This study analyzed 22 cases of primary oral melanoma through histopathological and immunohistochemical examination. The results showed that most cases occurred in females around 58 years of age and affected the hard palate. Microscopically, most cases showed deep invasion and a mixed epithelioid and plasmacytoid cell composition. Immunohistochemically, S-100 and HMB-45 stained positive in all cases, while Melan-A was negative in 3 cases. Proliferation rates as measured by Ki-67 were high. This highlights the utility of immunohistochemistry to diagnose oral melanoma.
Please find the power point (ppt.) on everything that you need to know about Malignant melanoma in very simple language by Sunil kumar Daha from very reliable references. Especially focused on surgical interventions. Thank you
Please find the power point (ppt.) on everything that you need to know about Malignant melanoma in very simple language by Sunil kumar Daha from very reliable references. Especially focused on surgical interventions. Thank you
Melanoma
Cutaneous Melanoma
also known as malignant melanoma, is a type of cancer that develops from the pigment-containing cells known as melanocytes.
Classification Of Melanoma
I : De novo melanoma
A. Melanoma in situ (MIS)
B. Lentigo maligna melanoma (LMM)
C. Superficial spreading melanoma (SSM)
D. Nodular melanoma (NM)
E. Acral-lentiginous melanoma (ALM)
F. Melanoma of the mucous membranes
G. Desmoplastic melanoma
II Melanoma arising from precursors
Melanoma arising in dysplastic nevomelanocytic nevi
B. Melanoma arising in congenital nevomelanocytic nevi
C. Melanoma arising in common NMN
Etiology And Pathogenesis
The etiology and pathogenesis of cutaneous melanoma are unknown.
Epidemiologic studies demonstrate a role for genetic predisposition and sun exposure in melanoma development.
The major genes involved in melanoma development reside on chromosome 9p21.
Etiology
UVR, mostly of the UVB spectrum (290–320 nm) that induces mutations in suppressor genes. The propensity for multiple BCC may be inherited. Associated with mutations in the PTCH gene in many cases.
Predisposing Factors
Genetic markers (CDKN2a mutation)
Skin type I/II
Family history of dysplastic nevi or melanoma
Personal history of melanoma
Ultraviolet irradiation, particularly sunburns during childhood and intermittent burning exposures
Number (>50) and size (>5 mm) of melanocytic nevi
Congenital nevi
Number of dysplastic nevi (>5)
Dysplastic melanocytic nevus syndrome
Immune suppression (debatable)
Number (>50) and size (>5 mm) of melanocytic nevi
Congenital nevi
Number of dysplastic nevi (>5)
Dysplastic melanocytic nevus syndrome
Immune suppression (debatable)
Six Signs of Malignant Melanoma (ABCDE Rule):
A- Asymmetry in shape—one-half unlike the other half.
B- Border is irregular—edges irregularly scalloped, notched, sharply defined.
C- Color is not uniform; mottled—haphazard display of colors; all shades of brown, black, gray, red, and white.
D- Diameter is usually large.
E- Elevation is almost always present and is irregular—surface distortion is assessed by side-lighting. others use E for Enlargement— a history of an increase in the size of lesion is one of the most important signs of malignant melanoma.
Lentigo Maligna Melanoma (LMM)
A presentation created by Dr. Henry N. Ho, Medical Director, Head and Neck Program, Florida Hospital Cancer Institute, discussing everything you need to know about head and neck melanoma.
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.
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Melanoma
Cutaneous Melanoma
also known as malignant melanoma, is a type of cancer that develops from the pigment-containing cells known as melanocytes.
Classification Of Melanoma
I : De novo melanoma
A. Melanoma in situ (MIS)
B. Lentigo maligna melanoma (LMM)
C. Superficial spreading melanoma (SSM)
D. Nodular melanoma (NM)
E. Acral-lentiginous melanoma (ALM)
F. Melanoma of the mucous membranes
G. Desmoplastic melanoma
II Melanoma arising from precursors
Melanoma arising in dysplastic nevomelanocytic nevi
B. Melanoma arising in congenital nevomelanocytic nevi
C. Melanoma arising in common NMN
Etiology And Pathogenesis
The etiology and pathogenesis of cutaneous melanoma are unknown.
Epidemiologic studies demonstrate a role for genetic predisposition and sun exposure in melanoma development.
The major genes involved in melanoma development reside on chromosome 9p21.
Etiology
UVR, mostly of the UVB spectrum (290–320 nm) that induces mutations in suppressor genes. The propensity for multiple BCC may be inherited. Associated with mutations in the PTCH gene in many cases.
