klaes (larry.klaes@incent.com)
Date: Mon Jun 18 2001 - 11:53:45 PDT


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Sent: Monday, June 18, 2001 11:36 AM
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Subject: SCIENCEWEEK EXPRESS June 15, 2001

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SCIENCEWEEK EXPRESS
An Abridged Version of SCIENCEWEEK

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June 15, 2001 -- Vol. 5 Number 24

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It is our responsibility as scientists, knowing
the great progress which comes from a satisfactory
philosophy of ignorance, the great progress which
is the fruit of freedom of thought, to proclaim
the value of this freedom, to teach how doubt is
not to be feared but welcomed and discussed, and
to demand this freedom as our duty to all coming
generations.

-- Richard P. Feynman (1918-1988)

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ScienceWeek Express, which you are now reading, is an abridged
version of SCIENCEWEEK. Read SCIENCEWEEK for complete reports,
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THIS WEEK IN SCIENCEWEEK:

1. CELL BIOLOGY:
ON THE TRANSFER OF MOLECULAR PROBES INTO CELLS
A major task of molecular biology is to identify the roles of
various proteins in cellular events. One method is to transfer
molecular probes into the cell, probes that modify or control
specific proteins. But most such probe molecules do not easily
penetrate cell membranes, so various methods have been developed
to achieve transfer in the laboratory.

2. CELL BIOLOGY: COOPERATIVE BEHAVIOR IN DIVIDING AMOEBA
At the end stage of binary fission, when connected daughter
amoebas have difficulty separating, the cells overcome this
problem by effectively calling upon a neighboring amoeba to help
them achieve separation. "The 'midwife' cell is chemotactically
recruited for this mechanical intervention in what is a
surprising example of primitive cooperation.

3. MEDICAL BIOLOGY: ON THE WAR ON CANCER
Ever since 1971, when President Nixon declared war on cancer,
oncologists and cancer patients have been caught in a cycle of
euphoria and despair as the prospect of new treatments has given
way to the sober realities of these treatments. The war on cancer
has turned out to be profoundly misconceived -- both in its
rhetoric and in its execution. ***(FULL TEXT BELOW)***

4. COSMOLOGY: THE EARLY UNIVERSE AND THE SZ EFFECT
Because the SZ effect is independent of distance, results of SZ
effect surveys will provide an incisive test of theories of the
structure and evolution of the Universe, as well as an
independent determination of fundamental cosmological parameters.

5. MATERIALS SCIENCE: SUPERCOOLED LIQUIDS
Despite the ancient history of glass, the molecular mechanisms
involved in liquids acquiring amorphous rigidity upon cooling are
not fully understood. One approach is that of the "energy
landscape" of the liquid -- the multidimensional surface
generated by the potential energy of the system as a function of
molecular coordinates.

6. QUANTUM PHYSICS:
ON THE UNCERTAINTY PRINCIPLE: WHO NEEDS HEISENBERG?
[An SW Commentary by Harry S. Lipkin (Weizmann Institute, IL)]
It was Einstein and not Heisenberg who opened the Pandora's box
of quantum-mechanical spookiness. Einstein tried vary hard to
close it afterwards, but he never succeeded. It is still there in
the next millennium.

