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  • Cancer: A Comprehensive Review of Classification, Etiology and Evolving Therapeutic Strategies with Special Emphasis on Chemotherapy

  • 1Assistant Professor, Department of Pharmaceutics, Eklavya College of Pharmacy, Tasgaon, Sangli–416416
    2Clinical Research Associate, Alkem Laboratories ltd., Mumbai- 400013
    3Assistant Professor, Department of Pharmacology, Eklavya College of Pharmacy, Tasgaon, Sangli–416416
    4Assistant Professor, Department of Pharmaceutical Chemistry, Eklavya College of Pharmacy, Tasgaon, Sangli–416416
     

Abstract

Cancer is a complex and heterogeneous group of diseases marked by the uncontrolled growth and dissemination of abnormal cells, contributing significantly to global morbidity and mortality. Its origins are multifactorial, involving both environmental influences such as tobacco exposure, radiation, and infectious agents and intrinsic factors like genetic alterations, hormonal disruptions, and immune system irregularities. Based on the tissue of origin, cancers are generally categorized into carcinomas, sarcomas, leukaemia, and lymphomas, each with unique biological characteristics and prognostic outcomes. Treatment approaches vary depending on the cancer type, stage, and molecular profile. Traditional methods include surgical intervention, radiation therapy, and chemotherapy. However, recent innovations have expanded the therapeutic landscape to include targeted treatments, immunotherapies, CAR-T cell therapy, and nanotechnology-based solutions. Chemotherapy remains a foundational systemic treatment, utilizing cytotoxic drugs to disrupt cell division and promote programmed cell death. Despite its effectiveness, chemotherapy poses challenges such as adverse side effects, resistance mechanisms, and lack of specificity. This review aims to provide a detailed exploration of cancer classification and therapeutic modalities, with a particular focus on the evolving role of chemotherapy in oncology. A deeper understanding of these elements is essential for advancing early diagnosis, tailoring personalized treatments, and improving patient outcomes.

Keywords

Cancer, Chemotherapy, Immunotherapy, Targeted therapy

Introduction

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Cancer encompasses a broad spectrum of diseases defined by the unregulated proliferation and dissemination of abnormal cells. Under physiological conditions, cellular growth, differentiation, and apoptosis are tightly regulated through complex molecular signalling networks. Disruption of these pathways through genetic mutations, epigenetic dysregulation, or environmental insults can trigger malignant transformation. According to WHO and GLOBOCAN 2020 estimates, cancer accounts for approximately one in every six deaths worldwide. The global burden is anticipated to escalate further due to aging populations, rising obesity rates, tobacco use, and environmental carcinogen exposure. In 2020, the five most incident cancers were breast (2.26 million), lung (2.21 million), colorectal (1.93 million), prostate (1.41 million), and non-melanoma skin cancers (1.20 million) [1,2]. Detailed global incidence and mortality data are presented [Table 1]. This review provides a structured synthesis of cancer etiology, histological classification, epidemiological trends, and multimodal treatment strategies, with special emphasis on the pharmacological basis and clinical role of chemotherapy in contemporary oncology.

Epidemiology and Global Burden

Cancer is the second leading cause of death globally [3]. In 2020, an estimated 19.3 million new cases were reported, with nearly 10 million cancer-related deaths. Projections indicate that by 2040, annual incidence may exceed 28 million cases if current trends persist. The distribution of cancer types varies considerably by geographic region, income level, and access to healthcare.

Table 1. Global Cancer Incidence and Mortality Statistics (GLOBOCAN 2020)

Cancer Type

New Cases (millions)

Deaths

% of Cancer Deaths

Mortality Rank

Breast

2.26

685,000

6.9%

2nd

Lung

2.21

1,800,000

18.0%

1st

Colorectal

1.93

916,000

9.4%

2nd

Prostate

1.41

375,000

3.8%

5th

Non-melanoma Skin

1.20

63,700

0.6%

—

Stomach

1.09

769,000

7.7%

4th

Liver

0.91

830,000

8.3%

3rd

Cervical

0.60

342,000

3.4%

—

Etiology and Risk Factors

Carcinogenesis is a multistep process involving the progressive accumulation of genetic and epigenetic alterations that transform a normal cell into a malignant phenotype. The IARC classifies etiological agents into physical, chemical, and biological categories [4]. [Table 2] summarizes the principal carcinogenic agents and their associated malignancies.

