View Article

Abstract

Cancer remains one of the leading global health challenges, characterized by uncontrolled cellular proliferation, genetic instability, and the potential for metastasis. cancers are broadly classified into carcinomas, sarcomas, leukemias, lymphomas, myelomas and mixed type cancer. The etiology of cancer involves a Multifactorial interplay between genetic mutations, environmental exposures, lifestyle factors, And infectious agents. Mutations in oncogenes and tumor suppressor genes, alongside chronic Exposure to carcinogens, initiate and promote malignant transformation. Preventive measures are categorized into primary, secondary, and tertiary levels, emphasizing lifestyle modification, Vaccination, early detection through screening, and post-treatment rehabilitation. Chemotherapy remains a cornerstone of cancer therapy, utilizing diverse drug classes such as alkylating agents, antimetabolites, mitotic inhibitors. Recent advances, Including immunotherapy, nanotechnology-based drug delivery, and precision oncology, have Revolutionized cancer management by enhancing selectivity and reducing systemic toxicity. Furthermore, gene-editing tools such as CRISPR/Cas9 and artificial intelligence applications in diagnostics signify promising future directions. Collectively, these multidisciplinary Approaches underscore the importance of integrating prevention, early diagnosis, and Personalized treatment to improve global cancer outcomes.

Keywords

Oncogenes, tumor suppressor genes, prevention strategies, chemotherapy, targeted therapy, precision oncology, CRISPR technology, nanomedicine

Introduction

Cancer: -

Cancer represents a group of diseases characterized by the abnormal and uncontrolled Proliferation of cells that invade and destroy surrounding tissues and can metastasize to distant Organs. According to the World Health Organization (WHO), Cancer remains one of the leading causes of death globally, responsible for nearly 10 million Deaths in 2022, accounting for one in six deaths worldwide [1]. The global burden of cancer continues to rise due to population aging, lifestyle changes, and exposure to carcinogenic factors. The most prevalent cancers include breast, lung, colorectal, and prostate cancers, with lung cancer being the leading cause of mortality [2]. Early diagnosis and effective treatment are crucial for improving survival outcomes, as most cancers exhibit better prognoses when detected in early stages. Cancer Can be classified according to various criteria, including histogenesis, tissue of origin, Molecular profile, and clinical behavior [3].

  1. Types of Cancer: -

Fig.1: Types of Cancer.

  1. Carcinoma: -

Carcinomas are malignant tumors that originate from epithelial tissues, which form the outer Coverings of the body, line internal organs, and constitute glandular structures. [4]. The development of carcinomas occurs when epithelial cells undergo genetic Mutations that disturb normal processes of differentiation, proliferation, and apoptosis, leading to uncontrolled cellular growth and eventual tumor formation. Several types are Breast carcinoma, Lung carcinomas, Prostate Carcinoma, Colorectal Carcinoma. Breast carcinoma, causes of cancer-related mortality in women worldwide [5]. Lung carcinoma is strongly associated with tobacco use and Environmental pollutants. Prostate carcinoma is particularly common in older men. Similarly, colorectal carcinoma occurrence influenced by dietary Habits, genetic predisposition, and chronic inflammatory conditions [6].

  1. Sarcoma: -

Sarcomas are malignant tumors that originate from mesenchymal tissues, which include bone, Cartilage, fat, and muscle. Unlike carcinomas that arise from epithelial cells, sarcomas develop from the connective and supportive structures of the body. [7]. Several distinct types of sarcomas have been identified based on their tissue of origin. Osteosarcoma, one of the most common primary bone malignancies, arises from bone-forming Osteoblasts and predominantly affects adolescents and young adults. Liposarcoma develops from adipose (fat) tissue and commonly occurs in deep soft tissues such as the thigh or Retro peritoneum. Chondrosarcoma, in contrast, originates from cartilage-producing cells and Tends to occur in middle-aged to older adults, frequently involving the pelvis, ribs, and long Bones [8].

  1. Leukemia: -

Leukemias are malignant disorders of the blood-forming tissues that originate from bone Marrow stem cells, leading to the uncontrolled production of abnormal white blood cells. These Malignant cells accumulate within the bone marrow and peripheral blood, disrupting normal Hematopoiesis and impairing the production of healthy red blood cells, platelets, and functional Leukocytes [9]. Leukemias are broadly classified based on the rate of disease progression and the lineage of The affected blood cells. Acute leukemias are characterized by a rapid onset and the Proliferation of immature precursor cells, or blasts, that fail to mature properly (Ex. Acute Myeloid Leukemia (AML)). Chronic leukemias have a More gradual onset and involve the accumulation of more mature, yet functionally defective, White blood cells. (Ex. Chronic Myeloid Leukemia (CML)) [10].

  1. Lymphoma:

Lymphomas are malignant neoplasms that originate from the lymphatic system, specifically Involving lymphocytes either B cells or T cells. These cancers typically arise within lymph Nodes but may also develop in extranodal sites such as the spleen, bone marrow, Gastrointestinal tract, or other organs. Lymphomas are broadly classified into two main categories: Hodgkin’s Lymphoma (HL) and Non-Hodgkin’s Lymphoma (NHL) [11].

  1. Myeloma: -

Myeloma, also known as Multiple Myeloma, is a malignant disorder originating from plasma Cells the antibody-producing B lymphocytes residing within the bone marrow. In this condition, Abnormal plasma cells undergo uncontrolled proliferation, leading to the excessive production of a single type of immunoglobulin or its fragments, known as monoclonal proteins (M-Proteins). These malignant cells not only accumulate within the bone marrow but also interfere with the normal production of red blood cells, white blood cells, and platelets, resulting in Widespread hematologic and systemic abnormalities [12].

  1. Mixed Type Cancers: -

Mixed-type cancers are neoplasms that originate from multiple germ cell or tissue lineages Within a single tumor, exhibiting both epithelial and mesenchymal characteristics. A classic example of this category is teratocarcinoma, a tumor that contains differentiated Tissues derived from all three embryonic germ layers—ectoderm, mesoderm, and endoderm. Teratocarcinomas are most commonly found in the gonads, particularly in the testes and Ovaries, although they may also have occur in extragonadal locations such as the mediastinum or Sacrococcygeal region. Histologically, these tumors combine features of benign teratomas, which contain mature tissue elements, with those of malignant embryonal carcinomas, Characterized by undifferentiated, rapidly proliferating cells [13].

  1. Causes and Risk Factors of Cancer: -

Cancer is a multifactorial disease resulting from the complex interaction of genetic, Environmental, biological, and lifestyle factors.

