Posted: April 24th, 2025

Analysis help

I have a PDF file for analysis, 7-8 sentences needed in a form of a memo (link below), so around 250 words in total should be the maximum word count, I’m fine with less.
Format: The memo should be in the format of a short letter to your boss, the Head of Drug Discovery. You may be creative with the names of people and companies if you wish. If you are unsure of the correct formatting for a memo, check out these

templates

.

• Length: The Memo should be approximately two paragraphs in length. Do not exceed 400 words. Managers don’t like to read lengthy articles. Keep everything very clear and brief. 
• Content: The Head of Drug Discovery does not remember all of the details about how enzymes work. The Memo needs to:

  Define enzymes. 
  Explain how enzymes function as catalysts for biochemical reactions.
  Discuss how reactions can be inhibited by inhibiting enzymes. (Note: enzymes themselves do NOT inhibit chemical reactions. Another inhibitory ligand binds to the enzyme, preventing it from catalyzing the reaction.) 
  Explain the importance of drugs that could be developed to interfere with the structure of telomerase to treat cancer. 
  https://create.microsoft.com/en-us/templates/memo

2/4/2021 Telomeres, Telomerase and Cancer [Reprint] – Scientific American

https://www.scientificamerican.com/article/telomeres-telomerase-and/ 1/15

H E A L T H

Telomeres, Telomerase and Cancer [Reprint]
An unusual enzyme called telomerase acts on parts of chromosomes known as telomeres. The

enzyme has recently been found in many human tumors and is being eyed as a new target for cancer
therapy

By Carol W. Greider, Elizabeth H. Blackburn on October 5, 2009

Editor’s note: We are posting the main text of this article from the February 1996 issue
of Scientific American for all our readers because the authors have won the 2009 Nobel
Prize in Physiology or Medicine. Subscribers to the digital archive may obtain a full
PDF version, complete with artwork and captions.

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2/4/2021 Telomeres, Telomerase and Cancer [Reprint] – Scientific American

https://www.scientificamerican.com/article/telomeres-telomerase-and/ 2/15

Often in nature things are not what they seem. A rock on the seafloor may be a
poisonous fish; a beautiful flower in a garden may be a carnivorous insect lying in wait
for prey. This misleading appearance extends to certain components of cells, including
chromosomes—the strings of linear DNA that contain the genes. At one time, the DNA at
the ends of chromosomes seemed to be static. Yet in most organisms that have been
studied, the tips, called telomeres, are actually ever changing; they shorten and lengthen
repeatedly.

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During the past 15 years, investigation of this unexpected flux has produced a number of
surprising discoveries. In particular, it has led to identification of an extraordinary
enzyme named telomerase that acts on telomeres and is thought to be required for the
maintenance of many human cancers. This last finding has sparked much speculation
that drugs able to inhibit the enzyme might combat a wide array of malignancies. The
research also opens the possibility that changes in telomere length over time may
sometimes play a role in the aging of human cells.

Modern interest in telomeres and telomerase has its roots in experiments carried out in
the 1930s by two remarkable geneticists: Barbara McClintock, then at the University of

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2/4/2021 Telomeres, Telomerase and Cancer [Reprint] – Scientific American

https://www.scientificamerican.com/article/telomeres-telomerase-and/ 3/15

Missouri at Columbia, and Hermann J. Muller, then at the University of Edinburgh.
Working separately and with different organisms, both investigators realized that
chromosomes bore a special component at their ends that provided stability. Muller
coined the term “telomere,” from the Greek for “end” (telos ) and “part” ( meros ).
McClintock noted that without these end caps, chromosomes stick to one another,
undergo structural changes and misbehave in other ways. These activities threaten the
survival and faithful replication of chromosomes and, consequently, of the cells housing
them.

It was not until the 1970s, however, that the precise makeup of the telomere was
determined. In 1978 one of us (Blackburn), then working with Joseph G. Gall of Yale
University, found that the telomeres in Tetrahymena, a ciliated, single-cell pond
dweller, contained an extremely short, simple sequence of nucleotidesÑ TTGGGG —
repeated over and over. (Nucleotides are the building blocks of DNA; they are generally
denoted as single letters representing the chemical bases that distinguish one nucleotide
from another. The base in T nucleotides is thymine; that in G nucleotides is guanine.)