7. IN FOCUS: ON CLAYS AND THE ORIGIN OF LIFE

8. FROM THE SCIENCEWEEK ARCHIVE:
MEDICINE: LOOKING BACKWARD 1000 YEARS

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The text below is abridged from ScienceWeek. Complete ScienceWeek
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other reports on the subject. To subscribe to the complete
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MEDICAL BIOLOGY: ON THE WAR ON CANCER
For the past 30 years, the phrase "war on cancer" has echoed in
the halls of government and popped in and out of the popular
press. "War" was declared a generation ago, but since that time
more than 15 million people have died of cancer in the US alone,
and the total cancer death rate has not significantly declined.
If this is a "war", it seems we are still far from winning it.
... ... Jerome Groopman (Harvard University, US), one of the
leading cancer researchers in the US, presents an essay on the
so-called "war on cancer", the author making the following
points.
     1) The author points out that important advances have been
made in oncology in recent years, and the current atmosphere of
hope is not without foundation. But it is also not without
precedent: ever since 1971, when President Nixon declared war on
cancer, oncologists and cancer patients have been caught in a
cycle of euphoria and despair as the prospect of new treatments
has given way to the sober realities of these treatments. The war
on cancer has turned out to be profoundly misconceived -- both in
its rhetoric and in its execution.
     2) The author points out that three decades after the
declaration of war, the high expectations of the early 1970s seem
almost willfully naive. This year alone, more than a million new
diagnoses of major cancers will be made and about 550,000
Americans will die of cancer, an average of 1500 a day. In the
course of a lifetime, one of every three American women will
develop a potentially fatal malignancy; for men, the odds are one
in two. Nevertheless, the triumphant rhetoric that animated the
war on cancer still shapes public opinion: many people believe
that cancer is, in essence, a single foe, that a single cure can
destroy it, and that the government is both responsible for and
capable of spearheading the campaign. "The military metaphors
have retained their potency -- even though they have proved to be
inappropriate and misleading."
     3) The author points out that in fact the principal benefits
from the war on cancer have been in other realms. The
technologies developed to identify cancer viruses in the 1970s
and 1980s coalesced in the new field of molecular biology, which
for the first time opened up the cell and its genetic blueprint
to examination. This revolutionary work on DNA also spawned a
highly profitable industry: using the tools developed via
contracts with the National Cancer Institute, biotechnology
companies have created lifesaving treatments for heart disease,
sepsis, colitis, and many other serious diseases. Equally
dramatic gains were made in AIDS research: the molecular
techniques and reagents used to search for human cancer viruses
proved essential to identifying HIV and mapping its genes. In
addition, the inventory of failed cancer drugs includes agents
like AZT, which proved beneficial in treating AIDS. These
unintended consequences of the war on cancer make it more
difficult to gauge its success or failure.
     4) The author suggests that the most promising results in
cancer research and treatment have stemmed from basic biological
investigations. And yet both Congress and the public continue to
view open-ended scientific investigations as nebulous, self-
indulgent, and wasteful of taxpayers' money, and are reluctant to
fund such research. For this reason, oncologists talk in terms of
imminent cures through directed research -- both in their
proposals for new projects and in their assessment of ongoing
work. The media attention that results further misleads the
public.
     5) The author concludes: "It is impossible to say which type
of currently intractable cancer will be cured first. In the next
10 years, the survival rate of people with a certain type of
melanoma or lung tumor or lymphoma or breast cancer may not
change. But it also might improve by 50 percent, or 90 percent.
Because of the uncertainty inherent in scientific discovery,
there is simply no way of knowing. Paradoxically, for cancer
patients and their families, this inability to predict the future
becomes their sustaining hope."
-----------
Jerome Groopman: The Thirty Years' War.
(The New Yorker 4 June 2001)
QY: Jerome Groopman: Harvard Univ. Medical School 617-432-1550.
-------------------
Summary by SCIENCE-WEEK http://scienceweek.com 15Jun01
For more information: http://scienceweek.com/swfr.htm
-------------------
Related Background:
MEDICAL BIOLOGY: ORIGINS OF CANCER
     In general, cancer involves a loss of normal cellular growth
control, the loss of control producing a growing tissue mass
called a "tumor" or "neoplasm". Uncontrolled growth occurs not
