Histological Grading Systems of Epithelial Dysplasia & Squamous Cell Carcinoma

Total Page:16

File Type:pdf, Size:1020Kb

Histological Grading Systems of Epithelial Dysplasia & Squamous Cell Carcinoma REVIEW ARTICLE HISTOLOGICAL GRADING SYSTEMS OF EPITHELIAL DYSPLASIA & SQUAMOUS CELL CARCINOMA Parikshit Sharma1, Diksha Singh2,*, Janhavi Dixit3, Manish Kumar Singh4, Naveen Kumar5 1Senior resident, 2Assistant Prof., 3Senior Resident, Oral Pathology FODS, KGMU Lucknow 4Asst. Prof., HOD, Social and Preventive Medicine, BRD Medical College, Gorakhpur 5PGT, Dr. R Ahmed Dental College, kolkata *Corresponding Author: Email: [email protected] Abstract: Oral precancer lesions or conditions are primary indication to be alert about oral health. As there are high chances of oral precancer to turn into malignant lesion. It is difficult to asses that which precancer lesion is highly malignant and which is not. There are lots of classification and grading systems about the grading of oral precancerous lesion, which shows great variabilty and inter observer bias. This review gets importance as we reviewd all grading systems for oral precancer and cancer lesions with their post and cones. Key words: Oral Precancer, Cancer, Tobacco, Dysplasia, Classification INTRODUCTION of the subsequent development of carcinoma. But dysplasia can be found in association with a variety The term ‘dysplasia’ was introduced by of non-neoplastic conditions, such as in the Reagon in 1958 in relation to the cells exfoliated neighbourhood of chronic inflammatory ulceration or from lesions of the uterine cervix. Dysplasia means burns. Furthermore, dysplasia may regress, as has abnormal, atypical proliferation, encountered been shown in the case of the cervix.1,2 principally in the epithelium. In past epithelial Oral precancer lesions can be defined as dysplasia, epithelial atypia and dyskeratosis were altered epithelial lesions which have an increased used synonymously. Pindborg (1977) defined likelihood of progressing to squamous cell epithelial dysplasia as the term used for “A lesion in carcinoma. The nomenclature, natural history and which part of the thickness of the epithelium is predictive value of this group of lesions was replaced by the cells showing varying degrees of reviewed at an expert workshop held in London in cellular atypia.”Burkhart and Maerker (1981) stated 2005, and has been reported in a series of recent that the degree of dysplasia is determined “As a papers3,4. The group recommended that the measure of tissue and cellular deviation from the distinction between potentially malignant lesions and normal.” Kumar et al (1992) defined dysplasia “as conditions should be abandoned in favour of a disturbance in the maturational sequence of the common terminology of Oral potentially malignant stratified squamous epithelium and disturbance in disorders3,5. This recognises the fact that even in cell kinetics of the proliferative compartment with patients with lesions such as leukoplakia, malignancy cytological changes.” Exposur of a cell to carcinogen may arise elsewhere as a result of field change. The leads to cyt5ological changes, depending on the most common disorders recognised as potentially extent and duration of stimuli. An increase in cell malignant are leukoplakia and erythroplakia. The proliferation, diminishing the cytosolic volume and WHO definition of these lesions is generally regarded the associated organelle load, could be an attempt in as unsatisfactory, since it largely a definition by this direction. In the context of oral epithelium, an exclusion. The Working group recommended a new accelerated growth phase depicted by broadening of definition for Leukoplakia which recognises the lack the progenitor compartment (hyperplasia) is the of evidence about risk and the nature of the lesions earlier sequel of exposure to an