Predisposing Factors
Genetic markers (CDKN2a mutation)
Skin type I/II
Family history of dysplastic nevi or melanoma
Personal history of melanoma
Ultraviolet irradiation, particularly sunburns during childhood and intermittent burning exposures
Number (>50) and size (>5 mm) of melanocytic nevi
Congenital nevi
Number of dysplastic nevi (>5)
Dysplastic melanocytic nevus syndrome
Immune suppression (debatable)
Number (>50) and size (>5 mm) of melanocytic nevi
Congenital nevi
Number of dysplastic nevi (>5)
Dysplastic melanocytic nevus syndrome
Immune suppression (debatable)
Six Signs of Malignant Melanoma (ABCDE Rule):
A- Asymmetry in shape—one-half unlike the other half.
B- Border is irregular—edges irregularly scalloped, notched, sharply defined.
C- Color is not uniform; mottled—haphazard display of colors; all shades of brown, black, gray, red, and white.
D- Diameter is usually large.
E- Elevation is almost always present and is irregular—surface distortion is assessed by side-lighting. others use E for Enlargement— a history of an increase in the size of lesion is one of the most important signs of malignant melanoma.
Lentigo Maligna Melanoma (LMM)
A presentation created by Dr. Henry N. Ho, Medical Director, Head and Neck Program, Florida Hospital Cancer Institute, discussing everything you need to know about head and neck melanoma.
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.
Hello! Today we prepared for you a biology capstone project example. If you need more go to https://www.capstonewritingservice.com/biology-capstone-project-ideas/
How to Make Awesome SlideShares: Tips & TricksSlideShare
Turbocharge your online presence with SlideShare. We provide the best tips and tricks for succeeding on SlideShare. Get ideas for what to upload, tips for designing your deck and more.
Histopathological patterns of cutaneous malignant melanoma in Sudaniosrjce
IOSR Journal of Dental and Medical Sciences is one of the speciality Journal in Dental Science and Medical Science published by International Organization of Scientific Research (IOSR). The Journal publishes papers of the highest scientific merit and widest possible scope work in all areas related to medical and dental science. The Journal welcome review articles, leading medical and clinical research articles, technical notes, case reports and others.
Yayan T. Sundara, Dokter di Klinik Jejaring Padjadjaran dan Master of Bio Medical Science Research dari Leiden University Medical Centrum, juga staff Departemen Pelayanan PT Rumah Sakit Padjadjaran
EXPRESSION OF CK5 BASAL CYTOKERATIN DURING METASTATIC DEVELOPMENT OF BREAST C...ANCA MARIA CIMPEAN
Objective. Breast cancer is a one of the most common cancers in females worldwide. Basal cytokeratin CK5 represent the marker of progenitors for glandular and myoepithelial lineages of mammary epithelium. During epithelial differentiation there is a gradual decrease of CK5 expression. The purpose of this study was to compare the expression of basal cytokeratin CK5 vs hormone receptors, HER2, Ki67 and molecular subtypes immunohistochemically defined in the primary breast carcinoma of NST type and axillar lymph node metastasis. Material and Methods. We processed immunohistochemically 91 invasive breast carcinomas of NST type and their ipsilateral axillar lymph node metastasis (LNM). Results. The majority of primary tumors were evaluated as CK5 negative (78 cases/85.7%). The majority of cases were evaluated as Luminal B (50 cases/54.9%) and Luminal A (28 cases/30.8%) tumors. The HER2 subtype was confirmed in 8 cases/8.8%, 5NP in 3 cases/3.3% and Basal-like in 2 cases/2.2%. The parallel comparison of CK5 expression at both sites, primary and metastatic, revealed that this marker is not stable during metastatic progression. The molecular subtypes were not stable during metastatic process in 21 cases/23.1%. Conclusions. The majority of NST invasive ductal breast carcinomas are CK5 negative. The molecular subtypes and CK5 are not stable during metastatic process. Cancerous cells prefer to lose this marker in the lymph node environment. The presence of cases with simultaneous expression of CK5 and hormone receptors is an open field to debate the existence of other, transient molecular subtypes. We expect a further confirmation in larger study groups.
Key Words: molecular subtypes, invasive carcinoma NST type, basal cytokeratin.
Clinicomycological profile of Dermatophytosis in a teaching hospitalinventionjournals
International Journal of Pharmaceutical Science Invention (IJPSI) is an international journal intended for professionals and researchers in all fields of Pahrmaceutical Science. IJPSI publishes research articles and reviews within the whole field Pharmacy and Pharmaceutical Science, new teaching methods, assessment, validation and the impact of new technologies and it will continue to provide information on the latest trends and developments in this ever-expanding subject. The publications of papers are selected through double peer reviewed to ensure originality, relevance, and readability. The articles published in our journal can be accessed online.