Since then, scientists have characterized the telomeres in a host of creatures, including
animals, plants and microorganisms. As is true of Tetrahymena, virtually all telomeres—
including those of mice, humans and other vertebrates— contain repeated short
subunits often rich in T and G nucleotides [see “The Human Telomere,” by Robert K.
Moyzis; SCIENTIFIC AMERICAN, August 1991]. For instance, human and mouse
telomeres feature the sequence TTAGGG; those of roundworms feature TTAGGC. ( A
stands for adenine, C for cytosine.)

2/4/2021 Telomeres, Telomerase and Cancer [Reprint] – Scientific American

https://www.scientificamerican.com/article/telomeres-telomerase-and/ 4/15

In Search of Telomerase

 The telomerase enzyme that is the object of so much attention today was found when
comparisons of telomere length suggested such an enzyme could resolve a long-standing
puzzle in biology. By the early 1980s investigations had revealed that, for some reason,
the number of repeated subunits in telomeres differs between organisms and even
between different cells in the same organism. Moreover, the number can fluctuate in a
given cell over time. (Every species, however, has a characteristic average. In
Tetrahymena, the average telomere has 70 repeats; in humans, 2,000.) The observed
heterogeneity led Blackburn, who had moved to the University of California at Berkeley,
Jack W. Szostak of Harvard University and Janis Shampay of Berkeley to propose a new
solution to what has been called the end-replication problem.

The problem has to do with the fact that cells must replicate their genes accurately
whenever they divide, so that each so-called daughter cell receives a complete set.
Without a full set of genes, a daughter cell may malfunction and die. (Genes are those
sequences of nucleotides that give rise to proteins and RNA, the molecules that carry out
most cellular functions. The genes in a chromosome are scattered throughout the large
expanse of DNA that is bounded by the chromosome’s two telomeres.)

In 1972 James D. Watson, working at both Harvard and Cold Spring Harbor Laboratory,
noted that DNA polymerases, the enzymes that replicate DNA, could not copy linear

A D V E R T I S E M E N T

2/4/2021 Telomeres, Telomerase and Cancer [Reprint] – Scientific American

https://www.scientificamerican.com/article/telomeres-telomerase-and/ 5/15

chromosomes all the way to the tip. Hence, the replication machinery had to leave a
small region at the end (a piece of the telomere) uncopied. In theory, if cells had no way
to compensate for this quirk, chromosomes would shorten with each round of cell
division. Eventually, the erosion would eliminate the telomeres and critical genes in
some generation of the cells. These cells would thus perish, spelling the end of that
cellular lineage. Clearly, all single-cell species subject to such shortening manage to
counteract it, or they would have vanished long ago. So do germ-line cells (such as the
precursors of sperm and eggs), which perpetuate the species in multicellular organisms.
But how do such cells protect their telomeres?

For Blackburn, Szostak and Shampay, the observed fluctuations in telomere length were
a sign that cells attempt to maintain telomeres at a roughly constant size. Yes, telomeres
do shorten during cell division, but they are also lengthened by the attachment of newly
synthesized telomeric subunits. The researchers suspected that the source of these
additional repeats was some undiscovered enzyme capable of a trick that standard DNA
polymerases could not perform.

When cells replicate their chromosomes, which consist of two strands of DNA twisted
around each other, they begin by separating the double helix. The polymerases use each
of these “parent” strands as a template for constructing a new partner. The special
enzyme the workers envisioned would be able to build extensions to single strands of
DNA from scratch, without benefit of an existing DNA template.

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2/4/2021 Telomeres, Telomerase and Cancer [Reprint] – Scientific American

https://www.scientificamerican.com/article/telomeres-telomerase-and/ 6/15

In 1984 the two of us, working in Blackburn’s laboratory at Berkeley, set out to discover
whether this putative telomere-lengthening enzyme—telomerase —actually existed. To
our delight, we found it did. When we mixed synthetic telomeres with extracts of
Tetrahymena cells, the telomeres gained added subunits, just as would be expected if
the proposed enzyme were present.

Within the next several years we and our colleagues learned much about how telomerase
works. Like all polymerases and virtually all enzymes, it consists mainly of protein, and
it requires that protein to function. Uniquely, though, it also includes a single molecule
of RNA (close cousin to DNA) that contains the critical nucleotide template for building
telomeric subunits. Telomerase places the tip of one strand of DNA on the RNA,
positioning itself so that the template lies adjacent to that tip. Then the enzyme adds one
DNA nucleotide at a time until a full telomeric subunit is formed. When the subunit is
complete, telomerase can attach another by sliding to the new end of the chromosome
and repeating the synthetic process.