Fig.2: Cancer Risk Factors

  1. Genetic Factors: -
  • Role of Oncogenes and Tumor Suppressor Genes: -

Genetic mutations play a central role in the process of carcinogenesis by disrupting normal cellular control mechanisms that regulate growth, division, and apoptosis. Two major classes of genes are primarily implicated in this process—oncogenes and tumor suppressor genes. Oncogenes are the mutated or overexpressed forms of proto-oncogenes, which are normal genes responsible for promoting controlled cell growth and differentiation. When altered, proto-oncogenes such as RAS, MYC, and HER2 become oncogenes that drive continuous and unregulated cell proliferation, contributing directly to tumor formation. Conversely, tumor suppressor genes, including TP53, RB1, and BRCA1/2, normally act as cellular safeguards by Inhibiting cell division, repairing damaged DNA, or triggering apoptosis in cells that have Sustained irreparable damage. Mutations that inactivate these genes lead to a loss of growth Regulation, enabling abnormal cells to survive and proliferate unchecked [14].

  1. Environmental Factors: -

Environmental carcinogens play a major role in the global burden of cancer, with the World Health Organization estimating that approximately 20% of all cancers are caused by Environmental exposures [15]. These carcinogenic influences include radiation, chemical Pollutants, and industrial emissions, all of which can induce genetic mutations or epigenetic Changes that lead to malignant transformation. Radiation exposure is one of the most well-established environmental causes of cancer. Ionizing radiation, such as X-rays and gamma rays, has sufficient energy to cause DNA double-Strand breaks, resulting in chromosomal aberrations and mutations that promote uncontrolled Cell growth. Individuals exposed to high doses of ionizing radiation—such as atomic bomb Survivors or patients receiving excessive medical radiation—are at increased risk for cancers Of the blood (leukemia), thyroid, and breast. Ultraviolet (UV) radiation, particularly UVB, Represents another potent environmental carcinogen. Chronic exposure to UVB radiation Induces the formation of pyrimidine dimers in DNA, leading to mutations in key genes such as TP53. This mechanism is strongly associated with the development of skin cancers, including Melanoma, squamous cell carcinoma, and basal cell carcinoma [16]. Airborne pollutants and industrial emissions also contribute significantly to carcinogenesis. Fine particulate matter (PM2.5), polycyclic aromatic hydrocarbons (PAHs), and diesel exhaust Are recognized as Group 1 carcinogens by the International Agency for Research on Cancer (IARC). These substances can generate reactive oxygen species, cause oxidative DNA damage, and promote chronic inflammation in exposed tissues. Long-term exposure to such pollutants Has been linked to an increased incidence of lung and bladder cancers, particularly in urban And industrialized regions [17].

  1. Lifestyle Factors: -
  • Tobacco: - Tobacco smoke contains more than 70 known carcinogens, including Benzo[a]pyrene and nitrosamines. It accounts for nearly 30% of all cancer deaths globally, Particularly lung, head, neck, and bladder cancers.
  • Alcohol consumption: -
    Chronic alcohol intake promotes carcinogenesis through acetaldehyde Formation, oxidative stress, and hormonal imbalance. It increases the risk of liver, breast, Esophageal, and colorectal cancers.
  • Diet and Obesity: - High-fat, low-fiber diets and obesity induce chronic inflammation, insulin Resistance, and altered adipokine signaling, predisposing individuals to colorectal, pancreatic, And postmenopausal breast cancers.
  • Physical Inactivity: - Sedentary behavior decreases metabolic rate and immune function, which Are protective against cancer. Regular physical activity reduces the risk of colorectal and breast Cancer by 20–30% [18].
  1. Prevention and Control of Cancer: -

Cancer prevention and control encompass a comprehensive public health strategy aimed at Reducing cancer incidence, promoting early detection, and improving patient quality of life Post- treatment. Prevention efforts are classified into three hierarchical levels primary, Secondary, and tertiary each addressing distinct stages of disease development and Management.

  • Primary Prevention: -

One of the most significant components of primary prevention is lifestyle modification. Modifiable risk factors such as tobacco use, excessive alcohol consumption, poor diet, physical Inactivity, and obesity account for a large proportion of preventable cancers. According to the World Health Organization (WHO), an estimated 30–50% of all cancers can be prevented Through healthy lifestyle choices [19]. Tobacco control remains the most critical measure, as Cigarette smoking is the leading cause of preventable cancer mortality globally. Effective Interventions, including taxation, advertising restrictions, smoke-free legislation, and cessation Support programs, have consistently demonstrated success in reducing cancer prevalence [20]. Diet and physical activity also play pivotal roles in cancer prevention. Consuming a balanced Diet rich in fruits, vegetables, whole grains, and dietary fiber while limiting red and processed Meats, saturated fats, and sugary foods helps lower the risk of colorectal, breast, and Gastrointestinal cancers. Similarly, moderating alcohol intake significantly decreases the Risk of liver, breast, and esophageal cancers. Another cornerstone of primary prevention is vaccination, which plays a decisive role in Preventing virus- associated cancers. [21].

  • Secondary Prevention: -

Secondary prevention focuses on the early detection and diagnosis of cancer, which significantly enhances treatment outcomes and survival rates. By identifying pre-cancerous lesions or early- stage malignancies before they progress, secondary prevention allows for timely intervention and improved prognosis [22]. The cornerstone of this preventive strategy lies in well-structured screening programs, which have proven effective in reducing cancer mortality across multiple cancer types. For cervical cancer, screening through Pap smear testing and HPV DNA testing remains one of the most successful public health interventions [23]. In the case of breast cancer, mammography is the standard screening tool for identifying small, Non-palpable tumors that are often curable with early intervention. [24]. Colorectal cancer screening employs Several techniques, including fecal occult blood testing (FOBT), sigmoidoscopy, and Colonoscopy, which allow for the detection and removal of adenomatous polyps before they Evolve into invasive cancer. These preventive measures have dramatically reduced both the Incidence and mortality associated with colorectal malignancies [25]. Similarly, prostate Cancer detection relies on prostate-specific antigen (PSA) testing, which can help identify early Disease, particularly in men at elevated risk. Although PSA screening remains controversial Due to concerns about overdiagnosis and overtreatment, it continues to be a valuable tool for Selected patient populations. For individuals at high risk of lung cancer, such as long-term heavy smokers, low-dose Computed tomography (LDCT) screening has emerged as a highly effective method. [26].

  • Tertiary Prevention: -

Tertiary prevention focuses on the rehabilitation, long-term management, and quality of life of Individuals who have already been diagnosed with cancer. Its primary objectives are to prevent Disease recurrence, minimize complications, and alleviate the physical and psychological Burdens associated with both the illness and its treatment [27]. Unlike primary and secondary Prevention, which target the onset and early detection of disease, tertiary prevention aims to Optimize health outcomes and functionality after diagnosis and therapy. Rehabilitation forms a Crucial component of tertiary prevention, encompassing physical, nutritional, and Psychological interventions that help cancer survivors regain strength, mobility, and emotional Well-being. Post-treatment complications such as chronic fatigue, peripheral neuropathy, musculoskeletal stiffness, and malnutrition are common and often require multidisciplinary management involving physiotherapists, dietitians, and mental health professionals. Psychological counseling and social support further aid in addressing anxiety, depression, and fear of recurrence, thereby improving overall quality of life [28]. With advancements in cancer treatment leading to increased survival rates, survivorship and palliative care have gained significant importance. Survivorship programs provide structured follow-up for detecting recurrences, managing chronic pain, and addressing the long-term effects of cancer therapies. They also focus on lifestyle modification, health education, and emotional resilience to promote holistic recovery [29].