because the replication rate of cancer cells is always greater
than the replication rate of normal cells, but because of the
difference between the replication rate of cancer cells and the
rate of loss of cancer cells. In normal tissue, a precise balance
between replication rate and rate of loss is maintained; in a
growing neoplasm, this balance is absent and the replication rate
exceeds the rate of loss.
... ... Daniel Haber (Massachusetts General Hospital, US)
presents a review of the etiology of breast cancer, the author
making the following points concerning the origins of cancer in
general:
     1) The author points out that cancer results from the
accumulation of mutations in genes that regulate cellular
proliferation. These mutations can occur early in the process of
malignant transformation or later, during progression to an
invasive carcinoma. The earliest mutations occur in the *germ
line, as in the case of cancer-prone families. In these
instances, the inheritance of a mutated *allele is commonly
followed by the loss of the second allele from a somatic cell,
leading to the inactivation of a tumor-suppressor gene and
triggering malignant transformation. A classic example is
hereditary retinoblastoma, in which there is inheritance of a
mutant germ-line _RBI_ allele (a *tumor-suppressor gene) followed
by somatic mutation of the normal _RBI_ allele.
     2) Genes important to the development of cancer regulate
diverse cellular pathways, including the progression of cells
through the *cell cycle, resistance to programmed cell death
(apoptosis), and the response to signals that direct *cellular
differentiation. Moreover, the inactivation of genes that
contribute to the stability of the genome itself can favor the
acquisition of errors in other genes that regulate proliferation.
     3) Errors in DNA that arise during normal replication of the
molecule (nucleotide mismatches), or that are induced by ionizing
radiation or genotoxic drugs, can cause mutations in coding
sequences or breaks in double-stranded chromosomal DNA. If the
nucleotide mismatch is not repaired before a round of DNA
replication occurs, that mutation is transmitted to daughter
cells. An unrepaired break in double-stranded DNA can cause a
mitotic catastrophe when the cell attempts to segregate broken
chromosomes. Studies of yeast have identified genes that sense
damaged DNA and cause the arrest of the cell cycle, which allows
time for the molecular defect to be repaired. These genes operate
at several specific "checkpoints" in the cell cycle as a means of
ensuring genomic integrity before DNA is synthesized.
     4) The most critical checkpoint gene yet identified that is
related to cancer in humans is the tumor suppressor gene _p53_.
This gene is not essential for cell viability, but it is critical
for monitoring damage to DNA. Inactivation of _p53_ is an early
step in the development of many kinds of tumors. In cases of
cancer without _p53_ mutations, there are frequently alterations
in two other genes (_MDM2_ and _p14_) that regulate the
expression of _p53_.
-----------
Daniel Haber: Roads leading to breast cancer.
(New England J. Med. 23 Nov 00 343:1566)
QY: Daniel Haber: Massachusetts General Hospital, Boston, MA
02114 US.
-----------
Text Notes:
... ... *germ line: A germ cell is any cell from which gametes
(sperm cells and egg cells) are derived. All other cells are
called "somatic" cells. In general, the term "germ line" refers
to the line of differentiated germ cells.
... ... *allele: An allele is one of two or more forms of a
given gene that control a particular characteristic, with the
alternative forms occupying corresponding loci on homologous
chromosomes.
... ... *tumor-suppressor gene: In general, cancer genes have
been divided into 2 classes, proto-oncogenes and tumor suppressor
genes. Proto-oncogenes are genes that sustain activating changes
in human cancer. These changes may take the form of point
mutations or gene rearrangements that lead to increased or
uncontrolled activity of the encoded protein, or they make take
the form of gene amplification, which results in increased levels
of protein expression. In contrast, tumor suppressor genes are
characterized by inactivating changes in human cancer, typically
point mutations that result in truncation or functional
inactivation of the encoded protein, or gross deletions of
chromosomal fragments carrying these genes.
... ... *cell cycle: In this context, the term "cell cycle"
refers to the entire life history of a single cell from mitosis
to mitosis, including the sequence of intervening phases.
... ... *cellular differentiation: In general, in this context,
the term "differentiation" refers to the structural and
functional specialization of cells, developmental cell
specialization (morphology and biochemistry) resulting from
activation of specific parts of the cell genome.
-------------------
Summary & Notes by SCIENCE-WEEK http://scienceweek.com 5Jan01
For more information: http://scienceweek.com/swfr.htm
-------------------
Related Background:
