PMC3320546_01
On histological examination both endometrial curettage (A: Haematoxylin-Eosin x 100) and cervical biopsy (B: Haematoxylin-Eosin x 200) specimens revealed the presence of a neoplasm characterized by neoplastic signet-ring cells and trabecular structures.
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F1
On histological examination, both specimens revealed the presence of a neoplasm characterized by neoplastic signet-ring cells and trabecular structures (Figure 1).
Immunohistochemical analysis of endometrial neoplasm showed findings consistent with a primary cervical neoplasm, i.e. positivity to Ca-125 (A x 200), CEA (B x 100), and p16 (C x 200) and negativity to Vimentin (D x 200).
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F2
Immunohistochemical analysis showed findings consistent with a primary cervical neoplasm, including positivity to keratin 7, Ca-125, CEA, and p16 and negativity to Vimentin in both endometrial (Figure 2) and cervical biopsy (Figure 3), oestrogen and progesterone receptors.
Immunohistochemical analysis of cervical neoplasm showed findings consistent with a primary cervical neoplasm, i.e. positivity to Ca-125 (A x 100), CEA (B x 200), p16 (C x 200) and negativity to Vimentin (D x 400).
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F3
Immunohistochemical analysis showed findings consistent with a primary cervical neoplasm, including positivity to keratin 7, Ca-125, CEA, and p16 and negativity to Vimentin in both endometrial (Figure 2) and cervical biopsy (Figure 3), oestrogen and progesterone receptors.
Results of HPV-PCR amplification using the L1 consensus primers Gp5+/Gp6+ showing strong positivity for HPV-DNA in both endometrial and biopsy specimens: Lanes 1, 2, 3: CL (Cervical neoplastic lesion) DNA at three different dilutions, with strong signal for HPV-DNA. Lanes 4:, 5, 6: EL (Endometrial neoplastic lesion) DNA at three different dilutions, with strong signal for HPV-DNA. M: molecular weight standard; + = HPV positive control; - = HPV negative control.
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F4
The cervical origin of the neoplasm was also supported by the presence of HPV DNA (Figure 4) by Polymerase chain reaction amplification (PCR) and sequencing analysis which demonstrated the presence of HPV 18 (Figure 5).
Sequence alignment illustrating 100% identities between Human papillomavirus type 18 reference sequence (PAVE entry X05015.1) and HPV DNA from both endometrial and cervical specimens. (End: endometrial lesion)
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F5
The cervical origin of the neoplasm was also supported by the presence of HPV DNA (Figure 4) by Polymerase chain reaction amplification (PCR) and sequencing analysis which demonstrated the presence of HPV 18 (Figure 5).
Microscopic examination of hysterectomy specimen revealed the presence of neoplasm with endometrial and myometrial involvement. The endometrial component of the neoplasm was formed by predominant trabecular and glandular structures (A: Haematoxylin-Eosin x 40) In the myometrial part, the tumour was characterized by lakes of mucus in which neoplastic elements floated (B: Haematoxylin-Eosin x 100).
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F6
The endometrial component consisted of trabecular and glandular structures and signet-ring elements which accounted for 30% of the tumour (Figure 6A). In the myometrial part, the tumour was characterized by lakes of mucus in which neoplastic elements were floating (Figure 6B).