Genetic Resistance to Infectious Diseases in the Era of Personalized Medicine...CrimsonpublishersCJMI
Genetic Resistance to Infectious Diseases in the Era of Personalized Medicine by Andrei Alimov in Cohesive Journal of Microbiology & Infectious Disease
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
2. Med Oral Patol Oral Cir Bucal. 2012 May 1;17 (3):e383-8. Primary oral melanoma
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Introduction
Melanoma is formed by malignant melanocytes, which are
cells derived from the neural crest that produce melanin
(1). Over 90% of melanomas occur in the skin, but they
may also arise from mucosal surfaces or at other sites
wherein neural crest migrate (1,2). Primary oral melano-
mas are rare, comprising 0.4-1.8% of all melanomas and
0.5% of oral malignances (3-5). Primary OM is more com-
mon in the palate and gingiva of adult patients, and initially
asymptomatic contributing to the delay of diagnosis (6-10).
Clinical features vary, but the most common presentation
is an initial dark blue or black irregular macule, turning
later to an ulcerated black nodule (4,10-12).
As in other types of melanomas, the histology of OM
is variable. Basically it is considered three patterns, in
situ, invasive and mixed, the latter is the most common
corresponding to about 55% of the cases (4,12). The
tumor is formed by epithelioid, spindle and plasmacy-
toid tumor cells arranged in a sheet-like, organoid, al-
veolar, solid or desmoplastic configuration (4,5,12,13).
Most primary OM are heavily pigmented, but some are
amelanotic and immunohistochemistry can be helpful
to confirm the diagnosis of these cases (14-25).
The aim of this study is to describe the histological character-
istics and expression of S-100, HMB-45, Melan-A and Ki-67
in 22 cases of primary OM of Latin American patients.
Materials and Methods
Formalin-fixed, paraffin-embedded tissue blocks were
obtained from 22 patients (8 men and 14 women, mean
age 58 years, range of 23-86 years) with primary OM.
Eleven cases were from Guatemala, 7 from Mexico, and
4 from Peru. Of the 22 OM, seven (31.82%) were locat-
ed on the hard palate, five (22.73%) on hard palate and
upper gingiva, four (18.18%) only on the upper gingiva,
and two each (9.09%), on hard and soft palate, on the
lower gingiva and on the buccal mucosa (Fig. 1).
Diagnosis of primary OM was confirmed by the clinical
and histological characteristics, excluding the presence of
melanoma at other anatomical sites and consequently the
possibility of oral metastasis. The parameters evaluated
included presence or absence of melanin in the tumor
(melanotic or amelanotic), level of tumor cells invasion,
cellular morphology (epithelioid, spindle, plasmacytoid
or mixed) and pattern (solid, alveolar, organoid or paget-
oid), necrosis, perineural and perivascular invasion.
Cellular invasion was considered according to Prasad et
al. (26) as noninvasive (in situ), microinvasive (level I, cell
clusters in the superficial lamina propria), invasive (level
II, cell invasion into the lamina propria), and deep invasive
(level III, invasion into skeletal muscle, bone or cartilage).
For immunohistochemical staining three-micrometer-
thick sections were used. Briefly, after antigen retrieval
with EDTA/Tris buffer (pH 9.0) in a microwave oven,
endogenous peroxidase activity was blocked with 20%
H2
O2
for 5 cycles of 5 minutes each. Primary antibodies
(Table 1), after overnight incubation, were detected by
secondary antibodies conjugated with polymer dextran
marked with peroxidase (Dako EnVision Labelled Poly-
mer; Dako, Glostrup, Denmark). The reaction was de-
veloped with Permanent Red (Permanent Red Substrate
System, Dako) for the primary antibodies S-100, HMB-
45 and Melan-A, and diaminobenzidine hydrochloride
(DAB, Dako) was used as chromogen for Ki-67. The
preparations were lightly counterstained with Carazzi
hematoxylin, mounted with Aquatex (MERCK, Ger-
many) and examined by light microscope.
Antibody Clone Dilution Source
HMB-45 HMB-45 1:200 �ako®*
Melan-A A�03 1:800 �ako®*
Ki-67 M�B-1 1:100 �ako®*
�-100 Polyclonal 1:10.000 �ako®*
Table 1. Antibodies used for immunohistochemical evalua-
tion of 22 cases of primary oral melanomas.
*Dako, Dako Corporation, Carpinteria, California.
Fig. 1. Clinical aspects of primary oral melanoma. A. Oral melanoma of the hard palate showing a large black, irregular macula with
a small nodular area. B. Large pigmented melanoma of the lower gingiva causing tooth displacement.