irritant. When the ‘The term leukoplakia should be used to recognise irritant persists, the epithelium shows features of white plaques of questionable risk having excluded cellular atrophy, again a well characterized feature of (other) known diseases or disorders that carry no adaptation. At a later stage when the stages of increased risk for cancer’ However even this remains adaptation and reversible cell damage surpasses, the unsatisfactory and a clear definition of precursor cells progressively slips into a stage of irreversible lesions may have to wait for further diagnostic cell damage, manifest either as cell death or criteria based on molecular or genetic markers. For neoplastic transformation. The changes of dysplasia, the present time, the prognostic significance of an are in many cases the earliest microscopic evidence individual lesion is difficult to determine, and none of Journal of Oral Medicine, Oral Surgery, Oral Pathology and Oral Radiology;2015;1(1):7-20 7 Sharma et al. Histological Grading Systems of Epithelial Dysplasia & Squamous Cell Carcinoma the currently available molecular markers have benign hyperplastic lesions which may be proved to be prognostically significant and none have encountered. In oral and maxillofacial pathology yet been evaluated in large prospective studies. The therefore, oral epithelial dysplasia is regarded as the gold standard for the assessment of oral potentially standard terminology 4,7. malignant disorders remains the microscopic evaluation of haematoxylin and eosin stained sections Criteria for the diagnosis of oral epithelial dysplasia for the presence of epithelial dysplasia. Some texts The diagnosis and grading of oral epithelial use the terms squamous intraepithelial neoplasia dysplasia is based on a combination of architectural (SIN) or squamous intraepithelial lesions (SIL)6. The and cytological changes6, but evaluation of these is categories under each scheme are similar, but the subjective and has been subject to considerable inter- terminology is different. In the oral cavity, use of the and intra-observer variations in the grading of SIL terminology of ‘atypical hyperplasia’ may lead to lesions, with Kappa values showing only fair to confusion because of the large number of common moderate agreement between observers8,9,10. Table 1: Cytological and architectural features of oral epithelial dysplasia 13. Cellular changes: Architectural (Tissue) changes: Abnormal variation in nuclear size and shape Loss of polarity (anisonucleosis and pleomorphism) Disordered maturation from basal to squamous Abnormal variation in cell size and shape cells (anisocytosis and pleomorphism) Includes top-to-bottom change of carcinoma in Increased nuclear/cytoplasmic ratio situ Enlarged nuclei and cells Increased cellular density Hyperchromatic nuclei Basal cell hyperplasia Increased mitotic figures Dyskeratosis (premature keratinization and Abnormal mitotic figures (abnormal in shape or keratin pearls deep in epithelium) location) Bulbous drop shaped rete pegs Increased number and size of nucleoli. Secondary extensions (nodules) on rete tips. Table 2: Observer variability in head and neck lesions. Studies/ localisation Number of Histopathological Number of agreement Kappa value references slides classification examinators Abbey et al. oral cavity/ 120 WHO° 6 35.8-57.5% 0.15–0.41 1995 oropharynx Fischer et al. oral cavity/ 87 WHO° 24 - 0.59 20041 oropharynx (95% CI: 0.45– 0.72) 0.70 (95% CI: 0.56–0.84)2 Karabulut et oral cavity/ 100 WHO° 4 49–69% 27–45%3 al. 1995 oropharynx Tabor et al. oral cavity/ 43 WHO° 3 53% 0.58 2003 oropharynx Abbey et al. oral cavity/ 120 WHO° 6 38.5% 0.174 1998 oropharynx Brothwell et oral cavity/ 64 WHO° 3 51% 0.37 al. 2003 oropharynx Kujan et al. oral cavity/ 68 WHO and binary 4 WHO: WHO: 2006. oropharynx system 37.7% 0.22 (95% CI: ("low-risk" or (unweighte 