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3.13 Ginseng (Panax ginseng., Araliaceae)
Myocardial ischemia–reperfusion (I/R) injury has been prevented and treated with Panax ginseng (P. ginseng). The
study set out to dene the preventive effects of P. ginseng and
its active components against myocardial I/R injury to give
clinical evidence and novel perspectives for P. ginseng inves-
tigation and utilization in myocardial I/R injury. The study by
Chen et al. [39] outlined the pathophysiological pathways
underlying myocardial I/R injury and active components of P.
ginseng, such as ginsenosides, ginseng polysaccharides, and
phytosterols. Prevention and treatment of cardiac diseases
using these active components of P. ginseng were broadly
outlined, along with preclinical trials of myocardial I/R injury
and probable mechanisms of action. The study concluded that
active ingredients of P. ginseng might prevent myocardial I/R
injury and control oxidative stress- related proteins, inammatory cytokines, and apoptotic factors.
3.14 Guggul (Commiphora mukul.,
Burseraceae)
Guggul is one of the most widely used herbs to boost cardiac
and vascular health. The cardioprotective potential of C.
mukul in rats with myocardial necrosis induced by isoprenaline is already established. C. mukul extract was given for 30
days orally at 100, 200, and 400 mg/kg doses. Isoprenaline
(85 mg/kg; s.c.) was given to the animals, control and C.
mukul pre-treatment groups consecutively on the 29th and
30th day, at intervals of 24 h. Administration of isoprenaline
resulted in a signicant (p < 0.05) rise in superoxide dismutase, catalase, glutathione peroxidase, glutathione, and a
fall in malondialdehyde. C. mukul increased the myocardial
anti-oxidant status and stopped the leakage of lactate dehydrogenase and creatine phosphokinase-MB from the heart. C.
mukul pre-treatment was shown to reduce necrosis, edema,
and inammation through histological analysis. According to
the data, C. mukul may be a preventative and therapeutic
agent against oxidative stress linked to ischemic heart disease
due to its anti-oxidant and anti-peroxidative activities.
Moreover, a histopathological study revealed that the necrosis, edema, and inammation were reduced after pre-treatment with C. mukul. The current research suggested that C.
mukul may be a promising preventive and therapeutic agent
against oxidative stress-related ischemic heart disease [40].
3.15 Haritaki (Terminalia chebula.,
Combretaceae)
The present investigation evaluates the hypolipidemic effect
of methanolic bark extract of Terminalia chebula (T. cheb-
ula) against high-fat diet-induced hypercholesterolemia in
rats. Atherosclerosis, coronary heart disease, and stroke are
cardiovascular diseases for which hypercholesterolemia is a
signicant risk factor. The methanolic extract of T. chebula at
doses of 200, 400, and 600 mg/kg was utilized to evaluate its
anti-hyperlipidemic effect in animals and fasting blood glucose levels after treatment with the same doses were assessed
using commercially available kits. In the groups of animals
treated with T. chebula extract and atorvastatin, the positive
control showed a signicant increase in serum levels of highdensity lipoprotein (HDL) cholesterol in rats with dietinduced hypercholesterolemia. Also, acute toxicity studies
showed no morbidity and mortality at different doses. Thus,
the study conrmed the potential of T. chebula to treat hyper-
lipidemia [41].
3.16 Henbane (Hyoscyamus niger.,
Solanaceae)
The research describes the anti-hypertensive and blood vessel dilatory properties of the crude extract of Hyoscyamus
niger (H. niger) on rats under anaesthetic conditions. It
showed dose-dependent (10–100 mg/kg) reduction of BP,
rate, and force of atrial contractions in guinea pig atria. In the
isolated rabbit aorta H. niger (0.01–1.0 mg/ml) relaxed contraction induced by phenylephrine (PE, 1 μM) and K+ (80
mM) and it also suppressed the PE (1 μM) control peaks
which are usually found in Ca+2 free medium. The vasodilator activity of H. niger in endothelium-intact rat aortic preparations was endothelium-independent as it was not opposed
by N (omega)-nitro-L-arginine methyl ester. These ndings
suggested that Hyoscyamus niger reduced blood pressure by
acting as a Ca+2 antagonist [42].