3. Med Oral Patol Oral Cir Bucal. 2012 May 1;17 (3):e383-8. Primary oral melanoma
e385
The intensity of staining for S-100, HMB-45 and Me-
lan-A was graded as follows: negative (-); weak (+) 1%
to 25%; moderate (++) 25% to 50%; and strong (+++)
50% to 100% of the neoplastic cells. To calculate the
labeling index (LI) for Ki-67, 1000 tumor cells were
counted for each case and the results were expressed in
percentage of positive cells.
Results
Twenty out of 22 primary oral melanomas studied were
melanotic, and only two were amelanotic. Fifteen cases
(68.18%) showed deep cellular invasion (level III) when
diagnosed, while 4 and 2 cases presented levels II and I
respectively, and only one case was classified as in situ.
Cellular morphology varied, with 8 cases formed by epi-
thelioid and one by spindle cells, while the other 13 cases
showedamixedpopulationofepithelioidandplasmacytoid
or spindle cells. Most cases showed a predominant cellu-
lar solid pattern (17 cases-77.27%), followed by alveolar (3
cases), with organoid and pagetoid pattern in only one case
each. Necrosis, perivascular and perineural invasion was
found in 6, 7 and 3 cases respectively (Fig. 2).
Fig. 2. Histological aspects of primary oral melanoma (H&E). A. Oral melanoma of the hard palate composed mainly by
amelanotic spindle cells (x200). B. Oral melanoma of the upper gingiva formed by epithelioid and plasmacytoid neoplastic
melanocytes (x400). C. Solid OM showing nodular pattern of neoplastic melanocytic cells (x25). D. Epithelioid and plasma-
cytoid neoplastic melanocytes arranged in organoid pattern (x100). E. In situ lesion with neoplastic melanocytes arranged in
pagetoid pattern (x100). F. Oral melanoma of the hard palate showing perivascular invasion (x400).
4. Med Oral Patol Oral Cir Bucal. 2012 May 1;17 (3):e383-8. Primary oral melanoma
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Immunostaining with three melanocytic markers S-100,
HMB-45 and Melan-A in melanoma cells was cytoplas-
mic, but nuclear staining was also noted with S-100.
S-100 and HMB-45 were expressed in all cases, while
Melan-A was negative in 3 cases. S-100 was positive in
more than 50% of tumor cells in all cases, and HMB-45
had a strong staining in 21 cases (95.45%), and in one it
was moderate. Melan-A was expressed in 19 out of 22
cases; in 16, one and 2 cases it was strong, moderate and
weak respectively. Cell proliferation with Ki-67 ranged
from 15.51% to 63% of positive cells (Fig. 3).
(13,23,24), but information of histological and immuno-
histochemical profile is scarce.
Different from the skin there is not a definitive clinico-
pathological classification of OM (10,12,23). Classifica-
tion and staging of cutaneous melanomas using Bres-
low and Clark levels cannot be applied to oral mucosa
tumors due to structural differences between skin and
mucosa (13,25). In fact OM differ from cutaneous in
several aspects, including risk factors as actinic radia-
tion, a family history and association with atypical nevi,
factors applied mainly to cutaneous melanoma (4). In
Fig. 3. Expression of S-100 (A), HMB-45 (B), Melan-A (C), and Ki-67 (D) in primary oral melanoma of hard palate and upper gingiva (x400).
Discussion
Primary OM is a rare neoplasm accounting for only
0.5% of all oral malignances, with an incidence of 1.2
cases per 10 million per year (4,10,13). As it is very rare,
there are few reported series of OM. It is considered that
in Europe and Australia the incidence of OM is lower
than in Japan and in other nonwhite populations like in
Uganda, India and North American Indian (2, 6-8). Se-
ries of OM cases in Latin America have been reported
our present study we used the histological classification
proposed by Prasad et al. (26) based on the level of cel-
lular invasion. As noted previously, in contrast to cuta-
neous melanomas where the majority are diagnosed in
the radial growth phase, OM are found predominantly
in the vertical growth phase (4,12). Most cases in our
study were diagnosed with deep invasion (level III)
and only one as in situ. Although lesions in the mouth
usually are easily visualized, particularly if pigmented,
5. Med Oral Patol Oral Cir Bucal. 2012 May 1;17 (3):e383-8. Primary oral melanoma
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most cases of OM are in advanced stages when diag-
nosed. Unfortunately, this is also true for oral squamous
cell carcinoma, despite extensive efforts for early de-
tection of this relatively common neoplasia. Our results
were similar to those found by Lourenço et al. (13), with
82.35% of the cases diagnosed as level III, with only one
case as level I. Oral melanomas have a poor prognosis,
and according to Prasad et al. (26) the most important
histopathological predictor is tumor histological level.