  1. Treatment Approaches for Cancer: -

Fig.3: Treatments of Cancer

  • Surgery: -

Surgery remains one of the most established and effective modalities in the management of Localized solid tumors, playing a vital role in cancer diagnosis, staging, curative treatment, Palliation, and reconstruction [30]. As a cornerstone of oncologic care, surgical intervention Often provides the best chance for long-term disease control, especially when the malignancy Is detected at an early stage. In the context of localized tumor removal, surgical excision with Clear margins (R0 resection) is the primary goal, as it ensures complete removal of the Malignant tissue while minimizing the risk of recurrence. The principles of surgical oncology Advocate not only the removal of the primary tumor mass but also the dissection of regional Lymph nodes to evaluate potential metastatic spread and guide postoperative treatment Strategies [31]. For instance, procedures such as mastectomy or lumpectomy for breast cancer, Colectomy for colon cancer, radical prostatectomy for prostate cancer, and lobectomy for lung Cancer exemplify curative surgical approaches that have significantly improved patient survival Outcomes [32]. In advanced cases where curative resection is not possible, Palliative surgery serves to relieve distressing symptoms such as obstruction, bleeding, or pain, thereby enhancing patient comfort and quality of life. The advent of minimally invasive Surgical techniques, including laparoscopic and robotic- assisted procedures, has further Revolutionized cancer surgery by reducing postoperative pain, minimizing scarring, shortening Hospital stays, and accelerating recovery [33]

  • Radiation Therapy: -

Radiation therapy (RT) is a localized treatment that utilizes high-energy ionizing radiation to Damage cancer cell DNA, leading to cell death or loss of reproductive potential. Approximately 50–60% of cancer patients receive radiation therapy during their treatment Course, either alone or in combination with other modalities [34].

  • Techniques and Applications-

Modern radiation therapy has undergone remarkable advancements, enabling precise targeting Of tumor tissues while minimizing exposure to surrounding healthy organs. These innovations Have significantly improved both the efficacy and safety of cancer treatment [35]. The most Commonly used modality, External Beam Radiation Therapy (EBRT), employs linear Accelerators to deliver high-energy radiation beams from outside the body directly to the tumor Site. Another important approach, brachytherapy, involves the placement of radioactive sources within or near the tumor, providing a localized and concentrated dose of radiation—commonly Used in cervical and prostate cancers. Further technological refinements such as Intensity Modulated Radiation Therapy (IMRT) and Image-Guided Radiation Therapy (IGRT) allow for precise modulation of radiation dose and real-time imaging during treatment, ensuring Maximum tumor control with minimal damage to adjacent normal tissues. Radiation therapy plays a vital role in various stages of cancer management [36].

  • Chemotherapy: -

Chemotherapy refers to the systemic administration of cytotoxic drugs designed to destroy Rapidly dividing cells, thereby targeting malignant cells that have spread beyond the primary Tumor site. It remains one of the fundamental pillars of systemic cancer treatment, playing a Crucial role in the management of hematologic malignancies as well as advanced solid tumors [37]. The therapeutic goals of chemotherapy can be broadly categorized into curative, Adjuvant, and palliative intents. In the curative setting, chemotherapy aims to achieve complete remission by eradicating all Cancerous cells from the body. This approach has been particularly successful in malignancies Such as testicular cancer and Hodgkin lymphoma, where chemotherapy alone or in combination with other modalities has resulted in high cure rates. As an adjuvant therapy, chemotherapy is Administered after primary treatments like surgery or radiotherapy to eliminate microscopic Residual disease that could lead to recurrence. This strategy is commonly employed in cancers such as breast, colorectal, and lung cancers to improve long-term survival outcomes. In the Palliative context, chemotherapy is used to control tumor growth, alleviate symptoms, and Prolong life in patients with advanced or metastatic disease, where cure is no longer feasible [38]

  • Advantages and Limitations -

Chemotherapy offers several important advantages that make it a cornerstone of modern cancer Treatment. It is highly effective against both primary and metastatic tumors, allowing systemic Control of disease that has spread beyond the original site. Moreover, chemotherapy can be Combined with surgery or radiotherapy to achieve synergistic effects, enhancing the likelihood of complete remission and reducing recurrence rates. It is particularly useful in hematological Malignancies, such as leukemias and lymphomas, where localized treatment modalities are Insufficient because the cancer involves circulating or diffuse cell populations [39]. Despite its therapeutic potential, chemotherapy also presents notable limitations. One of the Most significant challenges is non-selective toxicity, as cytotoxic agents target all rapidly Dividing cells, leading to systemic side effects that affect the bone marrow, gastrointestinal Tract, and hair follicles. Another major concern is the development of drug resistance, wherein Tumor cells adapt through mechanisms such as increased drug efflux, enhanced DNA repair, or Metabolic alterations, thereby reducing treatment efficacy [40]. Chemotherapy also induces Immunosuppression, rendering patients more susceptible to infections due to bone marrow Suppression and diminished immune function. Furthermore, it can profoundly affect quality of Life, causing fatigue, nausea, organ toxicity, and, in some cases, long-term complications such as secondary malignancies. These drawbacks highlight the ongoing need for more selective and targeted therapeutic strategies to improve patient outcomes and reduce adverse effects [41].

  • Recent Advances-

Newer therapeutic trends in oncology focus on improving drug selectivity and minimizing Systemic toxicity while enhancing treatment efficacy. One major advancement is the Development of targeted therapies, such as tyrosine kinase inhibitors like imatinib, which Specifically act on molecular pathways responsible for tumor growth and survival rather than Indiscriminately destroying all rapidly dividing cells. Another significant innovation involves Nanoparticle-based drug delivery systems, which improve the bioavailability and controlled Release of chemotherapeutic agents while reducing adverse effects on healthy tissues. Additionally, modern treatment protocols increasingly employ combination regimens that Integrate chemotherapy with immunotherapy and radiation therapy to achieve synergistic Effects, improving overall response rates and long-term outcomes. These emerging strategies Represent a paradigm shift toward precision medicine, offering more personalized and tolerable Cancer care [42].

  1. Drugs Used in Cancer Treatment: -
  1. Alkylating Agents: -

Example: Cyclophosphamide

Alkylating agents were among the first chemotherapeutic drugs developed and continue to be Widely used due to their broad-spectrum efficacy. Cyclophosphamide, a nitrogen mustard Derivative, is a prototype of this class.