0.11–0.35 "high-risk") d) unweighted) 92.8% 0.63 (95% CI: (weighted) 0.42–0.78 Binary weighted) system: Binary system: 74.3% 0.50 Mclaren et larynx 100 WHO and two 13 - WHO: 0.32 al. 2000 grade Two-grade: 0.52 (low and high Grade ° = WHO is not explicitely stated, but terms are in agreement with this system. Journal of Oral Medicine, Oral Surgery, Oral Pathology and Oral Radiology;2015;1(1):7-20 8 Sharma et al. Histological Grading Systems of Epithelial Dysplasia & Squamous Cell Carcinoma 1 = The unweighted kappa considers all disagreements to be equally important, while the weighted kappa (Kw) yields a higher reliability when disagreements between raters are small compared with when they are large. 2 = the pathologic diagnoses are restricted to three categories ('no abnormality/hyperkeratosis', 'mild, moderate, or severe dysplasia', 'carcinoma in situ/carcinoma'). 3 = when comparing the kappa values between the two pairs of pathologists with the same education, these values did not diverge from the general level of kappa values, indicating that the interobserver variability was due to individual differences rather than to educational background. 4 = Clinical information submitted with biopsy. More recently there has been an attempt to significant in the diagnosis of severe dysplasia. more carefully define the criteria for grading of Abnormal shaped rete pegs may also be seen, with epithelial dysplasia7,8. Largely this has involved an lateral extensions or small branches. These are quite adaptation of the scheme used in cervical pathology abnormal and may be the earliest signs of invasion. where it has been traditional to grade cervical Occasional lesions may show prominent acantholysis intraepithelial neoplasia (CIN) according to the with severe disruption of the architecture. Although thickness or levels of involved epithelium. It should the epithelium may be thickened, severe dysplasia is be noted however that full thickness change sometimes accompanied by marked epithelial analogous
Recommended publications
  • Senescence and Apoptosis in Carcinogenesis of Cervical Squamous Carcinoma
    Modern Pathology (2007) 20, 961–966 & 2007 USCAP, Inc All rights reserved 0893-3952/07 $30.00 www.modernpathology.org Senescence and apoptosis in carcinogenesis of cervical squamous carcinoma Wei Feng1, Jianguo Xiao1, Zhihong Zhang2, Daniel G Rosen2, Robert E Brown1, Jinsong Liu2 and Xiuzhen Duan1 1Department of Pathology, The University of Texas Medical School at Houston, Houston, TX, USA and 2Department of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA Senescence and apoptosis are two key mechanisms that protect against cancer development. Many cell cycle regulators, such as p14ARF, p15INK4b and p16INK4a, are important in G1 cell cycle arrest and oncogene-induced senescence. The bcl-2 protein is one of the key components that control apoptosis, while the p53 protein plays key roles in both mechanisms. The genes of these key regulator proteins are often mutated or deleted in various malignancies. It is unknown how senescence and apoptosis are regulated in one of the most common tumors of the female genital tract, cervical squamous cell carcinoma (SCC). In this study the, expression of senescence, apoptosis and proliferation markers in normal cervical epithelium, cervical intraepithelial neoplasia (CIN) and SCC are characterized via immunohistochemical staining for p14ARF, p15INK4b, p16INK4a, bcl-2, p53 and Ki-67 in tissue microarray blocks containing 20 samples each of normal cervix, moderate-to-severe cervical dysplasia (CIN II–III) and invasive SCC. Samples are derived from 60 total cases of cervical biopsies and cervical conizations. Results showed that the proliferation marker, Ki-67, is markedly increased, and the senescence markers, p15INK4b, p16INK4a and p14ARF are overexpressed in both dysplasia and carcinoma.