Table 2. Major Etiological Agents, Exposed Populations, and Associated Cancers

Category

Agent

Exposed Population

Associated Cancer(s)

IARC Class

Physical

Ionizing radiation

Uranium miners, radiologists, Chernobyl survivors

Leukemia, thyroid, lung

IARC Group 1

Physical

Ultraviolet (UV-B/C)

Outdoor workers, sunbed users

Melanoma, BCC, SCC of skin

IARC Group 1

Chemical

Tobacco smoke

Smokers, passive smokers

Lung, oral, bladder, esoph.

IARC Group 1

Chemical

Asbestos

Construction, shipyard workers

Mesothelioma, lung cancer

IARC Group 1

Chemical

Aflatoxins

Contaminated grain/peanut consumers

Hepatocellular carcinoma

IARC Group 1

Chemical

Arsenic (drinking water)

High-arsenic regions (S. Asia, S. America)

Skin, lung, bladder

IARC Group 1

Chemical

Alcohol

Heavy alcohol consumers

Liver, oropharynx, breast

IARC Group 1

Biological

HPV (types 16, 18)

Sexually active individuals

Cervix, oropharynx, vulva

IARC Group 1

Biological

HBV / HCV

Infected individuals

Hepatocellular carcinoma

IARC Group 1

Biological

EBV

Immunocompromised individuals

Burkitt lymphoma, NPC

IARC Group 1

Genetic

BRCA1/2 mutation

Hereditary breast/ovarian cancer families

Breast, ovarian, pancreatic

Germline

Genetic

APC mutation

FAP syndrome carriers

Colorectal cancer

Germline

Histological Classification of Cancer

From a histopathological perspective, cancers are classified according to tissue of origin into six major categories [5,6,7,8]. This classification is of fundamental prognostic and therapeutic relevance. Table 3 provides a structured overview of cancer categories, cell of origin, primary sites, key subtypes, and estimated proportional incidence.

Table 3. Histological Classification of Cancer by Cell of Origin.

Category

Cell of Origin

Primary Sites

Key Subtypes

% of Cancers

Carcinoma

Epithelial cells

Breast, lung, colon, prostate, cervix

Adenocarcinoma, SCC, transitional cell

80–90%

Sarcoma

Mesenchymal / connective tissue

Bone, muscle, fat, cartilage, tendons

Osteosarcoma, liposarcoma, Ewing sarcoma

1%

Myeloma

Plasma cells (bone marrow)

Bone marrow (multifocal)

Multiple myeloma, plasmacytoma

1.8%

Leukemia

Haematopoietic stem cells

Bone marrow / blood

ALL, AML, CLL, CML

3.5%

Lymphoma

Lymphocytes

Lymph nodes, spleen, extranodal

Hodgkin HL, Non-Hodgkin NHL, cutaneous

5%

Mixed Type

Multiple cell lineages

Uterus, testis, lung, ovary

Carcinosarcoma, teratocarcinoma, adenosquamous

Rare

Carcinoma

Carcinomas are malignant neoplasms arising from epithelial cells and constitute approximately 80–90% of all human cancers. The two principal subtypes are adenocarcinoma (glandular origin; breast, lung, colon, prostate) [9,10,11,12] and squamous cell carcinoma (squamous epithelium; skin, cervix, oropharynx, esophagus) [13,14].

    1.  Sarcoma

Sarcomas originate in mesenchymal connective tissues (bone, cartilage, fat, muscle). They are rare (~1% of adult malignancies) but disproportionately affect children and young adults [15,16]. Key subtypes include osteosarcoma, chondrosarcoma, Ewing sarcoma, and soft tissue sarcoma.