  • Mechanism of Action

Cyclophosphamide exerts its cytotoxicity by alkylating DNA at the N7 position of guanine, Resulting in cross-linking of DNA strands. This interferes with DNA replication and Transcription, ultimately triggering apoptosis in rapidly dividing cells [43].

  • Pharmacokinetics

It can be administered orally or intravenously. Cyclophosphamide is a prodrug, metabolized in the liver via cytochrome P450 enzymes to active metabolites such as phosphor amide mustard and acrolein. The metabolites are renally excreted.

  • Adverse Effects

Major toxicities include myelosuppression, nausea and vomiting, alopecia, and hemorrhagic Cystitis (due to acrolein accumulation). The latter can be prevented by co-administration of Mesna (2-mercaptoethanesulfonate) [44].

  1. Antimetabolites: -
    • Examples: Methotrexate, 5-Fluorouracil (5-FU)

Antimetabolites are structural analogues of natural metabolites involved in nucleotide synthesis and are cell cycle–specific, acting mainly during the S-phase.

  • Mechanism of Action

The mechanism of action of antimetabolite chemotherapeutic agents involves interference with Nucleotide synthesis and DNA replication. Methotrexate (MTX) functions by inhibiting the Enzyme dihydrofolate reductase (DHFR), thereby blocking the formation of tetrahydrofolate, A critical cofactor required for the synthesis of thymidylate and purine nucleotides. This Disruption halts DNA and RNA synthesis, leading to the inhibition of cell proliferation [45]. Similarly, 5- Fluorouracil (5-FU) is metabolically converted within cells to its active form, Fluorodeoxyuridine monophosphate (FdUMP), which binds irreversibly to thymidylate Synthase, preventing the conversion of deoxyuridine monophosphate (dUMP) to thymidine Monophosphate (dTMP). This inhibition results in the depletion of thymidine, an essential Building block for DNA synthesis, ultimately leading to cell death [46].

Adverse Effects

Both agents can cause myelosuppression, mucositis, diarrhea, and hepatotoxicity. MTX Toxicity can be reversed using leucovorin (folic acid) rescue [47].

  1. Antitumor Antibiotics: -
    • Examples: Doxorubicin, Bleomycin

These agents are derived from Streptomyces species and act by interfering with DNA function Through multiple mechanisms.

  • Mechanism of Action

The mechanism of action of anthracycline and glycopeptide antibiotics involves direct Interaction with DNA and the generation of cytotoxic free radicals. Doxorubicin acts primarily By intercalating between DNA base pairs, disrupting the helical structure and inhibiting the Activity of topoisomerase II, an enzyme essential for DNA replication and repair. Additionally, It generates reactive oxygen species that cause oxidative damage and double-strand DNA Breaks, ultimately triggering apoptosis in rapidly dividing cells. In contrast, Bleomycin Exerts its cytotoxic effect by binding to DNA and inducing strand scission through the Formation of free radicals in the presence of iron and oxygen. This oxidative cleavage of DNA Impairs cell division and promotes apoptosis, particularly in the G2 phase of the cell cycle [48].

  • Adverse Effects

The adverse effects of these chemotherapeutic agents vary based on their mechanisms and Target tissues. Doxorubicin is notably associated with dose-dependent cardiotoxicity, resulting From free radical–induced damage to myocardial cells, which can lead to irreversible Congestive heart failure if cumulative doses are exceeded. Other common side effects include Alopecia and myelosuppression, reflecting its cytotoxic impact on rapidly dividing cells. To Mitigate cardiac toxicity, dexrazoxane is often administered as a cardioprotective agent during Prolonged therapy. In contrast, Bleomycin primarily affects the lungs, with pulmonary Fibrosis being its most significant dose-limiting toxicity. Patients may also experience skin Hyperpigmentation, mucocutaneous changes, and fever, while bone marrow suppression is relatively minimal compared to other chemotherapeutic agents, making it useful in Combination regimens where myelotoxicity is a concern [49].

  1. Mitotic Inhibitors: -
    • Examples: Paclitaxel, Vincristine

Mitotic inhibitors disrupt microtubule dynamics, a process essential for mitosis.

  • Mechanism of Action

The mechanism of action of mitotic inhibitors such as paclitaxel and vincristine involves Disruption of the microtubule dynamics essential for cell division. Paclitaxel acts by stabilizing Microtubules, thereby preventing their normal depolymerization during mitosis. This Stabilization interferes with the mitotic spindle function, causing cell cycle arrest at the Metaphase stage and ultimately triggering apoptosis in rapidly dividing cancer cells [50]. In Contrast, Vincristine binds specifically to tubulin dimers, inhibiting the polymerization process Required for microtubule assembly. This disruption of spindle formation leads to mitotic arrest and programmed cell death, making vincristine particularly effective in hematologic Malignancies such as leukemias and lymphomas.

  • Adverse Effects

Common side effects include peripheral neuropathy, bone marrow suppression, and alopecia. Vincristine is notable for neurotoxicity, while paclitaxel often causes hypersensitivity reactions Requiring premedication with corticosteroids and antihistamines [51].

  1. Emerging Trends and Future Perspectives

Cancer research and treatment have evolved rapidly over the past decade, driven by advances in molecular biology, nanotechnology, genomics, and artificial intelligence (AI). These Emerging trends aim to overcome the limitations of conventional chemotherapy—such as systemic toxicity, multidrug resistance, and lack of specificity—by providing targeted, Efficient, and personalized therapeutic strategies. This section explores four major Frontiers: nanoparticle-based drug delivery, personalized and precision oncology, gene therapy with CRISPR, and AI in cancer diagnosis and treatment optimization [52].

  • Nanoparticle-Based Drug Delivery

Nanotechnology represents a revolutionary approach for improving drug delivery, Bioavailability, and tumor targeting. Nanoparticles (NPs) are engineered carriers ranging from 1 to 100 nm in size that can encapsulate chemotherapeutic agents, enhancing their delivery to Tumor tissues via the enhanced permeability and retention (EPR) effect [53].

  • Mechanism and Advantages

Nanoparticles exploit tumor vasculature leakiness to selectively accumulate in cancerous Tissues while minimizing off-target exposure. Common nano carrier systems include liposomes, Polymeric nanoparticles, dendrimers, micelles, and gold nanoparticles. For instance, Doxil® (liposomal doxorubicin)—an FDA-approved formulation—reduces Cardiotoxicity by confining drug release to tumor sites. Similarly, albumin-bound Paclitaxel (Abraxane®) enhances solubility and cellular uptake, improving treatment outcomes In breast and pancreatic cancers.

  • Emerging Research

Modern research focuses on stimuli-responsive nanoparticles that release drugs upon exposure to tumor-specific triggers like pH, temperature, or enzymes, and multifunctional “theranostic” Nanoparticles that combine therapy and imaging [54].