    [Show full text]
  • Reproductive Al Hyyan Naif Al Balhi Team Sara Al Saif Pathology
    Hazim Jokhadar Rawan Reproductive Al hyyan Naif Al balhi Team Sara Al saif Pathology Pathology of cervix Revised by: th Maria Al ayed 6 Lecture :"Important"infos."|""""""""box"(Males)/""""""""box"(Female):"for"the"extra"infos."in"the"comments"of"lecturer"slides"and"talks"|""""""""box:"for"the"infos."quoted"from"Robbins. PATHOLOGY OF THE CERVIX The Transformation Zone (aka: the Squamo-Columnar Junction) It is of great importance because it is the most common site for dysplasia and cancer. Erosion/Ectropion: IMP Characterized by columnar epithelium replacing squamous epithelium, grossly resulting in an erythematous area. It is a typical response to a variety of stimuli including hormones, chronic irritation and inflammation (chronic cervicitis). It is benign and has no malignant potential. It happens in women with multiple deliveries caused by the excessive pushing leading to prolapse. It is usually operated on and a hysterectomy may be indicated because most of the time it causes bladder prolapse with urgency and involuntary micturition. Cervical Polyp: Benign, very common and easily diagnosed This is a small, peDunculated, often sessile mass. They are inflammatory proliferations of cervical mucosa and are not true neoplasms. The lesion is characterized by overgrowth of benign stroma covereD by epithelium. The stroma contains thick-walleD blooD vessels and fibrous and some inflammatory cells. EnDocervical polyps Ectocervical polyps Originate from the endocervix Originate from the ectocervix Majority are this kind Not as common Covered by endocervical, squamo-columnar or Covered by stratified squamous epithelium. metaplastic squamous epithelium Pap Smears: • Important for early detection. • Once a year after age of 35 Method:Cervical scrapings of mucus anD lining cells dyed with PAP stain Mucus: Lining Cells: For detection of abnormalities Most importantly used for including organisms detection of dysplasia and inflammation and infection carcinoma.
    [Show full text]
  • Correlation Between Koilocytes and Human Papillomavirus Detection by PCR in Oral and Oropharynx Squamous Cell Carcinoma Biopsies
    166 Mem Inst Oswaldo Cruz, Rio de Janeiro, Vol. 106(2): 166-169, March 2011 Correlation between koilocytes and human papillomavirus detection by PCR in oral and oropharynx squamous cell carcinoma biopsies Glauco Issamu Miyahara/+, Luciana Estevam Simonato, Neivio José Mattar, Deolino João Camilo Jr, Eder Ricardo Biasoli Departamento de Patologia e Propedêutica, Centro de Oncologia Bucal, Faculdade de Odontologia de Araçatuba, Universidade Estadual Paulista, Araçatuba, SP, Brasil The purpose of this study was to compare the histopathological analysis with polymerase chain reaction (PCR) methods to predict the presence of human papillomavirus (HPV) infection in oral squamous cell carcinoma biopsies. Eighty-three paraffin-embedded tissue specimens from patients with oropharynx and mouth floor squamous cell carcinoma were submitted to histopathological analysis under light microscopy, specifically for the determination of the presence of koilocytes. Subsequently, DNA was purified from the same paraffin-embedded specimens and submitted to PCR. Fisher’s exact test showed no statistically significant correlation between the two methods. The results suggest that the presence of koilocytes is unreliable for the detection of HPV presence in oral and oropharynx squamous cell carcinoma. Key words: human papillomavirus - squamous cell carcinoma - microscopy - polymerase chain reaction Human papillomavirus (HPV) is considered to be an HPV infection. Koilocytosis consists of the presence of etiological factor for uterine cervix carcinoma and its as- abnormal koilocytes that are vacuolated with nuclear sociation with oral and oropharyngeal carcinomas has pyknosis and large clear perinuclear halos that usually recently been addressed. More than 130-200 HPV types occupy a greater volume than that of the cytoplasm. It have already been described (Lajer & von Buchwald is considered a pathognomonic sign of HPV-associated 2010).
