Nanogen - PharmXpert Academy

Squamous Cell Carcinoma (SCC)
An SCC is a malignant tumour arising from the cells above
the basal layer of the epidermis (prickle layer), usually after
many years of exposure to sunlight. The cells in the prickle
layer are maturing towards keratin formation and the cancer
occurs when they accelerate in growth and breakthrough the
basement membrane into the dermis. Although sunlight is the
most common cause of SCC, any cancer-producing substance
(carcinogen) may initiate its development. SCCs often arise
from precancerous conditions such as solar keratoses. SCCs
may also develop from skin ulcers, scar tissues, and x-ray
damaged tissues, if this occurs then the chance of metastasis
increases to approximately 20%. In addition, some 40% of
transplant patients who are on immunosuppressive drugs
develop SCCs within 5-years post-transplantation. This skin
cancer is a serious problem and is potentially deadly. The first
sign of an SCC is usually a thickening, with the lesion feeling
firm, and the limits are not discrete. In the early stages there
may be a crust that may later shed to show an ulcer. It may also
form as a crack (fissure) or a small ulcer on the lip, which fails
to heal and bleeds recurrently. The SCC may metastasise with
an incidence of generally less than 5%.
The Old Established Treatments
Surgery: There are various
surgical techniques available to treat
skin cancer in its various forms.
Surgical excision of a tumour has
the advantage that if done correctly,
removes the affected area virtually
completely. This treatment is
extensive, requires anaesthesia
and depending on the tumour,
may require skin grafting with its
accompanying cosmetic limitations.
The risks of surgical intervention are well known and
excision of BCCs or SCCs from the facial area often involves
reconstructive surgery, which can be both time consuming and
costly.
Radiotherapy: Radiotherapy, moreso prior to the 1950’s
than now, has been used to treat most skin cancers. The
disadvantage of this mode of treatment is the resulting scar
tissue which may be depressed, depigmented and may also
undergo degenerative and malignant changes at a later date.
Dermatological: Dermatological treatment consists
of curettage and diathermy/ cauterisation, cryotherapy,
chemosurgery and chemotherapy, and is generally used
for superficial skin cancers. With curettage and diathermy,
the tumour is scraped out and the bleeding stopped by
cauterisation, (application of heat) by an electric current
(diathermy). Cryotherapy, possibly the most widely used
method, involves an intensely cold probe, cooled by liquid
nitrogen, which is applied to the lesion. When the lesion thaws,
there is pain in the treated area, followed by blister formation.
Chemosurgery involves chemical fixation of the lesion and
the fixed tissue is shaved off in layers. Chemotherapy with
5-fluorouracil (5-FU), which is an anti-metabolite and inhibits
RNA and protein syntheses leading to cell death, is used to
treat superficial lesions, but it is not specific for cancer cells.
5-FU is supplied as an ointment and requires considerable care
in its application under medical supervision.
All of the above methods (surgery, radiotherapy and
dermatogical) have their own individual limitations.
However, the limitations common to all of these methods
are:
• Formation of scar tissue
• Lack of normal tissue regrowth
• Limited access to the lesion if it is deep within the skin
• A high rate of recurrence
• Cosmetic end result
New Specific Treatments
It is now well established that specific glycoalkaloids from
the Solanum family have anticancer properties. The specific
glycoalkaloids consist of BEC, which is a standardised
mixture of triglycosides, solasonine and solamargine and
their corresponding di- and mono-glycosides (1-12). All the
glycosides contain the same aglycone, (the alkaloid without a
sugar molecule) - solasodine.
Solasodine on its own does not have anticancer properties;
however the mono-, di- and triglycosides do have anticancer
properties. These glycosides contain a plant sugar rhamnose,
which is not usually found in mammalian species. Specific
endogenous lectins (EELS), which are specific receptors for
the sugar part of the glycoalkaloids and are present in the
plasma membranes of susceptible cancer cells but not normal
cells recognize and bind the sugar rhamnose of the BEC
glycoalkaloids. BEC subsequently enters the cancer cell and
causes cell death by destroying the lysosome (6, 13-17).
BEC has been shown to have antineoplastic activity in cell
culture, animals and in humans (1, 3-12). Currently Phase II
studies with BEC are being carried out on terminal internal
tumours in man. With these studies BEC is being administered
intravenously (18).
Precursor of BEC5 Curaderm®
A cream formulation of BEC in concentrations of 10% was
well tolerated in an open tolerance and dose-finding Phase I
and II studies in healthy volunteers and in patients with actinic
keratosis, BCC and SCC (3). Application of the cream in this
study resulted in swelling of the BCC and SCC lesions, with
erythema (reddening) of the surrounding skin, then ulceration
in about 2 days, followed over the next weeks by healing with
healthy new cell growth. The only reported adverse events
were mild itching and burning sensations at the site of the
lesions in a few patients.
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