    • Personalized and Precision Oncology

Traditional cancer treatment often employs a “one-size-fits-all” approach; however, Interpatient variability in tumor genetics has made personalized and precision oncology the Future of cancer care.

  • Concept and Application

Personalized oncology tailors’ therapeutic strategies based on the molecular and genetic profile Of an individual’s tumor. Precision medicine leverages genomic sequencing, biomarker profiling, and molecular diagnostics to identify driver mutations and select optimal therapies.

  • Examples of Targeted Therapies

Targeted therapies have revolutionized cancer treatment by focusing on specific molecular Alterations that drive tumor growth. For instance, epidermal growth factor receptor (EGFR) Mutations identified in non-small cell lung cancer (NSCLC) are effectively targeted by tyrosine Kinase inhibitors such as erlotinib and osimertinib, which block aberrant EGFR signaling Pathways responsible for uncontrolled cell proliferation. Similarly, HER2 amplification in Breast cancer is treated with trastuzumab, a monoclonal antibody that binds to HER2 receptors, Inhibiting downstream signaling and inducing immune-mediated tumor cell destruction. In Melanoma, the BRAF V600E mutation leads to constitutive activation of the MAPK pathway, and targeted therapy with vemurafenib effectively inhibits this mutated kinase, resulting in Significant tumor regression [55].

  • Future Directions

The integration of liquid biopsies, circulating tumor DNA (ctDNA), and next-generation Sequencing (NGS) is enabling non-invasive, real-time tumor monitoring, facilitating adaptive Treatment strategies. Furthermore, pharmacogenomic databases are advancing the Prediction of drug efficacy and toxicity for individualized dosing regimens [56].

  • Role of Gene Therapy and CRISPR Technology

Gene therapy introduces or modifies genetic material to correct defective genes responsible for Tumorigenesis. The development of Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR)/Cas9 technology has transformed this field, enabling precise and efficient Genome editing.

  • Mechanism

CRISPR-Cas9 uses a guide RNA (gRNA) to direct the Cas9 nuclease to a specific DNA Sequence, inducing double-stranded breaks repaired via non-homologous end joining (NHEJ) Or homology- directed repair (HDR), allowing gene knockout or correction.

  • Applications in Oncology

In oncology, gene-editing technologies such as CRISPR-Cas9 have opened new avenues for Precise genetic manipulation to combat cancer. One major application involves the knockout Of oncogenes like KRAS, MYC, or BCL2, which are commonly overexpressed or mutated in Various cancers. Disrupting these genes suppresses tumor cell proliferation and survival. Another promising strategy focuses on the restoration of tumor suppressor genes such as p53, whose loss of function is implicated in many malignancies; reactivating these genes can Reinstate normal cell cycle regulation and promote apoptosis of cancer cells. Additionally, Gene-editing techniques are being used to engineer immune cells, particularly chimeric antigen Receptor T cells (CAR-T cells), to enhance their ability to recognize and destroy tumor cells with greater specificity and potency [57].

  • Challenges and Ethical Considerations

Despite its promise, gene therapy faces challenges including off-target effects, immune Reactions, and delivery system limitations. Ethical issues surrounding germline editing also Demand strict regulatory oversight. Ongoing clinical trials are investigating CRISPR-based therapies for hematologic malignancies and solid tumors, marking a paradigm shift in cancer therapeutics [58].

  • Artificial Intelligence in Cancer Diagnosis and Treatment Optimization

Artificial Intelligence (AI) and machine learning (ML) are revolutionizing oncology by Enabling data-driven decision-making across diagnosis, prognosis, and therapy planning.

  • Applications in Cancer Care

Diagnostics and Imaging: AI algorithms can detect malignancies in radiographic and Histopathological images with accuracy comparable to expert pathologists. For example, deep Learning models outperform humans in detecting breast cancer metastases in lymph node Biopsies.

Prognostic Modeling: ML-based predictive models analyze multi-omic data to forecast Disease progression, recurrence, and survival outcomes, facilitating precision prognostics.

Drug Discovery and Treatment Optimization: AI accelerates drug development by Predicting molecular interactions and toxicity profiles. Personalized therapy algorithms Optimize drug combinations based on patient-specific molecular signatures.

Clinical Decision Support Systems (CDSS): Integrated AI platforms such as IBM Watson For Oncology analyze medical literature and patient data to suggest evidence-based treatment Regimens [59].

  • Future Outlook

AI is expected to synergize with genomics and imaging technologies to Establish real-time adaptive oncology systems, enabling continuous learning and improved Patient outcomes through predictive analytics and digital twins [60].

CONCLUSION: -

Cancer continues to be one of the most complex and devastating diseases, with a multifaceted Origin encompassing genetic, environmental, and lifestyle factors. Understanding its diverse Classification from carcinomas and sarcomas to hematologic malignancies—enables clinicians and researchers to adopt more precise diagnostic and therapeutic strategies. Preventive strategies, including vaccination, lifestyle modification, and screening programs, have proven effective in reducing the incidence and mortality of several cancers. Chemotherapy, although associated with systemic toxicity, remains a mainstay of treatment, now complemented by targeted therapies, immunotherapy, and nanomedicine-based delivery systems that enhance efficacy and minimize adverse effects. Emerging technologies such as CRISPR gene editing and artificial intelligence are paving the way for precision oncology, enabling early detection and individualized treatment optimization. Continued integration of molecular diagnostics, advanced therapeutics, and preventive measures holds the key to improving patient survival and quality of life. Ultimately, a multidisciplinary approach combining scientific innovation, clinical expertise, and public health strategies will be essential to effectively combat the global cancer burden.                                          