3.17 Kalmegh (Andrographis paniculata.,
Acanthaceae)
Cardiac hypertrophy typically manifests as an expansion of
the cardiac muscle and a rise in the volume of muscle cells
that occur in response to hemodynamic stress, acute myocardial damage, infection, or abnormalities in the genes producing sarcomeric proteins [43]. An herbaceous plant known as
Andrographis paniculata (A. paniculata) is often used as a
medicinal food. It is used to treat endocrine disorders and
hypertension in several regions of Asia as a decoction, powder, or tablet. The aqueous A. paniculata extract and its
active constituent, andrographolide, have anti-inammatory
and anti-apoptotic properties. Three groups of test mice were
divided and given different diets standard chow, an obese
high-fat diet, or a high-fat diet treated with A. paniculata
extract (2 g/kg/day, administered via gavage for a week). The
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results showed that the myocardial inammation pathwayrelated proteins were elevated in the obese mice, potentially
contributing to cardiac hypertrophy and myocardial apoptosis. The research strongly implies that obese persons may
benet from taking supplements containing A. paniculata
extract to prevent and treat cardiovascular disease [44].
3.18 Orchid (Orchis mascula., Orchidaceae)
Aziz etal. [45] explored the possible mechanisms of action
for the medicinal use of Orchis mascula (OM) as a medication for hypertension and dyslipidaemia. The hydroalcoholic
roots extract of OM is used as animal model hypertensive
rats (strain: SHR/NCrlBR; hypertensive, non-stroke) and
their normotensive controls, Wistar Koyoto (WKY) rats,
Sprague–Dawley rats (170–200 g), and rabbits (1.5–2 kg) of
either sex used. OM increased acetylcholine-induced relaxation and improved endothelial dysfunction. It considerably
(P < 0.05) in hypertensive rats reduced systolic blood pressure. In a dose-dependent manner, the extract of OM at 10
and 30 mg/kg in normotensive anaesthetized rats lowered
mean arterial pressure. OM also decreased serum triglycerides and high-fat diet and tyloxapol-induced hyperlipidaemia. In a second model, OM prevented weight gain. OM
causes concentration-dependent relaxation of phenylephrine
and high K+ (80 mM)-induced contractions in the isolated
rabbit aorta. This research demonstrated that OM showd
action against hypertension and endothelial-modulating.
3.19 Pushkarmool (Inula racemosa Hook. f.,
Compositae)
For precordial chest discomfort, Ayurveda recommends
Inula racemosa Hook. f. Mangathayaru etal. [46] aimed to
investigate how Inula racemosa extract in alcohol (IrA) and
hexane (IrH) affects high-fat diet-induced atherosclerosis in
guinea pigs. In the aforementioned research, 5 groups were
formed with 6 animals in each group and to them, pellets
were given as a diet for 90 days along with 0.15% w/w cholesterol (positive control), 100 mg/kg of atorvastatin, or 10
mg/kg of atorvastatin acetate and 100 mg/kg of atorvastatin
calcium also administered. To the control group, only a pellet
diet was given. Compared to the positive control, IrA lowered total cholesterol, triglycerides, low-density lipoprotein
cholesterol, and the atherogenic index while increasing highdensity lipoprotein cholesterol. Sesquiterpene lactones in
IrH and phenolics in IrA are probably responsible for the
reported effects. The outcomes conrmed that I. racemosa
has cardioprotective and anti-obesity activity by demonstrating its anti-atherogenic effect.
3.20 Radish (Raphanus sativus.,
Brassicaceae)
Ghayur et al. [47] described the anti-hypertensive,
endothelium- dependent vascular relaxant, and cardiacmodulatory activity of Raphanus sativus seed extract. In the
study, Balb/c mice (20–25 g), Sprague–Dawley rats (170–
200 g), and guinea pigs (500–600 g) of either sex were used.
The aqueous extract of R. sativus was prepared, and its phytochemical testing was performed. Blood pressure was
assessed in anaesthetized normotensive rats. It demonstrated
that an atropine-sensitive pathway mediated a dosedependent (0.1–3 mg/kg) decline in rats’ blood pressure and
heart rate. The extract reduced the force of contractions and
rate in separated guinea pig atria in a dose-dependent manner
(0.03–3.0 mg/mL). The aqueous extract reduced the contractions produced by phenylephrine in endothelium-intact rat
aortas. In mice, the extract did not show any side effects up
to a dose of 10 g/kg. The cardiovascular inhibitory effect of
R. sativus was mediated by muscarinic receptor stimulation,
which may justify its anti-hypertensive activity [47].