Telomerase and Human Aging

In 1988 Greider left Berkeley for Cold Spring Harbor Laboratory, and later our groups
and others found telomerase in ciliates distinct from Tetrahymena, as well as in yeast,
frogs and mice. In 1989 Gregg B. Morin of Yale also discovered it, for the first time, in a
human cancer cell line—that is, in malignant cells maintained for generations in culture

A D V E R T I S E M E N T

2/4/2021 Telomeres, Telomerase and Cancer [Reprint] – Scientific American

https://www.scientificamerican.com/article/telomeres-telomerase-and/ 7/15

dishes. Today it is evident that telomerase is synthesized by nearly all organisms with
nucleated cells. The precise makeup of the enzyme can differ from species to species, but
each version possesses a species-specific RNA template for building telomeric repeats.

The importance of telomerase in many single-cell organisms is now indisputable. Such
organisms are immortal in that, barring accidents or geneticists meddling in their lives,
they can divide indefinitely. As Guo-Liang Yu in Blackburn’s research group
demonstrated in 1990, Tetrahymena needs telomerase in order to retain this
immortality. When the enzyme is altered, telomeres shrink and cells die. Blackburn’s
team and others have similarly demonstrated in yeasts that cells lacking telomerase
undergo telomere shortening and perish. But what role does telomerase play in the
human body, which consists of a myriad of cell types and is considerably more complex
than Tetrahymena or yeast?

Surprisingly, many human cells lack telomerase. Greider and others made this discovery
in the late 1980s, when they pulled together the threads of research that investigators in
Philadelphia had initiated more than 25 years earlier. Before the 1960s, human cells that
replicated in the body were thought to be capable of dividing endlessly. But then
Leonard Hayflick and his co-workers at the Wistar Institute demonstrated unequivocally
that this notion was incorrect. Today it is known that somatic cells (those not part of the
germ line) derived from human newborns will usually divide 80 to 90 times in culture,
whereas those from a 70-year-old are likely to divide only 20 to 30 times. When human
cells that are normally capable of dividing stop reproducing—or, in Hay- flick’s words,
become “senescent”—they look different and function less eÛciently than they did in
youth, and after a while they die.

2/4/2021 Telomeres, Telomerase and Cancer [Reprint] – Scientific American

https://www.scientificamerican.com/article/telomeres-telomerase-and/ 8/15

In the 1970s a Soviet scientist named A. M. Olovnikov linked this programmed cessation
of cell division to the end-replication problem. He proposed that human somatic cells
might not correct the chromosomal shortening that occurs when cells replicate their
DNA. Perhaps division ceased when cells discerned that their chromosomes had become
too short.

We were unaware of Olovnikov ‘s ideas until 1988, when Calvin B. Harley, then at
McMaster University, brought them to Greider’s attention. Intrigued, Greider, Harley
and their collaborators decided to see if chromosomes do get shorter in human cells over
time.

Sure enough, most normal somatic cells they examined lost segments of their telomeres
as they divided in culture, a sign that telomerase was not active. Similarly, they and
Nicholas D. Hastie’s group at the Medical Research Council (MRC) in Edinburgh found
that telomeres in some normal human tissues shrink as people age. (Reassuringly,
Howard J. Cooke, also at the MRC in Edinburgh, had shown that telomeres are kept
intact in the germ line.) These results indicated that human cells might “count” divisions
by tracking the number of telomeric repeats they lose, and they might stop dividing
when telomeres decline to some critical length. But definitive proof for this possibility
has not yet been obtained.

A D V E R T I S E M E N T

2/4/2021 Telomeres, Telomerase and Cancer [Reprint] – Scientific American

https://www.scientificamerican.com/article/telomeres-telomerase-and/ 9/15

Could the reduction of telomeres and of proliferative capacity over time be a cause of
human aging? It is probably not the main cause. After all, cells can usually divide more
times than is required in a human life span. Nevertheless, the functioning of the older
body may at times be compromised by the senescence of a subset of cells. For instance,
local wound healing could be impaired by a reduction in the number of cells available to
build new skin at a site of injury, and a reduction in the number of certain white blood
cells could contribute to age-related declines in immunity. Further, it is known that
atherosclerosis typically develops where blood vessel walls have been damaged. It is
conceivable that cells at repeatedly injured sites could finally “use up” their replicative
capacity, so that the vessels ultimately fail to replace lost cells. Then damage would
persist, and atherosclerosis would set in.