REFERENCE

  1. Sung H, et.al., “Global Cancer Statistics 2023”, CA Cancer J Clin,2023;73(1):17–54.
  2. Bray F, et.al., “Global cancer transition according to the Human Development Index”, Lancet Oncol, 2022;23(9):1224–36.
  3. Ferlay J, et. al., “Cancer incidence and mortality worldwide”, Int J Cancer, 2021;149(4):778–89.
  4. Torre LA, et.al., “Global Cancer Epidemiology”, CA Cancer J Clin, 2020;70(2):87–108.
  5. Kumar V, Abbas AK, Aster JC, “Robbins and Cotran Pathologic Basis of Disease”,10th Ed., Elsevier; 2021.
  6. Mertens F, et.al., “Sarcomas of soft tissue and bone: a review. Genes Chromosomes Cancer”, 2020;59(12):575–91.
  7. Coindre JM, “Grading of soft tissue sarcomas, Histopatholog”,2018;72(1):51–63.
  8. Rowley JD, “Chromosomal translocations in leukemia”, Nature, 2008;451(7178):849–56.
  9. Jabbour E,   Kantarjian          H,      “Chronic myeloid         leukemia:         2020    update”, Blood, 2020;135(5):387–99.
  10. Carbone A, Gloghini A, “The pathogenesis of Hodgkin lymphoma”, Blood Rev, 2021;48:100798.
  11. Kyle RA, Rajkumar SV, “Pathogenesis of multiple myeloma. Blood”, 2008;111(6):2962- 72.
  12. Ulbright TM, “Germ cell tumors of the gonads: a review”, Mod Pathol, 2020;33(S1): S36– S55.
  13. Levine AJ, “P53: 800 million years of evolution and 40 years of discovery”, Nat Rev Cancer, 2020;20(8):471–80.
  14. Brash DE, “UV signature mutations. Photochem Photobiol”, 2015;91(1):15–26.
  15. Loomis D, et.al., “The carcinogenicity of outdoor air pollution”, Lancet Oncol, 2013;14(13):1262–3.
  16. Islami F, et.al., “Global burden of cancer attributable to tobacco smoking”, CA Cancer J Clin, 2020;70(6):426–45.
  17. Friedenreich CM, et. al., “Physical activity and cancer prevention”, Br J Sports Med, 2021;55(13):763–70.
  18. Bray F, Jemal A, Grey N, Ferlay J, Forman D, “Global cancer transitions according to the Human Development Index (2008–2030)”, Lancet Oncol, 2012;13(8):790–801.
  19. Islami F, Torre LA, Jemal A, “Global trends of lung cancer mortality and smoking Prevalence”, Transl Lung Cancer Res, 2015;4(4):327–38.
  20. Key TJ, et.al.,       “Diet,        nutrition         and the prevention        of         cancer, Public Health Nutr.”,2004;7(1A):187–200.
  21. Boffetta P, Hashibe M, “Alcohol and cancer”, Lancet Oncol, 2006;7(2):149–56.
  22. Schiffman M, Castle PE, Jeronimo J, et.al., “Human papillomavirus and cervical cancer”, Lancet, 2007;370(9590):890–907.
  23. Arbyn M, et.al., “Worldwide burden of cervical cancer”, Vaccine, 2020;38(5):802–11.
  24. Myers ER,  et.al., “Benefits   and    harms   of breast           cancer  screening”,       JAMA, 2015;314(15):1615–34.
  25. Rex DK, et.al., “Colorectal cancer screening: recommendations for physicians And patients”, Am J Gastroenterol, 2017;112(7):1016–30.
  26. Moyer VA, “Screening for prostate cancer: U.S. Preventive Services Task Force Recommendation statement”, Ann Intern Med,2012;157(2):120–34.
  27. Aberle DR, et.al., “Reduced lung-cancer mortality with low-dose computed Tomographic screening”, N Engl J Med, 2011;365(5):395–409.
  28. Silver JK, et.al., “Cancer rehabilitation and survivorship care Cancer”, 2013;119(11 Suppl):2209–16.
  29. Temel JS, et.al., “Early palliative care for patients with metastatic non–small-cell Lung cancer”, N Engl J Med. 2010;363(8):733–42.
  30. Curigliano G, et.al., “Management of cancer treatment–related toxicities”, Ann Oncol, 2020;31(10):1312–24.
  31. Fisher B, et.al., “Surgical adjuvant therapy in breast cancer”, N Engl J Med, 1989;320(8):479–84.
  32. He J, et.al., “Surgical management of lung cancer”, J Thorac Dis, 2018;10(Suppl 7): S863– S876.
  33. Law WL, et al., “Laparoscopic colorectal resection: a comparison with open Surgery”, Ann Surg, 2007;245(1):1–7.
  34. Veronesi U, et. al., “Sentinel-node biopsy to avoid axillary dissection in breast Cancer with clinically negative lymph nodes”, Lancet Oncol, 2013;14(7):607–15.
  35. Delaney G, Jacob S, Featherstone C, Barton M, “The role of radiotherapy in Cancer treatment”, Cancer, 2005;104(6):1129–37.
  36. Bernier J, Hall EJ, Giaccia A, “Radiation oncology: a century of achievements”, Nat Rev Cancer,2004;4(9):737–47.
  37. Bentzen SM, “Preventing or reducing late side effects of radiation therapy”, Nat Rev Cancer, 2006;6(9):702–13.
  38. DeVita VT Jr, “Chu E. A history of cancer chemotherapy”, Cancer Res, 2008;68(21):8643– 53.
  39. Longley DB, Johnston PG, “Molecular mechanisms of drug resistance”, J Pathol, 2005;205(2):275–92.
  40. Burstein HJ, et.al., “Chemotherapy for advanced breast cancer”, J Clin Oncol, 2001;19(6):1671–87.
  41. Holohan C, et. al., “Cancer drug resistance: an evolving paradigm”, Nat Rev Cancer, 2013;13(10):714–26.
  42. Curigliano G, et.al., “Management of cancer treatment–related toxicities”, Ann Oncol, 2020;31(10):1312–24.
  43. Davis ME, Chen ZG, Shin DM, “Nanoparticle therapeutics: an emerging Treatment modality for cancer”, Nat Rev Drug Discov, 2008;7(9):771–82.
  44. Brock N, “Mesna and other thiols for prevention of urotoxicity of Oxazaphosphorine cytostatics”, Cancer Chemother Pharmacol, 1983;11(1):1–6.
  45. Jolivet J, et. al., “The pharmacology and clinical use of methotrexate”, N Engl J Med, 1983;309(18):1094–104.
  46. Tacar O, et.al., “Doxorubicin: an update on anticancer molecular action”, Cancer Treat Rev, 2013;40(4):473–88.
  47. Sleijfer S, “Bleomycin-induced pneumonitis”, Chest. 2001;120(2):617–24.
  48. Swain SM, Whaley FS, Ewer MS, “Congestive heart failure in patients treated with doxorubicin”, Cancer. 2003;97(11):2869–79.
  49. O’Sullivan JM, et.al., “Bleomycin pulmonary toxicity: clinical features and Management”, J Clin Oncol, 2003;21(5):913–26.
  50. Rowinsky EK, “Donehower RC, Paclitaxel and docetaxel in cancer therapy”, J Natl Cancer Inst., 1995;87(16):1265–79.
  51. Weaver BA, “How taxol/paclitaxel kills cancer cells”, Mol Biol Cell, 2014;25(18):2677– 81.
  52.  Siegel RL, Miller KD, Fuchs HE, Jemal A, “Cancer statistics, 2025”, CA Cancer J Clin, 2025;75(1):3–24.
  53. Shi J, Kantoff PW, Wooster R, Farokhzad OC, “Cancer nanomedicine: progress, Challenges and opportunities”, Nat Rev Cancer, 2017;17(1):20–37.
  54. Wang AZ, Langer R, Farokhzad OC, “Nanoparticle delivery of cancer drugs”, Anna Rev Med, 2012;63:185–98.
  55. Dienstmann R, Rodon J, Barretina J, Tabernero J, “Genomic medicine frontier in oncology”, Nat Rev Clin Oncol, 2013;10(9):535–49.
  56. Doble B, Chan CL, Toh CK, Ho BK, Soo RA, “Personalized medicine in Oncology: strategies and future directions”, Front Med, 2021;8:652–81.
  57. Rosenblum D, et. al., “Progress and challenges towards CRISPR-based cancer Therapies”, Nat Commun, 2020;11(1):1–11.
  58. Stadtmauer EA, et.al., “CRISPR-engineered T cells in patients with refractory Cancer”, Science, 2020;367(6481): eaba7365.
  59. Esteva A, et. al., “A guide to deep learning in healthcare”, Nat Med, 2019;25(1):24 – 9.
  60. Bibault JE, et.al., “Artificial intelligence in precision oncology: current Applications and future perspectives”, Cancer Lett, 2021;532:95–105.