3.21 Rhubarb (Rheum palmatum Linn.,
Polygonaceae)
Evans et al. [48] evaluated the heart-protective actions of
emodin via inhibiting histone deacetylase (HDAC)dependent gene expression; for this reason, they primarily
believed that emodin would reduce a pathological increase in
cardiac size via prohibition of histone deacetylases enzyme
and rhubarb which is rich in emodin would exhibit these
effects. The data demonstrated that emodin altered gene
expression globally and raised histone acetylation in cardiomyocytes. Additionally, they evaluated that emodin prevented hypertrophy induced by phorbol myristate acetate
(PMA) and phenylephrine (PE) in newborn rat ventricular
myocytes (NRVMs). Lastly, they proved the emodin’s cardioprotective action by translating it to 10 weeks of age,
C57BL/6 male and female mice models who received angiotensin II (Ang II) they proved its cardioprotective effect. The
study lasted 14 days and showed the invitro histone deacetylase enzyme activity inhibited by emodin and Turkish rhubarb containing emodin with fast-on, slow-off rates. Emodin
partially prevented pathological cardiac hypertrophy by
inhibiting histone deacetylase-dependent gene expression
modications.
In another study, Gehlken et al. [49] demonstrated the
activity of rhubarb containing pectin. Pectin inhibits galectin3- related endomyocardial brosis. They performed an
invitro study, evaluated the inhibitory capacity, and nally
identied potent pectin. Compared to the well-known modi-
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ed citrus pectin, ndings showed that modied rhubarb
pectin is the highest effective inhibitor of galectin-3. Cardiac
brosis induced in mice by angiotensin II (AngII) infusion.
In comparison to the control, Ang II infusion showd 4–5
times more brosis signal in the left ventricle tissue.
Compared to Ang II alone, brosis decreased by 57% after
receiving rhubarb pectin therapy but by 30% with modied
citrus pectin. Natural rhubarb pectin, a galectin-3 inhibitor,
signicantly reduced myocardial brosis and maintained
heart function invivo. It also had a higher inhibitory ability
than other pectins.
3.22 Sarpagandha (Rauwola serpentina.,
Apocynaceae)
By monitoring the structure of the liver and kidney tissues
histologically, biochemical markers, and blood pressure in
albino rats, the given study was done to examine the therapeutic effects of Rauwola serpentina on hypertension and
hyperlipidaemia. Thirty albino rats were used for the analysis, which further separated into 5 groups (6in each). Group
1 regular diet was given; in group 2 high-salt diet with only
8% NaCl and in group 3, atenolol (standard drug control) 50
mg/kg was given. It contains major secondary metabolites
such as avonoids, tannin, and alkaloids, which may have
therapeutic potential against cardiovascular ailments. Due to
the binding action of catecholamine in nerve cells, reserpine
shows anti-hypertensive effects. Combined with a highsodium diet, the methanolic plant extract was administered
to groups 4 and 5 at 100 mg/kg body weight and 200 mg/kg
body weight daily for four weeks. Compared to G2 and G3,
Rauwola serpentina signicantly lowered blood pressure in
groups 4 and 5. In conclusion, Rauwola serpentina has
therapeutic benets that certainly lowered cholesterol and
blood pressure by safeguarding the renal and liver tissues
[50].
3.23 Tulsi (Ocimum sanctum Linn.,
Lamiaceae)
decreased glutathione levels, superoxide dismutase, thiobarbituric acid reactive elements, and LDH. It also inhibited
lipid peroxidation at 25, 50, 75, and 100 mg/kg concentrations. The optimum heart-protective effect of O. sanctum
was reported in the current investigation at a 50 mg/kg dose.
Histopathological ndings supported the preceding outcomes even more. In this way, we presume that O. sanctum
may be therapeutically and preventatively useful in managing myocardial infarction [51].
3.24 Viola (Viola odorata Linn., Violaceae)
Siddiqi etal. [52] studied the activity of hydroalcoholic leaf
extract of Viola odorata (V. odorata) against hypertension
and dyslipidaemia. Sprague–Dawley rats (180–200 g),
guinea pigs (450–500 g), and Balb-C mice (20–25 g) of
either sex were used in the research. Under anaesthesia, rats
exhibit a dose-dependent reduction in mean systemic arterial
blood pressure (0.1–1.0 mg/kg). When vasoconstriction was
induced by phenylephrine (PE, 1M) and potassium (K+, 80
mM), V. odorata showed a relaxation based on concentration
along with a rightward shift of Ca+2 concentration–response
curves and suppression of PE (1M) control peaks in Ca++free medium.