    [Show full text]
  • Grading Evolution and Contemporary Prognostic Biomarkers of Clinically Significant Prostate Cancer
    cancers Review Grading Evolution and Contemporary Prognostic Biomarkers of Clinically Significant Prostate Cancer Konrad Sopyllo 1, Andrew M. Erickson 2 and Tuomas Mirtti 1,3,* 1 Research Program in Systems Oncology, Faculty of Medicine, University of Helsinki, 00014 Helsinki, Finland; konrad.sopyllo@helsinki.fi 2 Nuffield Department of Surgical Sciences, University of Oxford, Oxford OX3 9DU, UK; [email protected] 3 Department of Pathology, HUS Diagnostic Centre, Helsinki University Hospital, 00029 Helsinki, Finland * Correspondence: tuomas.mirtti@helsinki.fi Simple Summary: Prostate cancer treatment decisions are based on clinical stage and histological diagnosis, including Gleason grading assessed by a pathologist, in biopsies. Prior to staging and grading, serum or blood prostate-specific antigen (PSA) levels are measured and often trigger diagnostic examinations. However, PSA is best suited as a marker of cancer relapse after initial treatment. In this review, we first narratively describe the evolution of histological grading, the current status of Gleason pattern-based diagnostics and glance into future methodology of risk assessment by histological examination. In the second part, we systematically review the biomarkers that have been shown, independent from clinical characteristics, to correlate with clinically relevant end-points, i.e., occurrence of metastases, disease-specific mortality and overall survival after initial treatment of localized prostate cancer. Abstract: Gleason grading remains the strongest prognostic parameter in localized prostate ade- nocarcinoma. We have here outlined the evolution and contemporary practices in pathological evaluation of prostate tissue samples for Gleason score and Grade group. The state of more observer- Citation: Sopyllo, K.; Erickson, A.M.; Mirtti, T. Grading Evolution and independent grading methods with the aid of artificial intelligence is also reviewed.
    [Show full text]
  • Metastatic Potential Prediction by a Visual Grading System of Cell Motility: Prospective Validation in the Dunning R-3327 Prostatic Adenocarcinoma Model1
    (CANCER RESEARCH 48. 4312-4317, August 1, 1988] Metastatic Potential Prediction by a Visual Grading System of Cell Motility: Prospective Validation in the Dunning R-3327 Prostatic Adenocarcinoma Model1 James L. Mohler,2 Alan W. Partin,3 John T. Isaacs, and Donald S. Coffey Department of Urology, The Johns Hopkins University School of Medicine and The Johns Hopkins Oncology Center, Baltimore, Maryland 21205 ABSTRACT At present many grading systems are used to assess the metastatic potential of prostatic carcinoma. Whether these A method for accurate prediction of prognosis in individual patients grading systems describe architectural (3), cytological (4), or with prostatic carcinoma does not exist. The limitations of pathological some combination of both features (5-8), they share the short grading systems may result from the failure of standard pathological examination of fixed dead tissue to accurately assess the biological and coming of relying upon the examination of dead tissue to predict metastatic behavior of live tumor cells. Many of the sublines of the the biological behavior of a living dynamic tumor system. At Dunning R-3327 rat prostatic adenocarcinoma are histologically similar present no grading system has utilized living cancer cells that yet differ in metastatic potential. Cells from the Dunning model were may possess biological properties that are related to the aggres grown in culture and filmed by time-lapse videomicroscopy. These cells siveness of neoplasms. Cancer cell motility is an obvious ex exhibited characteristic membrane ruffling, pseudopodal extension, and ample of a property that would be lost with fixation but may cellular translation that could be graded with 80% reproducibility.
    [Show full text]
  • Breast Cancer Grading Poster
    Breast Cancer Grading Nottingham Criteria Accurate grading of invasive breast cancer requires good fixation, processing, section cutting, staining and careful application of grading criteria. In the UK, about 20% of symptomatic breast cancers are grade 1, 30% grade 2, and 50% grade 3. These proportions may be different in asymptomatic cancers detected by mammographic screening. Special type cancers (lobular, etc) should also be graded. Three separate scores are given: ThisGland (acinus) formation Score 1: more than 75% of the whole carcinoma forms acini Only score clearly formed glandular lumens surrounded Score 2: 10–75% of the whole carcinoma forms acini by polarised cancer cells Score 3: less than 10% of the whole carcinoma forms acini Nuclearpublication atypia/pleomorphism Only about 5% of symptomatic cancers score 1 for nuclear atypia; about 50% score 3. Score 1: nuclei only slightly larger than benign breast epithelium (< 1.5 × normal area); minor variation in size, shape and chromatin pattern Score 2: nuclei distinctly enlarged (1.5–2 × normal area), often vesicular, nucleoli visible; may be distinctly variable in size and shape but not always Score 3: markedly enlarged vesicular nuclei (> 2 × normal area), nucleoli often prominent; generally marked variation in size and shape but atypia not necessarily extreme was archived Nuclei of 20 consecutive breast cancers by increasing mean nuclear area (left to right, top to bottom). Paired non-neoplastic breast epithelium is shown above each case for comparison. Only one cancer (top left) has nuclei which score 1. The others in the top row score 2. All 10 in the bottom row score 3.