Myeloma

Multiple myeloma is characterised by clonal plasma cell proliferation in the bone marrow, overproduction of monoclonal immunoglobulin (M protein), osteolytic bone lesions, hypercalcemia, renal insufficiency, and immunodeficiency [17].

Leukaemia

Leukemias originate from haematopoietic precursor cells and are classified by cell lineage (lymphoid vs. myeloid) and clinical course (acute vs. chronic). Principal subtypes include ALL, AML, CLL, and CML. CML is pathognomonically associated with the BCR-ABL1 fusion arising from the Philadelphia chromosome translocation [18,19,20].

Lymphoma

Lymphomas arise from lymphocytes and are divided into Hodgkin Lymphoma (HL) defined by pathognomonic Reed-Sternberg cells and Non-Hodgkin Lymphoma (NHL), encompassing over 60 biologically distinct subtypes [21,22].

Mixed-Type Tumors

Mixed-type cancers contain neoplastic elements from more than one tissue type or germ cell layer. Notable examples include carcinosarcoma (uterus, ovaries), adenosquamous carcinoma (lung, pancreas, cervix), and teratocarcinoma (testis).

Therapeutic Strategies in Cancer Management

The oncological management of cancer has evolved from single-modality approaches to integrated, multidisciplinary treatment paradigms. [Table 4] provides a comparative overview of the principal treatment modalities, their scope, advantages, limitations, and representative clinical examples.

Table 4. Comparative Overview of Cancer Treatment Modalities

Modality

Scope

Key Advantages

Limitations

Clinical Examples

Surgery

Local / locoregional

Curative; immediate removal

Invasive; limited to localised disease

Appendicectomy (colon), mastectomy (breast)

Radiation Therapy

Local / locoregional

Curative or palliative; organ-sparing

Radiation toxicity; treatment-resistant hypoxic cells

IMRT (prostate), SBRT (lung)

Chemotherapy

Systemic

Broad spectrum; adjuvant/palliative

Non-selective; systemic toxicity; resistance

FOLFOX (CRC), R-CHOP (lymphoma)

Targeted Therapy

Systemic (molecular)

High selectivity; improved OS/PFS

Resistance mutations; high cost

Imatinib (CML), osimertinib (NSCLC)

Immunotherapy

Systemic (immune-based)

Durable responses; memory immunity

Immune-related adverse events (irAEs)

Pembrolizumab (melanoma, NSCLC)

Hormonal Therapy

Systemic (endocrine)

Well tolerated; oral formulations

Limited to hormone-receptor+ tumours

Tamoxifen (breast), enzalutamide (prostate)

Gene Therapy

Systemic / local

Curative potential; precision

Delivery challenges; high cost; early-stage

CAR-T (ALL, DLBCL)

HSCT

Systemic

GvL effect; curative in haematology

High treatment-related mortality; graft failure

Allogeneic HSCT (AML, ALL)

Chemotherapy

Chemotherapy employs cytotoxic agents to interrupt cellular proliferation, predominantly by targeting rapidly dividing cells [23]. Despite its broad clinical utility, chemotherapy is constrained by dose-limiting adverse effects, non-selectivity, and acquired drug resistance. [Table 5] details the principal chemotherapeutic drug classes, their mechanisms of action, representative agents, clinical indications, and cell-cycle specificity [24,25].