In tyloxapol-induced dyslipidaemia, V. odorata reduced
total cholesterol and triglyceride levels. A high-fat dietinduced dyslipidaemia model reected increased highdensity lipoprotein cholesterol and signicant reduction of
total cholesterol, atherogenic index, low-density lipoprotein
cholesterol, and preventing weight gain. As per the result,
drug extract showed a decrease in blood pressure results
probably due to pathways like inhibition of Ca+2 inux via
membranous Ca+2 channels, the release of Ca+2 from intracellular stores and nitric oxide-mediated pathways. Inhibition
of synthesis, absorption of lipids, and anti-oxidant activities
are responsible for decreased body weight and antidyslipidaemic activity of the extract. The study provided
pharmacological justication for using V. odorata as an anti-
hypertensive and anti-dyslipidaemic medication.
Ocimum sanctum has therapeutic potential with anti-oxidant
characteristics, yet, nothing is known about its cardioprotective efcacy against myocardial infarction. Isoproterenol
was administered at a dose of 85, 200, and 300 mg/kg twice
at intervals of 24 h to induce myocardial infarction changes
in anti-oxidant markers, lactate dehydrogenase (LDH), and
morphological and histological alterations were analysed.
Aqueous alcoholic extract of O. sanctum signicantly
4 Active Phytoconstituents forCVD
In addition to medicinal plants, several phytoconstituents are
present in the medicinal plants showing very high cardioprotective activity. Table1 represents detailed information on
different phytoconstituents isolated from the specic parts of
the medicinal plant, their dose, specic model, and use with
the mechanism of action.
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[53]
A study supported the utilization of
allicin as an effective therapeutic
agent for pathophysiological
abnormalities that may be related to
or linked with cardiac and renal
model for kidney
disease
40 mg/kg Rats were used as a
[54]
algorithms
The blood pressure in SHR-CP rats
was lowered, and endothelial
hypertensive rat
40 mg/kg Spontaneously
[55]
dysfunction was mitigated by
trans-cinnamaldehyde
Angiotensin-converting enzyme
model
Cyclosporine-induced
10 and 15
[56]
There was the potential for
activity, acetylcholinesterase,
butyrylcholinesterase, and arginase
activity were all considerably
decreased by caffeine and
hypertension in rat
model
mg/kg,
respectively
andrographolide to serve as a
chlorogenic acid
myocardial infarction
20 mg/kg/day Isoproterenol-induced
[57]
medicine that can help to protect
heart tissue in the case of myocardial
infarction
Arjunolic acid prevents myocardial
necrosis-related damage
in rats
has been driven by
isoproterenol in rats
15 mg/kg Myocardial necrosis
[58]
According to the study’s ndings,
rutin and digoxin can potentially treat
cardiovascular problems since it can
Ischemic–
reperfusion-induced
myocardial infarction
100 mg/kg
and 500 μg/
kg,
[59]
counteract I/R-induced myocardial
functional alterations
A potential treatment approach for
cardiac protection over myocardial
infarction is provided by the
anti-inammatory, protective effect
against oxidation, anti-stress, and
BDNF modulatory action by
induced by
isoproterenol
respectively
50 mg/kg Myocardial infarction
(continued)
rosmarinic acid in comorbidly
depressed rats
Act by reducing the
vasoconstrictor effects of
angiotensin II, oxidative stress,
Pharmacological
activity Mechanism of action Dose Animal model Study outcome References
Anti-
hypertensive
Name of medicinal
plant and parts used
for extraction
diallyl disulde
and increasing the expression of
Nrf2, as well as by upregulating
the AT1R and downregulating the
Keap1 protein
2+
By promoting nitric oxide release
via the nitric oxide synthase
pathway
By downregulating activities of
an angiotensin-I converting
enzyme, acetylcholinesterase,
butyrylcholinesterase, and
arginase
Mostly through L-type Ca
Anti-
hypertensive
–
Anti-
hypertensive
–
currents
+
Lowering the levels of
myeloperoxidase, lipid
channel inactivation and an
elevation in cardiac transient
outward K
infarction
peroxidation, ascorbic acid,
Myocardial
necrosis
bark
-ATPase activity
+
-K
glutathione, ceruloplasmin, and
+
glutathione peroxidase
Due to its potential to scavenge
free radicals and inhibit
Na
Through increasing the activity of
infarction
glutathione, superoxide
dismutase, interleukin-10,
infarction
brain-derived neurotrophic factor,
and other cardioprotective
molecules
Name of the
isolated compound
Table 1 Phytoconstituents reported for cardiovascular diseases
Allicin Synthesized from
Trans-
cinnamaldehyde
Caffeic acid and
chlorogenic acid
Andrographolide – Myocardial
Arjunolic acid Terminalia arjuna/
Rutin and digoxin – Myocardial
Rosmarinic acid – Myocardial
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[60]
The study revealed a concentration-
dependent effect of the vaccine
against myocardial infarction through
the proposed mechanism