MEDICAL BIOLOGY:
ENVIRONMENT VS. HEREDITY IN THE CAUSATION OF CANCER
     There is considerable public confusion concerning the origin
of cancer. What we call "cancer" is essentially a set of diseases
of genes (see related background material below), but most
cancers are not inherited: the gene damage responsible for most
cancers is apparently produced by environmental factors affecting
the genetic information that controls replication of ordinary
tissue cells. In other words, the damaged gene (or genes)
responsible for a cancer is usually not inherited; most often the
damage is produced (or occurs spontaneously) during the life of
the individual.
     Certain types of cancer are indeed apparently familial,
determined primarily by hereditary factors, but most types of
cancer are non-familial ("sporadic"), with an unclear
contribution of hereditary factors to the response of the
individual to environmental factors. In general, studies of twins
make it possible to estimate the overall contribution of
inherited genes to the development of cancer, and such studies
form the basis of current views of the heritability of various
cancers.
... ... P. Lichtenstein et al (9 authors at 7 installations, SE
DK FI) now report a study of data on 44,788 pairs of twins listed
in the Swedish, Danish, and Finnish twin-registries, the purpose
of the study to assess the risks of cancer at 28 anatomical sites
for the twins of persons with cancer. Statistical modeling was
used to estimate the relative importance of heritable and
environmental factors in causing cancer at 11 of those sites. The
authors conclude as follows: "We conclude that the overwhelming
contributor to the causation of cancer in the population of twins
that we studied was the environment. For some of the forms of
cancer, in which a shared environment is important, it may be
possible to find clues in studies of childhood environment or
long-lasting family habits. The relatively large heritability
proportions for cancers at some sites, despite the wide
confidence intervals, suggest major gaps in our understanding of
hereditable cancer. Even for cancers for which there is
statistically significant evidence of a heritable component, most
pairs of twins were discordant for the cancer -- indicating that,
on the population level, the increase in the risk of cancer even
among close relatives of affected persons is generally moderate."
-----------
P. Lichtenstein et al: Environmental and heritable factors in the
causation of cancer.
(New England J. Med. 13 Jul 00 343:78)
QY: Paul Lichtenstein [paul.lichtenstein@mep.ki.se]
-------------------
Summary by SCIENCE-WEEK http://scienceweek.com 28Jul00
For more information: http://scienceweek.com/swfr.htm
-------------------
Related Background:
MEDICAL BIOLOGY: ON MUTATIONS AND CANCER
The term "cancer", which means "crab" in Latin, was introduced by
Hippocrates (460-370 B.C.) to describe diseases in which tissues
grow and spread unrestrained throughout the body, eventually
causing death. Cancers can originate in almost any tissue of the
body, including nerve, muscle, blood, connective tissue, etc.
Depending on the cell type involved, cancers are grouped into 3
main categories: a) carcinomas, the most common types of cancer,
arise from the *epithelial cells that cover external and internal
body surfaces, with lung, breast, and colon cancers the most
frequent cancers of this type; b) sarcomas originate in
supporting tissues of *mesodermal origin, such as bone,
cartilage, fat, connective tissue, and muscle; c) lymphomas and
leukemias arise from cells of blood and *lymphatic origin, the
term "leukemia" used when such cancer cells circulate in large
numbers in the bloodstream rather than growing mainly as solid
masses of tissue. Cancer is a disease of the genomic apparatus of
the cell, in particular of the growth-regulation apparatus, and
considering the vast number of activities that must be
coordinated and regulated by the genomic apparatus during the
lifetime of each cell, it is not surprising that malfunctions
arise. In general, cancer is the most prominent of the many
diseases arising from aberrations in cell function, with more
than 25 percent of people in the US now expected to develop
cancer in their lifetime.
... ... C.R. Boland and L. Ricciardiello (2 installations, US)
present a review of current research on the genomic basis of
cancer, the authors making the following points:
     1) It has been known during most of this century that cancer
is often associated with visible derangements in the nucleus of
the cell. The cells of solid tumors commonly exhibit chromosome
duplications, deletions, and rearrangements, but before the
organization of the human cell nucleus was understood, these
chromosome aberrations were difficult to categorize and were of
little help in understanding the biological basis of cancer.
     2) Within a few decades after the discovery of the structure
of DNA, cancer-related genes (oncogenes) were isolated, and these
were frequently found to be mutant versions of normal cellular