Presence of melanin was observed in 20 cases, as 2
were amelanotic. In fact, it is known that over 90% of
oral melanomas contain melanin that can be easily ob-
served in routine hematoxilin and eosin (5,27). Bachar
et al. (28) studied 61 cases of head and neck mucosal
melanoma finding 6 amelanotic cases (12.8%), similar
to the values found in our study.
Different cell types, showing epithelioid, spindle and
plasmacytoid morphology have been described in OM
(5,12,13). In our series epithelioid cells predominated
in most cases, either as a monomorphous or polymor-
phous infiltrate, usually mixed with plasmacytoid or
spindle cells. The type of cellular infiltrate seems to
have no impact in prediction of tumor behavior; how-
ever, Lourenço et al. (13) observed in their series that
polymorphous tumors had a slightly higher incidence
of vascular infiltration and necrosis. Primary OM are
composed of nests or sheets of malignant cells in solid,
alveolar or organoid patterns, as found in our series
where the solid pattern (77.27%) predominated. As for
the cell type, the cellular pattern also does not seem to
influence the prognosis (5,12,13).
Vascular and perineural invasion was seen in 7 and 3
cases respectively, and similar results were described
by Lourenço et al. (13), who identified 45.71%, 60.61%
and 25.71% of cases with necrosis, perivascular and
perineural invasion respectively. It is interesting that
vascular invasion is more common than perineural, dif-
ferent from other more common oral tumors, as carci-
nomas and adenocarcinomas such as adenoid cystic car-
cinoma and polymorphous low-grade adenocarcinoma.
Although not commonly observed, and therefore not
considered to be an independent factor in most prognos-
tic models, vascular invasion when present in cutaneous
melanoma appears to be associated with a worse prog-
nosis (14). As suggested by Prasad et al. (29) presence
of vascular invasion potentially is an important indica-
tor of poor prognosis in OM, as this is the first step for
regional and distant metastases.
It is important to determine whether OM is a primary
or metastatic lesion. Clinical and microscopical char-
acteristics should be considered as site of involvement,
presence or absence of pigmentation, overlying mucosal
ulceration, extension along salivary glands ducts, and
vascular and perineural invasion (4,6). Pigmented le-
sions involving the palate and gingiva, with ulcerated
mucosa and extension along minor salivary gland are
common findings in primary OM. On the other hand
involvement of base of tongue with intact overlying
mucosa, palatal and gingival sparing, vascular and
perineural invasion are more commonly seen in meta-
static melanoma (4,6).
It is well known that melanoma has a wide spectrum
of histological features which mimic epithelial, hema-
tological, mesenchymal and neural tumors, and when
necessary immunohistochemistry is the primary tool to
establish the correct diagnosis (14-16, 30). Yu et al. (17)
studied the expression of melanocytic differentiation
markers in 6 primary OM. They showed that HMB-45,
S-100 and Melan-A were positive in 100%, 83% and 67%
of the cases respectively, suggesting that both HMB-45
and S-100 are good markers for immunohistochemical
diagnosis of primary OM. In this study, we found that
S-100 was a more sensitive marker than HMB-45 and
Melan-A, although it is much less specific. On the other
hand Prasad et al. (16) found that in sinonasal and OM
the least sensitive marker was HMB-45, marking 85%
of the cases, while S-100 and Melan-A were positive in
about 95% of the cases. In cutaneous melanomas, S-100
is the most sensitive marker with expression in about
98% of cases, but again it is the least specific (14-17).
HMB-45 and Melan-A show similar specificity in cu-
taneous melanomas with expression varying from 77-
100% (14-17, 20). Ki-67 staining is reported as positive
in 13-30% of the cells in cutaneous melanoma, although
individual cases can show almost 100% of nuclear posi-
tivity (14,15,31). In our study Ki-67 showed proliferat-
ing index ranging from 15.51% to 63% of positive cells.
The present study did not consider treatment and prog-
nosis of OM, but it is well established that treatment is
surgical with a very poor prognosis, with 1 and 5 years
survival of 75% and 15% respectively (4).
In summary, primary OM is rare, occurs in adult and
elderly patients and usually are diagnosed at advanced
stages, with very poor prognosis. It is formed by epi-
thelioid, spindle, plasmacytoid or a mixture of these
cells arranged in solid, alveolar and pagetoid pattern.
S-100 and HMB-45 are more frequently expressed than
Melan-A and these markers are helpful to confirm the
diagnosis.
References
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