The Cancer Connection

Some investigators suspect that the loss of proliferative capacity observed in human cells
lacking telomerase may have evolved not to make us decrepit but to help us avoid
cancer. Cancers arise when a cell acquires multiple genetic mutations that together cause
the cell to escape from normal controls on replication and migration. As the cell and its
offspring multiply uncontrollably, they can invade and damage nearby tissue. Some may
also break away and travel to parts of the body where they do not belong, establishing
new malignancies (metastases) at distant sites. In theory, a lack of telomerase would
retard the growth of tumors by causing continually dividing cells to lose their telomeres
and to succumb before they did much damage. If cancer cells made telomerase, they
would retain their telomeres and would potentially survive indefinitely.

2/4/2021 Telomeres, Telomerase and Cancer [Reprint] – Scientific American

https://www.scientificamerican.com/article/telomeres-telomerase-and/ 10/15

The notion that telomerase might be important to the maintenance of human cancers
was discussed as early as 1990. But the evidence did not become compelling until
recently. In 1994 Christopher M. Counter, Silvia Bacchetti, Harley and their colleagues
at McMaster showed that telomerase was active not only in cancer-cell lines maintained
in the laboratory but in ovarian tumors in the human body. Later that year groups led by
Harley, who had moved to Geron Corporation in Menlo Park, Calif., and by Jerry W.
Shay of the University of Texas Southwestern Medical Center at Dallas detected
telomerase in 90 of 101 human tumor samples (representing 12 tumor types) and in
none of 50 samples of normal somatic tissue (representing four tissue types).

Even before such evidence was obtained, however, researchers had begun exploring
some of the details of how telomerase might contribute to cancer. That work suggests
telomerase probably becomes active after a cell has already lost its brakes on
proliferation.

The first clue was an initially mystifying discovery made independently by Titia de
Lange, now at the Rockefeller University, and by Hastie’s group. In 1990 these
investigators reported that telomeres in human tumors were shorter than telomeres in
the normal surrounding tissue—sometimes dramatically so.

Studies by Greider’s, Bacchetti’s and Harley’s laboratories explained why the telomeres
were so small. The teams had induced normal cells from humans to make a viral protein

A D V E R T I S E M E N T

2/4/2021 Telomeres, Telomerase and Cancer [Reprint] – Scientific American

https://www.scientificamerican.com/article/telomeres-telomerase-and/ 11/15

causing cells to ignore the alarm signals that usually warn them to stop dividing. The
treated cells continued to proliferate long after they would normally enter senescence. In
most of the cells, telomeres shortened drastically, and no telomerase was detected;
eventually death ensued. Some cells, however, persisted after their siblings died and
became immortal. In these immortal survivors, telomeres were maintained at a
strikingly short length, and telomerase was present.

These outcomes imply that telomeres in cancer cells are small because cells synthesize
telomerase only after they have already begun to replicate uncontrollably; by then, the
cells have presumably lost a substantial number of telomeric subunits. When the enzyme
is finally activated, it stabilizes the severely clipped telomeres, allowing overly prolific
cells to become immortal.

These findings and others have led to an attractive but still hypothetical model for the
normal and malignant activation of telomerase by the human body. According to this
model, telomerase is made routinely by cells of the germ line in the developing embryo.
Once the body is fully formed, however, telomerase is repressed in many somatic cells,
and telomeres shorten as such cells reproduce. When telomeres decline to a threshold
level, a signal is emitted that prevents the cells from dividing further.

If, however, cancer-promoting genetic mutations block issuance of such safety signals or
allow cells to ignore them, cells will bypass normal senescence and continue to divide.
They will also presumably continue to lose telomeric sequences and to undergo
chromosomal alterations that allow further, possibly carcinogenic mutations to arise.
When telomeres are completely or almost completely lost, cells may reach a point at
which they crash and die.

But if the genetic derangements of the pre-crisis period lead to the manufacture of
telomerase, cells will not completely lose their telomeres. Instead the shortened
telomeres will be rescued and maintained. In this way, the genetically disturbed cells will
gain the immortality characteristic of cancer.

This scenario has generally been borne out by the evidence, although, once again, things
may not be entirely as they seem. Some advanced tumors lack telomerase, and some
somatic cells—notably the white blood cells known as macrophages and lymphocytes —

2/4/2021 Telomeres, Telomerase and Cancer [Reprint] – Scientific American

https://www.scientificamerican.com/article/telomeres-telomerase-and/ 12/15

have recently been found to make the enzyme. Nevertheless, on balance, the collected
evidence suggests that many tumor cells require telomerase in order to divide
indefinitely.