myocardial infarction
in rats
10 mg/kg Isoproterenol-induced
[61]
The research outcomes indicated that
6 mg/kg Chronic myocardial
[62]
vitexin is a cardioprotective
compound that could serve as a
valuable alternative to traditional
treatment for individuals suffering
from coronary heart disease
Taxifolin is an active component
against ISO-induced myocardial
ischemia/reperfusion
injury model
cardiac injury
50 mg/kg Isoproterenol-induced
[63]
injury and probably other heart-
related problems
Arjunic acid has a cardioprotective
Cobalt chloride-
8 μg/mL
[64]
activity by reducing mitochondrial
damage, apoptosis, hypoxia injury,
and damage from oxidative stress
Hesperidin may be used
therapeutically to alleviate
atherosclerosis and atherosclerosis
associated with metabolic disruption,
induced hypoxia in
rats
the LDL receptor,
high-fat diet-induced
atherosclerosis
200 mg/kg Using mice lacking
[65]
This work provided a novel
according to the established data
results
0.1% (w/w) Atherosclerosis-prone
[66]
understanding of the mechanisms by
which quercetin protects from
atherosclerosis
It was anticipated that using
zingerone as an active ingredient
could help prevent and treat
[67]
diet-induced atherosclerosis and its
health consequences
Salvianolic acid B may slow the
development of atherosclerosis,
)
−/−
mice model
apolipoprotein
E-decient (ApoE
diet-induced
atherosclerosis in
Wistar rat
20 mg/kg High cholesterol
analysis
30 ug/mL Done by invitro
according to ndings. Its potential to
modulate the YAP/TAZ/JNK
signalling pathway is associated with
anti-atherosclerosis capabilities
Pharmacological
activity Mechanism of action Dose Animal model Study outcome References
Name of medicinal
plant and parts used
for extraction
Name of the
Table 1 (continued)
isolated compound
Cardioprotective potential via
lowering oxidative stress,
excessive autophagy, and
regulating apoptosis by triggering
the PI3K/Akt/mTOR signalling
infarction
Vasicine – Myocardial
excess, and suppressing
2+
pathway
Act via improving the anti-
cardiac apoptosis
oxidant defence system, reducing
Ca
myocardial
ischemia
Vitexin – Chronic
Taxifolin may act by mediating
the Nrf2/HO-1 pathway,
injury
Taxifolin – Myocardial
capacity and reducing the activity
of proteins involved in apoptosis
decreasing reactive oxygen
species, inammation, and death
of cells
Arjunic acid – Cardioprotective via improving the anti-oxidant
in H9c2 cardiomyocytes
Hesperidin reduces
atherosclerosis by improving
insulin resistance, and lipid
Anti-
atherosclerotic
Hesperidin –
proles, inhibiting the production
of macrophage foam cells and
having an anti-oxidative impact
Through minimizing oxidative
stress, macrophage pyroptosis
and associated mechanism
promote NRF2 activation by
competitively binding to the
Arg483 site of KEAP1
Anti-atherosclerotic effect by
modulating lipid gene expression
Anti-
atherosclerotic
Quercetin –
Anti-
atherosclerotic
Zingerone –
and promoting anti-oxidant
potential
The yes-associated protein/TAZ/
JNK signalling pathway controls
both the production of oxidized
low-density lipoprotein and
inammation, which are both
inhibited as part of the
Anti-
atherosclerotic
Salvianolic acid B –
mechanism
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[68]
The ndings concluded that
pre-incubation with sophocarpine
mitigated the cytotoxic effects, DNA
fragmentation, and apoptosis
Completed by invitro
analysis
100 μg/mL
[69]
triggered by ox-LDL in endothelial
cells in a dose-dependent approach
A study indicates that crocin
enhanced the expression of
connexin-43in an experimentally
induced ischemic injury, which had a
myocardial infarction
caused by arterial
ligation
50 mg/kg Rat model for
[70]
preventative effect on the arrhythmia
The study revealed the
pharmacological potential of potent
anti-coagulant fraction/clerobrase
as a naturally obtained active agent
for the prevention and/or
management of cardiovascular
disorders linked to blood clotting
thrombus in mice by
employing carrageen
using supportive
invitro and invivo
analysis
100 mg/kg Formation of
By the modulation of NF-B
signalling, sophocarpine lowered
vascular endothelium apoptosis
and inammatory responses
induced by oxidized low-density
lipoprotein
expression
atherosclerotic
Sophocarpine – Anti-
Crocin – Anti-arrhythmic By decreasing Connexin-43
inuenced by brinogenolytic
action as well as anti-platelet
activity
Anti-coagulant The anti-coagulant impact is
Clerodendrum
colebrookianum/
leaves
Clerobrase from
anti-coagulant
fraction
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5 Conclusion
In conclusion, we have attempted to represent cumulative
data of all the medicinal plants’ investigation strategies for
various CVDs and their specic mode of action against a
particular disease. Thus, the chapter will act as a referential
source for scientic and general people to utilize natural
resources to prevent conventional drugs’ side effects in combating different cardiovascular diseases.
