Skin diseases are among the widespread
human health challenges, affecting 900 million people globally. Five common
conditions account for over 80% of all skin diseases. Understanding the unique
nature of skin cancer is crucial in the context of this broader burden. Skin
cancer primarily arises from the epidermis, the outermost layer of the skin.

Skin cancer is a malignant condition
characterised by the uncontrolled proliferation of any one of the many skin
cell types, disrupting the normal, regulated process of skin regeneration. Whereas
the normal process of regeneration of skin involves replication of the cells in
a controlled manner. As one of the most prevalent forms of cancer worldwide,
skin cancer encompasses various subtypes, each cancer has unique
characteristics and effects.

Types

Basal and squamous cell carcinomas are the
two most prevalent types of skin cancer, originating in the basal and squamous
layers of the epidermis, respectively. Basal cell carcinoma typically arises from
the basal cells, which are responsible for producing new skin cells.

On the other hand, squamous cell carcinoma,
develops in the squamous cells, which make up the outermost layer of the skin
and serve as a protective barrier to our body. Unlike basal cell carcinoma,
squamous cell carcinoma can sometimes spread to nearby lymph nodes or distant
parts of the body, though this is rare.

Both types of cancer generally grow slowly
and rarely spread to other parts of the body, making them highly treatable.
However, the treatments for these carcinomas, such as surgical excision,
radiation, or topical therapies, can be costly and often result in permanent
scarring, posing a cosmetic and emotional challenge for patients.

Non-melanoma skin
cancers,
comprising basal cell carcinomas and squamous cell carcinomas are rarely lethal
but require surgical treatment, which is painful and results in disfiguring of
the skin.

• Non-melanoma skin cancers are most
  frequent on parts of the body that are commonly exposed to the sunlight
  such as ears, face, neck and forearms, implying the hazardous role of
  long-term, repeated UV radiation exposure is a major causal factor.
• Within some countries there is a clear
  relationship between increasing incidences of non-melanoma skin cancers
  with decreasing latitude, i.e. higher UV radiation levels.
• Skin cancer burden in the older age
  groups will be due to occupational exposures to solar ultraviolet
  radiation much earlier in working life because non-melanoma skin cancer
  can take years or even decades to develop through DNA damage and genetic
  mutations.

Melanoma, the third most common type of skin cancer, is far more aggressive.
It originates in the melanocytes, the cells responsible for producing melanin,
the pigment that gives skin its colour. Unlike basal and squamous cell
carcinomas, melanoma has a higher possibility of metastasising to other parts
of the body, including vital internal organs such as the brain and liver. This
propensity for spreading makes melanoma a lethal form of skin cancer despite
its lower incidence rate.

Malignant melanoma, although significantly less prevalent than non-melanoma skin
cancers, is the leading cause of death due to skin cancer and is more likely to
be reported than non-melanoma skin cancers. A good number of studies substantiate
that the risk of developing malignant melanoma correlates with genetic predispositions
and personal characteristics such as skin type, and UV exposure behaviour of
the particular individual.

The World Health Organization (WHO) has
identified solar ultraviolet radiation as causing cancer of the skin in humans.
Among the working-age population, mortality rates from non-melanoma skin cancer
are higher in males (0.4 deaths per 100,000) compared to females (0.2 deaths
per 100,000). This disparity highlights the heightened vulnerability of males
working outdoors to prolonged UV exposure.

Major Pathophysiological Transformations

The development of skin cancer involves
several critical changes at the cellular and molecular levels such as DNA
damage and genetic mutations.

A. DNA Damage

The formation of cyclobutane pyrimidine
dimers (CPDs) and photoproducts due to ultraviolet radiation, leading to DNA breaks
and mutations. Mutations in genes that regulate cell growth and programmed cell
death (apoptosis) play a central role in skin cancer.

Production of immunosuppressive cytokines and
recruitment of regulatory T cells that suppress anti-tumour immune responses
create a favourable condition for the malignant cells to immune evasion.

Alterations in DNA methylation, histone
modification and microRNA expression can silence tumour suppressor genes or
activate oncogenes, contributing to skin cancer progression.

Symptoms

The most typical sign of skin cancer is a
visible change in the skin. This could present as a new growth or an unhealed
sore or a change in an existing mole or lesion. It is essential to note that
not all skin cancers look alike, and their appearance can vary widely depending
on the type and stage of the cancer.

However, for melanoma, the signs are;

·
The shape of one half of the mole or spot does
not match the other, which is larger than 6 millimetres even though smaller
when first detected with irregular edges or notched.

·
Eventually, the size shape, and colour of the
skin lesion will change with itching and sometimes bleeding.

·
Similarly, the colour of the skin or lesion is
uneven and may include different shades of brown, black, or even patches of
pink, red, white, or blue.

For non-melanoma skin cancers, the symptoms
may include;

·
A pearly or waxy bump associated with basal cell
carcinoma.