    [Show full text]
  • Lung Cancer: Clinical Presentation, Epidemiology, 1 Tumor Staging, Classification, Histologic Grading, and Spread Through Air Spaces
    LUNG CANCER: CLINICAL PRESENTATION, EPIDEMIOLOGY, 1 TUMOR STAGING, CLASSIFICATION, HISTOLOGIC GRADING, AND SPREAD THROUGH AIR SPACES CLINICAL PRESENTATION vena cava, or metastasis to distant sites such as Lung cancer presents in different ways, the bone or brain (Table 1-1). largely depending on the location and size of Although the presentation of primary lung the tumor and whether it remains localized to cancer varies with the location and size of the the lung or is metastatic (Table 1-1). One third tumor mass, its extent of spread, and its cell of lung cancer patients present with early stage type, there are many features of lung cancers disease and the rest with advanced disease. Pa- that overlap. Five to 20 percent of patients are tients with early stage tumors may have mini- asymptomatic at the time of diagnosis. These mal or no symptoms; lung cancer screening has patients usually have a chest radiographic im- led to the increased detection of such cancers, aging procedure that reveals a small lung mass resulting in a greater than 20 percent reduction which gets sampled for pathology. However, in mortality (1). Patients with advanced disease over 80 percent of new lung cancer patients can present with symptoms related to invasion have one or more symptoms referable to their or compression of major structures, such as the disease at the time of initial diagnosis, many of Table 1-1 LUNG CANCER PRESENTING SYMPTOMSa Category Symptom Pathogenesis Primary tumor Cough Airway obstruction, atelectasis, infection, airway infammation Hemoptysis
    [Show full text]
  • Coding Guidelines PROSTATE GLAND C619 Grade Note
    SEER Program Coding and Staging Manual 2012 Coding Guidelines PROSTATE GLAND C619 Grade Note: These guidelines pertain to the data item Grade. Refer to the Collaborative Stage Data Collection Manual for instructions on coding site-specific factors for prostate cases. Priority Rules for Grading Prostate Cancer Code the tumor grade using the following priority order 1. Gleason score (Use the table to convert Gleason score to the appropriate code) 2. Terminology Differentiation (well differentiated, moderately differentiated, etc) 3. Histologic grade Grade i, grade ii, grade iii, grade iv 4. Nuclear grade only Gleason Pattern Prostate cancers are commonly graded using Gleason score or pattern. Gleason grading is based on a 5- component system, based on 5 histologic patterns. The pathologist will evaluate the primary pattern (most predominant) and secondary patterns (second most predominant) for the tumor. Example: A Gleason pattern of 2 + 4 means that the primary pattern is 2 and the secondary pattern is 4. Gleason Score The primary and secondary patterns are added together to create a score. Primary pattern is doubled when there is no secondary pattern. Tertiary pattern is not used to determine Gleason score. Example: If the patterns are 2 + 4, the score is 6. If the pathology report contains only one number, and that number is less than or equal to 5, it is a pattern. If the pathology report contains only one number, and that number is greater than 5, it is a score. If the pathology report specifies a specific number out of a total of 10, the first number given is the score.