Reference

  1. Sung H, et.al., “Global Cancer Statistics 2023”, CA Cancer J Clin,2023;73(1):17–54.
  2. Bray F, et.al., “Global cancer transition according to the Human Development Index”, Lancet Oncol, 2022;23(9):1224–36.
  3. Ferlay J, et. al., “Cancer incidence and mortality worldwide”, Int J Cancer, 2021;149(4):778–89.
  4. Torre LA, et.al., “Global Cancer Epidemiology”, CA Cancer J Clin, 2020;70(2):87–108.
  5. Kumar V, Abbas AK, Aster JC, “Robbins and Cotran Pathologic Basis of Disease”,10th Ed., Elsevier; 2021.
  6. Mertens F, et.al., “Sarcomas of soft tissue and bone: a review. Genes Chromosomes Cancer”, 2020;59(12):575–91.
  7. Coindre JM, “Grading of soft tissue sarcomas, Histopatholog”,2018;72(1):51–63.
  8. Rowley JD, “Chromosomal translocations in leukemia”, Nature, 2008;451(7178):849–56.
  9. Jabbour E,   Kantarjian          H,      “Chronic myeloid         leukemia:         2020    update”, Blood, 2020;135(5):387–99.
  10. Carbone A, Gloghini A, “The pathogenesis of Hodgkin lymphoma”, Blood Rev, 2021;48:100798.
  11. Kyle RA, Rajkumar SV, “Pathogenesis of multiple myeloma. Blood”, 2008;111(6):2962- 72.
  12. Ulbright TM, “Germ cell tumors of the gonads: a review”, Mod Pathol, 2020;33(S1): S36– S55.
  13. Levine AJ, “P53: 800 million years of evolution and 40 years of discovery”, Nat Rev Cancer, 2020;20(8):471–80.
  14. Brash DE, “UV signature mutations. Photochem Photobiol”, 2015;91(1):15–26.
  15. Loomis D, et.al., “The carcinogenicity of outdoor air pollution”, Lancet Oncol, 2013;14(13):1262–3.
  16. Islami F, et.al., “Global burden of cancer attributable to tobacco smoking”, CA Cancer J Clin, 2020;70(6):426–45.
  17. Friedenreich CM, et. al., “Physical activity and cancer prevention”, Br J Sports Med, 2021;55(13):763–70.
  18. Bray F, Jemal A, Grey N, Ferlay J, Forman D, “Global cancer transitions according to the Human Development Index (2008–2030)”, Lancet Oncol, 2012;13(8):790–801.
  19. Islami F, Torre LA, Jemal A, “Global trends of lung cancer mortality and smoking Prevalence”, Transl Lung Cancer Res, 2015;4(4):327–38.
  20. Key TJ, et.al.,       “Diet,        nutrition         and the prevention        of         cancer, Public Health Nutr.”,2004;7(1A):187–200.
  21. Boffetta P, Hashibe M, “Alcohol and cancer”, Lancet Oncol, 2006;7(2):149–56.
  22. Schiffman M, Castle PE, Jeronimo J, et.al., “Human papillomavirus and cervical cancer”, Lancet, 2007;370(9590):890–907.
  23. Arbyn M, et.al., “Worldwide burden of cervical cancer”, Vaccine, 2020;38(5):802–11.
  24. Myers ER,  et.al., “Benefits   and    harms   of breast           cancer  screening”,       JAMA, 2015;314(15):1615–34.
  25. Rex DK, et.al., “Colorectal cancer screening: recommendations for physicians And patients”, Am J Gastroenterol, 2017;112(7):1016–30.
  26. Moyer VA, “Screening for prostate cancer: U.S. Preventive Services Task Force Recommendation statement”, Ann Intern Med,2012;157(2):120–34.
  27. Aberle DR, et.al., “Reduced lung-cancer mortality with low-dose computed Tomographic screening”, N Engl J Med, 2011;365(5):395–409.
  28. Silver JK, et.al., “Cancer rehabilitation and survivorship care Cancer”, 2013;119(11 Suppl):2209–16.
  29. Temel JS, et.al., “Early palliative care for patients with metastatic non–small-cell Lung cancer”, N Engl J Med. 2010;363(8):733–42.
  30. Curigliano G, et.al., “Management of cancer treatment–related toxicities”, Ann Oncol, 2020;31(10):1312–24.
  31. Fisher B, et.al., “Surgical adjuvant therapy in breast cancer”, N Engl J Med, 1989;320(8):479–84.
  32. He J, et.al., “Surgical management of lung cancer”, J Thorac Dis, 2018;10(Suppl 7): S863– S876.
  33. Law WL, et al., “Laparoscopic colorectal resection: a comparison with open Surgery”, Ann Surg, 2007;245(1):1–7.
  34. Veronesi U, et. al., “Sentinel-node biopsy to avoid axillary dissection in breast Cancer with clinically negative lymph nodes”, Lancet Oncol, 2013;14(7):607–15.
  35. Delaney G, Jacob S, Featherstone C, Barton M, “The role of radiotherapy in Cancer treatment”, Cancer, 2005;104(6):1129–37.
  36. Bernier J, Hall EJ, Giaccia A, “Radiation oncology: a century of achievements”, Nat Rev Cancer,2004;4(9):737–47.
  37. Bentzen SM, “Preventing or reducing late side effects of radiation therapy”, Nat Rev Cancer, 2006;6(9):702–13.
  38. DeVita VT Jr, “Chu E. A history of cancer chemotherapy”, Cancer Res, 2008;68(21):8643– 53.
  39. Longley DB, Johnston PG, “Molecular mechanisms of drug resistance”, J Pathol, 2005;205(2):275–92.
  40. Burstein HJ, et.al., “Chemotherapy for advanced breast cancer”, J Clin Oncol, 2001;19(6):1671–87.
  41. Holohan C, et. al., “Cancer drug resistance: an evolving paradigm”, Nat Rev Cancer, 2013;13(10):714–26.
  42. Curigliano G, et.al., “Management of cancer treatment–related toxicities”, Ann Oncol, 2020;31(10):1312–24.
  43. Davis ME, Chen ZG, Shin DM, “Nanoparticle therapeutics: an emerging Treatment modality for cancer”, Nat Rev Drug Discov, 2008;7(9):771–82.
  44. Brock N, “Mesna and other thiols for prevention of urotoxicity of Oxazaphosphorine cytostatics”, Cancer Chemother Pharmacol, 1983;11(1):1–6.
  45. Jolivet J, et. al., “The pharmacology and clinical use of methotrexate”, N Engl J Med, 1983;309(18):1094–104.
  46. Tacar O, et.al., “Doxorubicin: an update on anticancer molecular action”, Cancer Treat Rev, 2013;40(4):473–88.
  47. Sleijfer S, “Bleomycin-induced pneumonitis”, Chest. 2001;120(2):617–24.
  48. Swain SM, Whaley FS, Ewer MS, “Congestive heart failure in patients treated with doxorubicin”, Cancer. 2003;97(11):2869–79.
  49. O’Sullivan JM, et.al., “Bleomycin pulmonary toxicity: clinical features and Management”, J Clin Oncol, 2003;21(5):913–26.
  50. Rowinsky EK, “Donehower RC, Paclitaxel and docetaxel in cancer therapy”, J Natl Cancer Inst., 1995;87(16):1265–79.
  51. Weaver BA, “How taxol/paclitaxel kills cancer cells”, Mol Biol Cell, 2014;25(18):2677– 81.
  52.  Siegel RL, Miller KD, Fuchs HE, Jemal A, “Cancer statistics, 2025”, CA Cancer J Clin, 2025;75(1):3–24.
  53. Shi J, Kantoff PW, Wooster R, Farokhzad OC, “Cancer nanomedicine: progress, Challenges and opportunities”, Nat Rev Cancer, 2017;17(1):20–37.
  54. Wang AZ, Langer R, Farokhzad OC, “Nanoparticle delivery of cancer drugs”, Anna Rev Med, 2012;63:185–98.
  55. Dienstmann R, Rodon J, Barretina J, Tabernero J, “Genomic medicine frontier in oncology”, Nat Rev Clin Oncol, 2013;10(9):535–49.
  56. Doble B, Chan CL, Toh CK, Ho BK, Soo RA, “Personalized medicine in Oncology: strategies and future directions”, Front Med, 2021;8:652–81.
  57. Rosenblum D, et. al., “Progress and challenges towards CRISPR-based cancer Therapies”, Nat Commun, 2020;11(1):1–11.
  58. Stadtmauer EA, et.al., “CRISPR-engineered T cells in patients with refractory Cancer”, Science, 2020;367(6481): eaba7365.
  59. Esteva A, et. al., “A guide to deep learning in healthcare”, Nat Med, 2019;25(1):24 – 9.
  60. Bibault JE, et.al., “Artificial intelligence in precision oncology: current Applications and future perspectives”, Cancer Lett, 2021;532:95–105.