Table 5. Classification of Chemotherapeutic Agents by Mechanism of Action

Drug Class

Mechanism of Action

Key Agents

Clinical Indications

Cell Cycle

Alkylating Agents

Covalent DNA cross-linking → replication arrest

Cyclophosphamide, cisplatin, temozolomide, oxaliplatin

Lymphoma, breast, ovarian, glioblastoma

Non-cell cycle specific

Antimetabolites

Competitive inhibition of DNA/RNA synthesis cofactors

Methotrexate, 5-FU, gemcitabine, capecitabine

Colorectal, breast, pancreatic, leukemia

S-phase specific

Topoisomerase I Inhibitors

Prevent re-ligation of single-strand DNA breaks

Irinotecan, topotecan

Colorectal, ovarian, cervical, SCLC

S-phase preferential

Topoisomerase II Inhibitors

Prevent re-ligation of double-strand DNA breaks

Doxorubicin, etoposide, epirubicin

Leukemia, lymphoma, breast, sarcoma

Late S/G2-phase

Taxanes

Microtubule hyperstabilisation → mitotic arrest

Paclitaxel, docetaxel, cabazitaxel

Breast, ovarian, lung, prostate

M-phase specific

Vinca Alkaloids

Tubulin depolymerisation inhibition

Vincristine, vinblastine, vinorelbine

ALL, lymphoma, lung, breast

M-phase specific

Miscellaneous

Multiple / unique mechanisms

Bleomycin, asparaginase, arsenic trioxide

Testicular, ALL, APL

Variable

Targeted Therapy

Targeted therapies exploit specific molecular aberrations in cancer cells, achieving superior selectivity over conventional chemotherapy. [Table 6] summarizes the principal targeted drug classes, molecular targets, representative agents, indications, and predictive biomarkers [26,27,28,29,30,31,32,33,34,35,36].

Table 6. Major Targeted Therapy Classes, Molecular Targets, and Clinical Indications

Drug Class

Molecular Target

Representative Agents

Key Indications

Predictive Biomarker / Notes

EGFR inhibitors

EGFR

Erlotinib, gefitinib, osimertinib

NSCLC (EGFR-mutant)

Exon 19 del / L858R mutation required

HER2-directed

HER2/ErbB2

Trastuzumab, pertuzumab, T-DXd

Breast, gastric (HER2+)

HER2 IHC 3+ or FISH amplification

BCR-ABL1 TKIs

BCR-ABL1 fusion

Imatinib, dasatinib, ponatinib

CML, Ph+ ALL

Philadelphia chromosome t(9;22)

VEGF/VEGFR inhibitors

VEGF / VEGFR

Bevacizumab, sunitinib, sorafenib

RCC, HCC, colorectal, GIST

Anti-angiogenic mechanism

CDK 4/6 inhibitors

CDK4/CDK6

Palbociclib, ribociclib, abemaciclib

HR+ HER2− breast cancer

Used with aromatase inhibitor

PARP inhibitors

PARP-1/2/3

Olaparib, niraparib, rucaparib

BRCA-mutant ovarian/breast

Synthetic lethality mechanism

BRAF/MEK inhibitors

BRAF V600 / MEK

Vemurafenib, dabrafenib, trametinib

BRAF V600E melanoma, NSCLC

Combination recommended to prevent resistance

PD-1/PD-L1 ICIs

PD-1 / PD-L1

Pembrolizumab, nivolumab, atezolizumab

Multiple solid tumors

PD-L1 TPS / TMB as predictive biomarkers

ALK inhibitors

ALK fusion

Alectinib, brigatinib, lorlatinib

ALK-rearranged NSCLC

EML4-ALK fusion most common

Immunotherapy

Cancer immunotherapy harnesses the host immune system to eliminate tumor cells. Approved modalities include immune checkpoint inhibitors (anti-CTLA-4, anti-PD-1/PD-L1), CAR-T cell therapies, bispecific T-cell engagers (BiTEs), and cancer vaccines. CAR-T therapy has demonstrated durable complete remissions in relapsed/refractory B-cell ALL and diffuse large B-cell lymphoma [37,38].

Hormonal Therapy

Endocrine therapy is the standard of care for hormone receptor-positive cancers. ER-positive breast cancer is managed with selective estrogen receptor modulators (tamoxifen), selective estrogen receptor degraders (fulvestrant), or aromatase inhibitors (anastrozole, letrozole). Prostate cancer employs LHRH agonists/antagonists (leuprolide, degarelix) or androgen receptor antagonists (enzalutamide, apalutamide) [39,40].

Gene Therapy and HSCT

Gene therapy encompasses oncogene suppression, tumor suppressor gene restoration, suicide gene therapy, and CRISPR-Cas9-mediated genome editing. Hematopoietic stem cell transplantation (HSCT) enables dose-intensified chemotherapy with haematopoietic rescue and confers graft-versus-leukaemia (GvL) immune effects in allogeneic settings [41,42,43,44,45].