    [Show full text]
  • Grading of Prostatic Adenocarcinoma: Current State and Prognostic Implications Jennifer Gordetsky1,2 and Jonathan Epstein3,4*
    Gordetsky and Epstein Diagnostic Pathology (2016) 11:25 DOI 10.1186/s13000-016-0478-2 REVIEW Open Access Grading of prostatic adenocarcinoma: current state and prognostic implications Jennifer Gordetsky1,2 and Jonathan Epstein3,4* Abstract Background: Despite significant changes in the clinical and histologic diagnosis of prostate cancer, the Gleason grading system remains one of the most powerful prognostic predictors in prostate cancer. The correct diagnosis and grading of prostate cancer is crucial for a patient’s prognosis and therapeutic options. However, this system has undergone significant revisions and continues to have deficiencies that can potentially impact patient care. Main Body: We describe the current state of grading prostate cancer, focusing on the current guidelines for the Gleason grading system and recent changes from the 2014 International Society of Urological Pathology Consensus Conference on Gleason Grading of Prostatic Carcinoma. We also explore the limitations of the current Gleason grading system and present a validated alternative to the Gleason score. The new grading system initially described in 2013 in a study from Johns Hopkins Hospital and then validated in a multi-institutional study, includes five distinct Grade Groups based on the modified Gleason score groups. Grade Group 1 = Gleason score ≤6, Grade Group 2 = Gleason score 3 + 4 = 7, Grade Group 3 = Gleason score 4 + 3 = 7, Grade Group 4 = Gleason score 8, Grade Group 5 = Gleason scores 9 and 10. Conclusion: As this new grading system is simpler and more accurately reflects prostate cancer biology, it is recommended by the World Health Organization (WHO) to be used in conjunction with Gleason grading.
    [Show full text]
  • “Leukoplakia- Potentially Malignant Disorder of Oral Cavity -A Review”
    DOI: 10.26717/BJSTR.2018.04.001126 Neha Aggarwal. Biomed J Sci & Tech Res ISSN: 2574-1241 Review Article Open Access “Leukoplakia- Potentially Malignant Disorder of Oral Cavity -a Review” Neha Aggarwal*1 and Sumit Bhateja2 1Department of Oral Medicine & Radiology, Manav Rachna Dental College & Hospital, Faridabad, India 2Reader Dept of Oral Medicine and Radiology, Manav Rachna Dental College, India Received: May 18, 2018; Published: May 29, 2018 *Corresponding author: Neha Aggarwal, Senior Lecturer (MDS), Department of Oral Medicine & Radiology, Manav Rachna Dental College & Hospital, Faridabad, India Abstract The term Leukoplakia simply means a “white patch”, and it has been used in a sense to describe any white lesion in the mouth. This lesions. Some investigators tried, although unsuccessfully, to restrict this term only to those white lesions that histologically indicated epithelial non-specific usage led to confusion among physician, surgeons and researchers who attributed a precancerous nature to many innocuous dysplasia. Since the mid-1960s there has been a considerable understanding and clarification in the concept of leukoplakia, and now leukoplakia isKeywords: recognized Leukoplakia; as a specific Potentially entity. malignant disorder Introduction increased risk for cancer. Leukoplakia is a clinical term and the le Leukoplakia is a greek word- Leucos means white and Plakia- - (acanthosis) and may or may not demonstrate epithelial dysplasia. ry by the Hungarian dermatologist, Schwimmer in 1877 [1,2]. WHO sion has no specific histology. It may show atrophy or hyperplasia means patch. It was first coined in the second half of the 19th centu It has a variable behavioural pattern but with an assessable tenden- (1978) [3]- A white patch or plaque that cannot be characterized cy to malignant transformation.