genes in which an activating *point mutation or an aberrant
*genetic amplification process resulted in a gain of function for
that gene product, and a growth advantage for that aberrant cell.
But as more and more oncogenes were identified, researchers
realized that tumor growth was also associated with loss of
function of certain "tumor suppressor genes". These tumor
suppressor genes were often inactivated by their deletion from
the nucleus, and the phrase "loss of heterozygosity" (LOH) was
applied to genetic loci in which both *alleles were present in
normal tissues, but one copy was lost in tumor tissue. In many
instances, tumor suppressor genes were first identified by virtue
of germ-line mutations that were present at a high frequency in a
rare tumor, e.g., retinoblastoma, but it soon became apparent to
researchers that many tumor suppressor genes were associated with
a variety of different tumors, many of which were not rare at
all.
     3) There are no oncogenes or tumor suppressor genes that are
activated or deleted in and from all cancers. Even tumors of a
single organ rarely have uniform genetic alterations, although
tumor types from one specific organ do have a tendency to share
mutations in certain genes or in different genes within a single
growth-regulatory pathway.
     4) At the present time, it is not known how many critical
mutations are required to convert a single normal cell into a
malignant cell. Human cells have been difficult to transform in
vitro, and the basis for this difficulty is not yet understood.
The simplest model of tumorigenesis is as follows:
... ... a) Human cells experience a certain number of mutations
each day as a result of exposure to carcinogens or as a result of
ordinary biological degradation, both of which can alter
nucleotide sequences. Errors will also occur during new DNA
synthesis and in the process of disentangling the chromosomes
during *mitosis. Most of these errors would be either irrelevant
to the life of the cell or deleterious because of the loss of a
gene critical for cellular viability.
... ... b) By chance, an occasional genomic mutation might create
a growth advantage for a cell, permitting increased net cellular
growth, because of increased proliferation or a reduction in
programmed cell death (reduction in apoptosis), with a resulting
*clonal expansion of that lineage. A second genomic alteration
might then occur within this expanding clone, again by chance,
providing an additional growth advantage for that cell and its
progeny. By virtue of these two advantages, the cells of this
clone would eventually overgrow neighboring cells, creating yet
another expanding clone. This scenario would repeat as a
consequence of each new mutation that provided an additional
growth advantage. The accumulation of these growth promoting
mutations is the basis of the current view of "multistep
carcinogenesis".
-----------
C.R. Boland and L. Ricciardiello: How many mutations does it take
to make a tumor?
(Proc. Natl. Acad. Sci. US 21 Dec 99 96:14675)
QY: C. Richard Boland [crboland@ucsd.edu]
-----------
Text Notes:
... ... *epithelial cells: In animals, "epithelial cells"
compose the cell layers that form the interface between a tissue
and the external environment, for example, the cells of the skin,
the lining of the intestinal tract, and the lung airway passages.
... ... *mesodermal: In the embryos of higher animals, there
occurs the transformation of a single-layer "blastula" into a
3-layered "gastrula" consisting of ectoderm (outermost layer),
mesoderm (middle layer), and endoderm (innermost layer)
surrounding a cavity with one opening. The 3 layers are called
the "germ layer", and these layers, via further cell
differentiation and proliferation, determine the development of
all the major body systems and organs.
... ... *lymphatic: The lymphatic system is a complex network
for the distribution of lymph fluid (which is similar to blood
plasma -- blood without red cells). Lymph is collected by
drainage from the tissues throughout the body, flows in the
lymphatic vessels through the lymph nodes, and is eventually
added to the venous blood circulation.
... ... *point mutation: A minor changes in the genome; a single
base-pair substitution.
... ... *genetic amplification process: The production, by
various means, of additional copies of a stretch of genomic DNA.
... ... *alleles: One of two or more forms of a given gene that
control a particular characteristic, with the alternative forms
occupying corresponding loci on homologous chromosomes.
... ... *mitosis: Programmed division of the nucleus during cell
replication.
... ... *clonal expansion: This refers to the expansion of a
population of cells all derived from repeated replications of
progeny of a single cell.
-------------------
Summary & Notes by SCIENCE-WEEK http://scienceweek.com 14Jan00
For more information: http://scienceweek.com/swfr.htm

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as subject and "manual remove swx" as text.)
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