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Role ofLifestyle Modification andDiet
https://t.me/medicina_free
inthePrevention ofCancer
MoumitaChatterjee , SharmisthaGanguly ,
andSubhajitDutta
Abstract
Cancer is a multifactorial disease that is still leading the
chart in terms of mortality rate. Almost 90% of the cancers are sporadic in nature, with only 10% being genetic
and inherited in an autosomal dominant manner. Although
accumulated evidence suggests a drop in mortality rates
in recent years, we are still far away from fully understanding the pathophysiological mechanisms associated
with such complex phenotypes. Moreover, anti-cancer
medications possess a plethora of mild aftereffects without much relief. Hence, there is a need to explore the natural protective mechanisms that can limit the mortality rate
with minimal or no adverse consequences. This book
chapter entails a story citing different natural mechanisms
that can lower the risk of developing different types of
cancer. We focussed on lifestyle modications and
changes in nutritional diet that can modulate different
regulatory players associated with cancer signalling axes.
We have presented an avalanche of evidence ranging from
molecular mechanisms to implications of different natural
diets in cancer, thereby providing a strong correlation
between lifestyle modications and their mitigation.
Through this chapter, readers will understand the mitigating roles of low bre, omega-3- and omega-6 fatty acids,
red meat, ax seeds, fruits, and vegetables in protecting
different cancer types ranging from breast to lung to prostate carcinoma. Finally, the clinical evidence of lifestyle
M. Chatterjee
V.Sivaram Research Foundation, Bangalore, Karnataka, India
S. Ganguly
University Department of Botany, Ranchi University,
Ranchi, Jharkhand, India
S. Dutta (*)
Functional Genomics and Metabolism Research Unit, Department
of Biochemistry and Molecular Biology, University of Southern
Denmark, Odense, Denmark
Ronin Institute for Independent Scholarship, Montclair, NJ, USA
e-mail: subhajit@bmb.sdu.dk
modications will establish a positive association between
reduced cancer progression with increased chances of
survival.
Keywords
Lifestyle modication · Diet · Cancer
1 Introduction
Cancer is a group of diseases characterized by the unchecked
invasion and growth of aberrant cells. Normal cells become
cancer cells through a multistep process involving changes to
both the metabolic phenotype and molecular signature. The
“metastasis” or the concluding phase of the invasion process
can be lethal [1]. The International Agency for Research on
Cancer’s GLOBOCAN 2020 estimated the status of cancer
incidencence as well as mortality of cancer patients (Fig.1a,
b). They predicted around new 19.3 million cases worldwide
(18.1 million excluding non-melanoma skin cancer) and
reported more than 10 million deaths from cancer (9.9 million excluding non-melanoma skin cancer). Female breast
cancer has surpassed lung cancer as the most commonly
diagnosed malignancy, with an estimated 2.3 million new
cases (11.7%). Colorectal (10.0%), lung (11.4%), stomach
(5.6%), and prostate (7.3%) cancers are next in line. Lung
cancer remained the most common type, with an estimated
1.8 million deaths (18%). It was then followed by colorectal
(8.3%), liver (9.4%), female breast (6.9%) cancers, and
stomach (7.7%) [2]. In the last few years, immuno-oncology
and targeting actionable changes in oncogene-driven tumours
have revolutionized cancer treatment paradigms. Both cancer remedy sectors carry on with signicant obstacles.
Evaluating the curative impact of druggable genomic alteration in biomarker-driven clinical trials is hampered because
they are not only heterogeneous but also represent small subsets of patients in some tumour types. Even though the use of
NGS (next-generation sequencing) technologies for molecular pre-screening in clinical research is growing, difculties
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