·
A firm, red nodule or a scaly, crusted lesion
that may bleed, commonly linked to squamous cell carcinoma.

·
A flat, flesh-coloured or brown scar-like
lesion, which may also indicate basal cell carcinoma.

Risk Factors

• The presence of numerous atypical irregular
  and larger nevi (moles) is the strongest risk factor for malignant
  melanoma especially in fair-skinned populations.
• People with a pale complexion, blue eyes,
  and red or fair hair are more susceptible to malignant melanoma. Studies
  demonstrate that in melanoma patients, the amount of UV radiation needed is
  at lower minimum dose to cause redness or erythema than in control groups.
• High, intermittent exposure to ultraviolet
  radiation appears to be a significant risk factor for the development of
  malignant melanoma. That is, intense sun exposure occasionally during
  vacations is a potential threat to skin cancer.
• The incidence of malignant melanoma increases
  with decreasing latitude. As a result, populations closer to the equator
  face greater risk due to higher UV radiation levels.
• Several epidemiological studies support a
  positive association with history of sunburn, mostly at an early age.
• Malignant melanoma risk is higher in
  people with a history of non-melanoma skin cancers and of solar keratosis
  or precancerous sun-induced lesions. Both history and precancerous lesions
  are indicators of cumulative UV exposure.

The incidence of both non-melanoma and
melanoma skin cancers has been increasing over the past decades. Currently,
between 2 and 3 million non-melanoma skin cancers and 132,000 melanoma skin
cancers occur globally each year. One in every three cancers diagnosed is a
skin cancer.

Racial and Geographical Factors

Skin pigmentation plays a crucial role in
determining an individual’s susceptibility to skin cancer. Due to the relative low
level of skin pigmentation, Caucasian populations generally have a much higher
risk of developing non-melanoma or melanoma skin cancers than dark-skinned
populations.

Naturally people with brown and black skin can
resist sunburn or UV radiation. They safely tolerate relatively high levels of
sun exposure without greatly increasing their skin cancer risk due to higher
melanin level.

In contrast, people with pale or freckled
skin, fair or red hair and blue eyes are in the highest risk group. People with
dark hair and eyes who do not normally get sunburnt are at medium risk of
developing skin cancer. They usually include Mediterranean, Middle Eastern, and
Indian subcontinent populations.

Nevertheless excessive exposure to intense
sunlight can lead to skin damage, pigmentation disorders, the risk of eye
damage and heat stroke is the same irrespective of the skin types.

Causes

·
Tobacco Smoking is a significant risk factor for
Squamous Cell Carcinoma. The carcinogens in tobacco damage DNA in skin cells,
increasing the risk of malignant transformation.

·
Human papillomavirus infection (genital warts),
particularly for mucosal sites such as oral mucosa, lips, and genitals are
linked to skin cancer. HPV can disrupt normal cell cycle regulation, leading to
cancerous changes.

·
Drug-induced immune suppression reduces the
body’s ability to detect and destroy cancerous cells. They are at higher risk
for skin cancers, particularly SCC and basal cell carcinoma (BCC).

·
Certain medicines such as hydrochlorothiazide results
in the photosensitizing effects that make the skin more vulnerable to UV damage
leading to skin cancer.

·
Exposure to carcinogenic chemicals can causes to
SCC.

·
Longstanding skin diseases such as lichen
sclerosus and linear porokeratosis damage the tissues and can predispose
individuals to skin cancer.

·
A longstanding wound or scar or ulcers known as
Marjolin ulcer undergo malignant transformation to SCC.

·
Genetic conditions significantly increase the
risk of skin cancer due to defects in DNA repair mechanisms or tumour
suppressor genes

Treatment

The majority of skin cancers are, in
allopathy, treated surgically, using a local anaesthetic to numb the skin. The malignant
tumour, along with a margin of surrounding healthy tissue, is surgically
removed. The size of the margin depends on the type and aggressiveness of the
cancer. Risk of scarring, infection, or functional impairment, especially in
sensitive areas are significant concerns of such treatment method. Following
treatment and protein supplementary are also necessary to prevent recurrence. As
usual, such methods are very painful and expensive.

Homoeopathy Treatment

Alternatively, homeopathic remedies
influence the body’s immune system, gene expression, and cellular responses.
These remedies work by modulating gene expression and influencing epigenetic
mechanisms. It also affects tumour suppressor genes that regulates cell cycle
arrest and apoptosis or genes involved in DNA repair, potentially supporting
cellular defence against cancer progression. Homeopathic medicines exert
apoptotic (programmed cell death) effects on cancer cells, promoting their destruction
while leaving healthy cells unaffected. Homoeopathy believes disruption of the
vital balance manifests as disease symptoms and focuses restoring disrupted
balance by addressing the root cause of the disease. Homeopaths focus on to
revitalise the intrinsic energy that maintains health and harmony in the body. As
a result, it promotes overall health and wellbeing of individuals without any
harmful surgical exertion.