Prospects for Cancer Therapy

The presence of telomerase in various human cancers and its absence in many normal
cells mean the enzyme might serve as a good target for anticancer drugs. Agents able to
hobble telomerase might kill tumor cells (by allowing telomeres to shrink and disappear)
without disrupting the functioning of many normal cells. In contrast, most existing
anticancer therapies disturb normal cells as well as malignant ones and so are often
quite toxic. Further, because telomerase occurs in numerous cancers, such agents might
work against a broad array of tumors.

These exciting possibilities are now being actively explored by pharmaceutical and
biotechnology companies. Nevertheless, a number of questions must be answered. For
instance, researchers need to determine which normal cells (beyond the few already
identified) make telomerase, and they need to assess the importance of the enzyme to
those cells. If telomerase is crucial, drugs that interfere with it might in fact prove
unacceptably toxic. The shortness of telomeres in certain tumor cells may obviate this
problem, however. Telomerase- inhibiting agents might cause cancer cells to lose their
telomeres and die well before normal cells, with their much longer telomeres, lose
enough of their telomeres to suffer any ill effects.

Investigators must also demonstrate that inhibition of telomerase can destroy
telomerase-producing tumors as expected. Last September, Harley, Greider and their
co-workers showed that an inhibitory agent could cause the telomeres of cultured tumor
cells to shrink; the affected cells died after about 25 cycles of cell division. Blackburn,
now at the University of California at San Francisco, and her group have found, however,
that cells sometimes compensate for the loss of telomerase. They repair their shortened
ends by other means, such as by a process called recombination, in which one
chromosome obtains DNA from another. If activation of alternative, “telomere-
salvaging” pathways occurs frequently in human tumors, therapy targeted to telomerase
would fail.

2/4/2021 Telomeres, Telomerase and Cancer [Reprint] – Scientific American

https://www.scientificamerican.com/article/telomeres-telomerase-and/ 13/15

Studies of animals should help resolve such concerns. They should also help reveal
whether inhibitors of telomerase will eliminate tumors in the living body and whether
they will do so quickly enough to prevent cancers from injuring critical tissue.

To develop agents that will block telomerase in the human body, investigators must also
have a sharper picture of exactly how the enzyme functions. How does it attach to DNA?
How does it “decide” on the number of telomeric subunits to add? DNA in the nucleus is
studded with all manner of proteins, including some that specifically bind to the
telomere. What part do telomerebinding proteins play in controlling the activity of
telomerase? Would altering their activity disrupt telomere elongation? Within the next
10 years we expect to learn a great deal about the interactions among the various
molecules that influence telomere length.

Research into the regulation of telomere size could also yield benefits beyond new
therapies for cancer. A popular approach to gene therapy for various diseases involves
extracting cells from a patient, inserting the desired gene and then returning the
genetically corrected cells to the patient. Frequently, though, the extracted cells
proliferate poorly in the laboratory. Perhaps insertion of telomerase alone or in
combination with other factors would temporarily enhance replication capacity, so that
larger numbers of therapeutic cells could be delivered to the patient.

Modern research into telomeres has come a long way from the initial identification of
repetitive DNA on the ends of chromosomes in a unicellular pond dweller. Elongation of
telomeres by telomerase, initially considered to be merely a “cute” mechanism by which
some single-cell creatures maintain their chromosomes, has proved, as ever, to be other
than it seemed. Telomerase is, in fact, the predominant means by which nucleated cells
of most animals protect their chromosomal end segments. And, now, study of this once
obscure process may lead to innovative strategies for fighting a range of cancers.

In the early 1980s scientists would not have set out to identify potential anticancer
therapies by studying chromosome maintenance in Tetrahymena. The research on
telomerase reminds us that in studies of nature one can never predict when and where
fundamental processes will be uncovered. You never know when a rock you find will
turn out to be a gem.

2/4/2021 Telomeres, Telomerase and Cancer [Reprint] – Scientific American

https://www.scientificamerican.com/article/telomeres-telomerase-and/ 14/15

F O L LOW U S

S C I E N T I F I C A M E R I CA N A R A B I C

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A B O U T T H E A U T H O R ( S )

CAROL W. GREIDER and ELIZABETH H. BLACKBURN began collaborating in 1983,
when Greider joined Blackburn’s laboratory at the University of California, Berkeley.
Greider, who earned her PhD in molecular biology from U.C. Berkeley in 1987, is senior
staff scientist at Cold Spring Harbor Laboratory. Blackburn holds a 1975 doctorate in
molecular biology from the University of Cambridge. She has been a professor of
microbiology and immunology at the University of California, San Francisco, since 1990
and department chair since 1993.

N E W S L E T T E R

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