War on Cancer

On July 21, 2004, in Cancer
Substantial investments by pharmaceutical firms in biotech firms that are developing cancer drugs
is bad news for cancer, as are major efforts to improve on the first generation
of anti-angiogenesis drugs,
such as one that destroys a tumor’s blood supply without affecting the patient’s
normal blood vessels, and an Abbott Labs cancer drug showing promise after initial
trial setbacks.

A more direct and easier route than angiolytics to curing cancer might be
through a virus genetically-modified to kill
cancer but not normal cells
, which has proved potent, safe for healthy
tissue, and effective in the test tube.

We wrote in May about a method of detecting cancer molecules. Another new
method less ambitiously detects cancer masses as small as a millimeter and zaps them
directly with chemo.

Even if targeted cancer drugs
take as long as a decade to replace chemotherapy completely, they could still
result in lower chemotherapy doses in the meantime.

Given the acceleration over the past three decades, it is not surprising that
five-year cancer survival rates
are significantly better today than they were 30 years ago. The advances
described in the rest of this section guarantee they will continue to get
significantly better.

War on Cancer

Merck is partnering with biotech firm Vertex Pharmaceuticals to develop and
market an experimental aurora kinase inhibitor drug called VX-680 that
has shown promise in shrinking tumors. Aurora kinase has been identified as
overly abundant in leukemia and colon, breast, and some other cancers. In animal
tests the drug shrank colon tumors by 56 percent and pancreatic tumors by 22
percent, as well as “positive effects” on animals with leukemia.

Another partnership joins Japanese brewer and pharmaceutical firm Kirin with
US biotech Merix Bioscience to develop and market Merix’s “personalized” cancer
vaccine. Making the vaccine is labor-intensive, and the plan is apparently to
draw on Kirin’s expertise in robotic automation technology to produce it faster
and cheaper. Merix already has a deal with biotech firm Geron, and an analyst
sees the deals as validation of Merix’s technology, which introduces genetic
material from a patient’s tumor into dendritic cells collected from their own
blood. When reintroduced in the patient’s bloodstream, the altered cells trigger
the patient’s immune function to attack and destroy cancer cells.

A human trial in kidney cancer patients is underway, with preliminary results
expected by the end of the year. If they are positive, accelerated FDA approval
for a larger Phase II trial will be sought, but the vaccine will not be on the
market until 2007 at the earliest.

Reference: Rowland, Christopher (2004). “Vertex
in $34m deal for anticancer drug
.” Boston Globe, June 23.

Reference: Fisher, Jean P. (2004). “Merix
secures rich partner: Kirin deal eases fiscal pressures
.” News &
Observer, June 22.


The next generation of anti-angiogenesis drugs under development improve on
Avastin, which extends life for colorectal cancer patients by an average
of five months, by targeting proteins that help cancer cells grow and by being
administered as pills, rather than intravenously. Pfizer’s SU11248
targets VEGF (as does Avastin), KiT (as does Gleevec), and FLT-3.

Increasing the targets may increase side effects and toxicity, but one expert
told Reuters the side effects are “still very manageable” compared to

Bayer and Onyx Pharmaceuticals are co-developing BAY 43-9006 that
targets RaF kinase and VEGF. Genentech and OSI Pharmaceuticals are trialling
Avastin in combination with Tarceva, each of which targets a
different protein. These drugs are being trialed in renal cell carcinoma
patients, the leading kidney cancer, affecting about 31,000 patients a year.

Novartis and Schering are co-developing a drug for colorectal cancer, PTK
, which turns all three VEGF receptors so none of the five VEGF signals
can bind to them (Avastin blocks only one of the five). The hoped-for
result will be “a more complete blockade of the angiogenesis process,” said a
Schering executive.

Reference: Unknown (2004). “Cancer Drugs Aim
at More Targets
.” Reuters via Wired News, June 6.