CONCLUSION

Cancer represents a diverse group of diseases unified by dysregulated cellular growth and the potential for systemic dissemination. This review has systematically outlined the etiological determinants, histological classification schema, and principal treatment modalities currently employed in oncology. Chemotherapy, while central to cancer treatment, must be contextualized within a broader multimodal framework that increasingly incorporates targeted therapy, immunotherapy, and precision medicine. Continued investment in translational oncology research, biomarker discovery, and international healthcare equity is essential to improving survival outcomes and quality of life for cancer patients globally.

Author Contributions: Not relevant

Funding: Not relevant

Acknowledgements: Not relevant

Conflicts of interest:  The authors declare no conflict of interest.

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Reference

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  2. Ferlay J, Soerjomataram I, Dikshit R, Eser S, Mathers C, Rebelo M, Parkin DM, Forman D, Bray F. Cancer incidence and mortality worldwide: sources, methods and major patterns in GLOBOCAN 2012. International journal of cancer. 2015 Mar 1;136(5):E359-86.
  3. Saini A, Kumar M, Bhatt S, Saini V, Malik A. Cancer causes and treatments. Int J Pharm Sci Res. 2020 Jul;11(7):3121-34.
  4. Murphy PK, Sellers ME, Bonds SH, Scott S. The SEER Program’s longstanding commitment to making cancer resources available. JNCI Monographs. 2024 Aug;2024(65):118-22.
  5. Zolfaghari B, Mirsadeghi L, Bibak K, Kavousi K. Cancer prognosis and diagnosis methods based on ensemble learning. ACM Computing Surveys. 2023 Mar 3;55(12):1-34.
  6. Abedizadeh R, Majidi F, Khorasani HR, Abedi H, Sabour D. Colorectal cancer: a comprehensive review of carcinogenesis, diagnosis, and novel strategies for classified treatments. Cancer and Metastasis Reviews. 2024 Jun;43(2):729-53.
  7. Rajput JM. Cancer: a comprehensive review. International Journal of Research in Pharmacy and Allied Science. 2023 Jan 1;1(3):42-9.
  8. Van Dooijeweert C, Van Diest PJ, Ellis IO. Grading of invasive breast carcinoma: the way forward. Virchows Archiv. 2022 Jan;480(1):33-43.
  9. Padinharayil H, Varghese J, John MC, Rajanikant GK, Wilson CM, Al-Yozbaki M, Renu K, Dewanjee S, Sanyal R, Dey A, Mukherjee AG. Non-small cell lung carcinoma (NSCLC): Implications on molecular pathology and advances in early diagnostics and therapeutics. Genes & diseases. 2023 May 1;10(3):960-89. https://www.cancer.gov/publications/dictionaries/cancer-terms
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Photo
Satyajeet Jagdale
Corresponding author

Assistant Professor, Department of Pharmaceutics, Eklavya College of Pharmacy, Tasgaon, Sangli–416416

Photo
Siddhant Bansode
Co-author

Clinical Research Associate, Alkem Laboratories ltd., Mumbai- 400013

Photo
Saurabh Joshi
Co-author

Assistant Professor, Department of Pharmacology, Eklavya College of Pharmacy, Tasgaon, Sangli–416416

Photo
Shrirang Kharmate
Co-author

Assistant Professor, Department of Pharmaceutics, Eklavya College of Pharmacy, Tasgaon, Sangli–416416

Photo
Deepak Phalle
Co-author

Assistant Professor, Department of Pharmaceutical Chemistry, Eklavya College of Pharmacy, Tasgaon, Sangli–416416

Satyajeet Jagdale*, Siddhant Bansode, Saurabh Joshi, Shrirang Kharmate, Deepak Phalle, Cancer: A Comprehensive Review of Classification, Etiology and Evolving Therapeutic Strategies with Special Emphasis on Chemotherapy, Int. J. Med. Pharm. Sci., 2026, 2 (8), 712-719. https://doi.org/10.5281/zenodo.22055367

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