    [Show full text]
  • Bizarre Atypia of the Cervical Epithelium Due to Chemotherapy with Busulfan and Cyclophosphamide
    Turkish Journal of Pathology 2007;23(3):173-176 Bizarre atypia of the cervical epithelium due to chemotherapy with busulfan and cyclophosphamide Servikal epitelde busulfan ve siklofosfamid kemoterapisine ba¤l› bizar atipi Özgür EK‹NC‹, Ifl›lay Bilge YILMAZ, Ömür ATAO⁄LU Gazi Üniversitesi T›p Fakültesi Patoloji Anabilim Dal›, ANKARA ABSTRACT ÖZET We present a 20 year-old female patient with highly aty- Yaz›m›zda uterus serviksinde sitoloji ve biyopsi ile a¤›r pical epithelial changes in the uterine cervix discovered epitelyal atipik de¤ifliklikler gösterilen 20 yafl›ndaki on cervical smear and biopsy specimens. She had re- kad›n hastay› sunmaktay›z. Hasta yak›n zamanda akut cently been diagnosed with acute lymphoblastic lenfoblastik lenfoma tan›s› alm›fl olup alkilleyici ajanlar lymphoma and received alkylating agent chemothe- ile kemoterapi alm›flt›r. Hastam›zda izlenen atipik de¤i- rapy. We thought that the epithelial atypia was related fliklikler, konuyla ilgili literatürün de ›fl›¤›nda kullan›- to chemotherapy in the light of the reports in the litera- lan alkilleyici ajanlara ba¤lanm›fl olup, bu yaz›da ilgili ture which are discussed in the present text along with histopatolojik ve sitolojik kriterler tart›fl›lm›flt›r. a brief review of related histopathological and cytologi- cal criteria. Key words: Cervical dysplasia, chemotherapy, busul- Anahtar sözcükler: Servikal displazi, kemoterapi, bu- fan, cyclophosphamide sulfan, siklofosfamid INTRODUCTION ceived a regimen of busulfan and cyclophospha- mide. She had a cervical smear in her follow-up. Chemotherapy with alkylating agents has The smear slide stained with Papanicolaou stain been known to cause high grade dysplastic alte- revealed severely enlarged cells with hyperchro- rations in epithelial cells (1-4).
    [Show full text]
  • (NCCN) Breast Cancer Clinical Practice Guidelines
    NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines®) Breast Cancer Version 5.2020 — July 15, 2020 NCCN.org NCCN Guidelines for Patients® available at www.nccn.org/patients Continue Version 5.2020, 07/15/20 © 2020 National Comprehensive Cancer Network® (NCCN®), All rights reserved. NCCN Guidelines® and this illustration may not be reproduced in any form without the express written permission of NCCN. NCCN Guidelines Index NCCN Guidelines Version 5.2020 Table of Contents Breast Cancer Discussion *William J. Gradishar, MD/Chair ‡ † Sharon H. Giordano, MD, MPH † Sameer A. Patel, MD Ÿ Robert H. Lurie Comprehensive Cancer The University of Texas Fox Chase Cancer Center Center of Northwestern University MD Anderson Cancer Center Lori J. Pierce, MD § *Benjamin O. Anderson, MD/Vice-Chair ¶ Matthew P. Goetz, MD ‡ † University of Michigan Fred Hutchinson Cancer Research Mayo Clinic Cancer Center Rogel Cancer Center Center/Seattle Cancer Care Alliance Lori J. Goldstein, MD † Hope S. Rugo, MD † Jame Abraham, MD ‡ † Fox Chase Cancer Center UCSF Helen Diller Family Case Comprehensive Cancer Center/ Comprehensive Cancer Center Steven J. Isakoff, MD, PhD † University Hospitals Seidman Cancer Center Massachusetts General Hospital Amy Sitapati, MD Þ and Cleveland Clinic Taussig Cancer Institute Cancer Center UC San Diego Moores Cancer Center Rebecca Aft, MD, PhD ¶ Jairam Krishnamurthy, MD † Karen Lisa Smith, MD, MPH † Siteman Cancer Center at Barnes- Fred & Pamela Buffet Cancer Center The Sidney Kimmel Comprehensive Jewish Hospital and Washington Cancer Center at Johns Hopkins University School of Medicine Janice Lyons, MD § Case Comprehensive Cancer Center/ Mary Lou Smith, JD, MBA ¥ Doreen Agnese, MD ¶ University Hospitals Seidman Cancer Center Research Advocacy Network The Ohio State University Comprehensive and Cleveland Clinic Taussig Cancer Institute Cancer Center - James Cancer Hospital Hatem Soliman, MD † and Solove Research Institute P.
    [Show full text]