Photo
Pallavi Ghankar
Corresponding author

Navsanjeevan Shikshan Mandal’s College of Pharmacy, Darwha, Dist-Yavatmal Maharashtra India

Photo
Anisha Bhowate
Co-author

Navsanjeevan Shikshan Mandal’s College of Pharmacy, Darwha, Dist-Yavatmal Maharashtra India

Photo
Tejaswini Tidke
Co-author

Navsanjeevan Shikshan Mandal’s College of Pharmacy, Darwha, Dist-Yavatmal Maharashtra India

Photo
Avinash Jiddewar
Co-author

Navsanjeevan Shikshan Mandal’s College of Pharmacy, Darwha, Dist-Yavatmal Maharashtra India

Pallavi Ghankar*, Anisha Bhowate, Tejaswini Tidke, Avinash Jiddewar, The Role of Medicine in Cancer with Emerging Trend and Future Perspective, Int. J. Sci. R. Tech., 2025, 2 (11), 671-683. https://doi.org/10.5281/zenodo.17720050

More related articles
A Review on the Role of the Herbal Ingredients Use...
Harshal Pagar, Vaishali Pagar, Yash Tambe, Vaibhav Thakare, ...
Advancing the Radiopharmaceutical Revolution: Inno...
Alok Kumar, Ankita Singh, Mahesh Kumar Yadav, Aryan Singh, Faizan...
Overview on the Recent in Pharmacological Profile of Terminalia Catappa...
Suvarna Borade, Ghule U. V., Dr. V. A. Kashid, Fiza Shaikh, Mayur Vare, Darshan Pagar, Pratik Pagar,...
Emerging Multidrug-Resistant Fungal Pathogens: Epidemiology, Mechanisms, and Nov...
Haider Abbas, Amulya Singh, Arpit Maurya , Kavya Singh, Dr. Anupam Singh, ...
Characterizing the Role of Suzetrigine Drug as A Non-Opioid Analgesic for Acute ...
Shraddha Ghadage, Snehal Kadbhane, Dr. Vijaykumar kale, Shweta Mahajan, Shweta Dandawthe, ...
Related Articles
Assessment of the Effects of X-Ray Leakage Exposure in Some Selected Teaching Ho...
O. O. Oladapo, Z. A. Akinwale, E. A. Oni, A. A. Aremu, ...
Review -Phytomedicine (Ginger)...
Pragya Yadav, Pramod Mishra, Sujeet Pratap Singh, Tarkeshwar Prasad. Shukla, ...
Harnessing Nature: The Cosmeceutical Promise of Medicinal Plants...
Rutuja Suryawanshi, Vaishali Pagar, Rutuja Gunjal, ...
A Review on the Role of Transdermal Drug Delivery: Microneedles, Patches, and Na...
Yash Tambe, Vaishali Pagar, Harshal Pagar, Vaibhav Thakare, ...
A Review on the Role of the Herbal Ingredients Used in Hair Oil...
Harshal Pagar, Vaishali Pagar, Yash Tambe, Vaibhav Thakare, ...
More related articles
A Review on the Role of the Herbal Ingredients Used in Hair Oil...
Harshal Pagar, Vaishali Pagar, Yash Tambe, Vaibhav Thakare, ...
Advancing the Radiopharmaceutical Revolution: Innovation, Challenges, and Expand...
Alok Kumar, Ankita Singh, Mahesh Kumar Yadav, Aryan Singh, Faizan Raza, Md Raja Ansari, Md Affan, Ra...
A Review on the Role of the Herbal Ingredients Used in Hair Oil...
Harshal Pagar, Vaishali Pagar, Yash Tambe, Vaibhav Thakare, ...
Advancing the Radiopharmaceutical Revolution: Innovation, Challenges, and Expand...
Alok Kumar, Ankita Singh, Mahesh Kumar Yadav, Aryan Singh, Faizan Raza, Md Raja Ansari, Md Affan, Ra...