Reference: Stein, Rob (2004). “Cancer
Drugs Show Promise: ‘Targeted’ Therapies Block Disease’s Molecular Signals
Washington Post, June 6.

Reference: Rosenberg, Daniel (2004). “Study Backs
Wider Use For ImClone’s Erbitux
.” Wall Street Journal, June 7.

Reference: Rosenberg, Daniel (2004). “Abbott
Studies Show Drug Delays Prostate Cancer
.” Wall Street Journal, June 7.

Another Angiolytic Drug Under

Adherex Technologies’ experimental drug Exherin inhibits proteins
called N-cadherin that hold together cancerous blood vessels. Normal blood
vessels are stronger than those in tumors and were unaffected in laboratory

Reference: Ranii, David (2004). “Adherex
hedging potential blockbuster cancer treatment
.” News & Observer, June

Promising Cancer Pill

Abbott Laboratories’ experimental prostate cancer drug Atrasentan
taken in pill form — is showing promise after early setbacks in trials. Though
it failed to slow progression of the disease in patients with end-stage prostate
cancer, it may work for the sickest of cancer patients. The drug is also being
studied in cancers of the kidney, ovaries, and brain.

Reference: Japsen, Bruce (2004). “Prostate
cancer drug promising for Abbott
.” Chicago Tribune, June 3.

Cancer Bomb

British researchers “deleted” a gene from an adenovirus, enabling it to
infect and burst cancer cells while leaving normal tissues unharmed. They took
advantage of the fact that normal cells can self-destruct when infected by a
virus, to prevent its spread, whereas cancer cells don’t care.

In tests, the virus was immediately detected by normal cells and was unable
to spread very far in healthy tissue, but it thrived among the cancer cells and
spread rapidly — more rapidly than normal — killing them in the process.

The modified virus was tested on pancreatic, lung, ovarian, liver, and
colorectal cancers in the test tube, as well as on live tumor-bearing mice.
Human clinical trials are planned for next year.

Reference: Bhattacharya, Shaoni (2004). “Genetically-modified
virus explodes cancer cells
.” New Scientist, June 4.

Search & Destroy Small Masses

New tools to diagnose and destroy millimeter-sized tumors are expected to
enter clinical trials in 2005. Both tools track the same protein biomarker that
signal angiogenesis as a tumor seeks additional blood supply. Upon finding the
biomarker, the diagnostic tool attaches an oil droplet carrying gadolinium,
which glows under MRI, and the therapeutic tool releases a small, precise dose
of paclitaxel (Taxol). Experts caution that not enough is yet
known about the behavior and attributes of very small tumors to be certain of

Reference: Philipkoski, Kristen (2004). “Nano Killers Aim
at Mini Tumors
.” Wired News, June 22.

Targeting Cancer

Most of the new, targeted, cancer therapies such as Tarceva (lung) and
Avastin (colon) are approved only as last-ditch efforts, notes Hollister
Hovey in the Wall Street Journal, who quotes one researcher as thinking
that chemotherapy will continue to be used for “at least a decade,” though
possibly at lower doses.

Reference: Hovey, Hollister H. (2004). “Targeted
Cancer Drugs Wait in the Wings
.” Wall Street Journal, June 1.

Cancer Survival Rate Triples In Three

The Associated Press, reporting a study by the US National Cancer Institute
and the Centers for Disease Control and Prevention, quotes the following

  • The number of cancer survivors (defined as anyone in whom cancer has been
    diagnosed, no matter how recently) rose from three million in 1971 to 9.8
    million in 2001.
  • The five-year survival rate for children with cancer has risen from about 50
    percent in the 1970s to 80 percent currently.
  • The five-year survival rate for adults with cancer has risen from about 50
    percent in the 1970s to 64 percent currently.

Reference: Unknown (2004). “Number
of Cancer Survivors Soars
.” Associated Press via Washington Post, June 25.


Leave a Reply

Your email address will not be published. Required fields are marked *