Some recent studies have suggested that patients with Hodgkin lymphoma who undergo remission following treatment are likely to experience significant weight gain and may become overweight or obese. The association between treatment for Hodgkin lymphoma and subsequent weight gain has not been explored in Pakistan. We undertook a review of weight changes in adult Hodgkin lymphoma patients who received treatment at Shaukat Khanum Memorial Cancer Hospital and Research Centre, Lahore.

Abnormal uterine bleeding is one of the most common clinical problems in gynaecological practice and is an indicator of various underlying disorders. An endometrial biopsy should be done in all women over 35 years with AUB to rule out endometrial cancer or pre-malignant lesion and to initiate treatment. However, wide range of histological patterns on endometrial biopsy offer a diagnostic challenge to practicing pathologists. The objective of this study was to determine histological patterns of endometrium in postmenopausal women with abnormal uterine bleeding.

The purpose of this study is to characterize the effect of KAI1 overexpression on the biological behavior of nasopharyngeal carcinoma (NPC) cells.

Dermoid cysts are rare masses of the oral cavity derived from ectodermal elements. These are benign, slow-growing tumors that are typically asymptomatic but cause complications of inflammation or dysphagia, dystonia, and airway encroachment due to mass effects. We report the case of a 17 year old female with a painless mass in the left side of the oral cavity. Ultrasound findings demonstrated non-specific findings of a cystic lesion, and definite diagnosis was made with contrast-enhanced CT and intraoperatively with pathologic confirmation. This retrospective report highlights the challenges in evaluating masses of the oral cavity with imaging and provides a comprehensive discussion on imaging of oral masses on various imaging modalities to guide diagnosis and management.

Uterine leiomyomas (fibroids) are common benign neoplasms, which develop from the muscular tissue of the uterus with an estimated incidence of 20-40% in women of reproductive age. In the early nineties, power morcellators were introduced and became commonly used during hysterectomy for symptomatic fibroids. However, if all fragments are not removed, they may parasitize to other blood supply and present as abdominal or pelvic masses. Unfortunate cases have also been reported in which uterine sarcomas seeded throughout the abdomen and pelvis secondary to morcellation. The Food and Drug Administration (FDA) estimates that 1 in 350 women undergoing hysterectomy or myomectomy for fibroids is found to have an unsuspected uterine sarcoma. As a result, the FDA issued a press release in 2014 discouraging the use of power morcellators. Recently, the FDA approved a new containment device, the PneumoLiner, for use with certain power morcellation devices. However, it is unknown if this device will help to reduce the risk of seeding fibroids and unsuspected uterine malignancies. We present a case in which a patient who underwent morcellation therapy for symptomatic fibroids presented with recurrent abdominal and pelvic leiomyomas mimicking malignancy.

Uterine leiomyosarcoma is an uncommon pathology, predominantly found in aged population. Patients with metastatic disease have poor survival and therapy mainly consists of palliative systemic chemotherapy. However, more aggressive strategies such as radiofrequency ablation (RFA) may benefit patients with limited secondary disease. RFA is considered a simple and safe modality for treatment of hepatic lesions. The benefits related to RFA include low morbidity, short hospital stay and the possibility to repeat the procedure when necessary due to recurrences. However, minor and major complications related to mechanical and thermal damage may occur, especially in cases of tumors adjacent to extrahepatic organs and those at subcapsular position. This case report shows a successful RFA of two hepatic subcapsular leiomyosarcoma metastases neighbouring the gallbladder, without a safe cleavage plane from it. Combined hydrodissection, percutaneous cholecystostomy and continuous irrigation were performed as effective techniques to prevent thermal injury. Clinical and radiological follow up demonstrates no local complication.

A change in tumor size is a well-validated and commonly used value for evaluating response to chemotherapy in cancer. Metabolic changes induced by chemotherapy are related to prognosis in several tumor types. However, the clinical implication of metabolic changes in patients with advanced gastric cancer (AGC) undergoing chemotherapy remains unclear. We aimed to evaluate response of tumor size and metabolism in AGC during chemotherapy and to reveal the relationship between them in view of their impact on patient survival. Methods: We prospectively enrolled patients with AGC before the initiation of first-line palliative chemotherapy. Using baseline and follow-up contrast-enhanced CT and 18F-FDG PET, we assessed the tumor diameter, SUVmax, and total lesion glycolysis in each lesion and their changes during chemotherapy at the same time. We included all lesions with the maximal longest diameters over 1 cm on CT, and each lesion was evaluated by matched 18F-FDG PET. We analyzed the association between changes in tumor metabolism and tumor size and performed outcome analysis on overall survival (OS) and progression-free survival (PFS). Results: Seventy-four patients were enrolled, and the number of all lesions included in this study was 620. Compared with adenocarcinomas, poorly cohesive carcinomas demonstrated lower SUVmax irrespective of tumor size (P < 0.001). Human epidermal growth factor receptor 2 (HER2)-positive tumors showed higher SUVmax than HER2-negative tumors (P = 0.002). The changes in SUVmax due to chemotherapy had a linear correlation with the changes in tumor size of each lesion, and a 30% tumor size reduction was associated with a 50% SUVmax reduction (P < 0.001). Total lesion glycolysis changes also correlated with tumor size changes (P < 0.001). Better OS and PFS were obtained in patients with both tumor size and SUVmax reduction than in patients with either size or SUVmax reduction only (OS, P = 0.003; PFS, P = 0.038). Conclusion: Changes in tumor metabolism induced by chemotherapy correlated with changes in tumor size in AGC. Considering both changes in metabolism and size could help predict a more accurate prognosis for AGC patients undergoing chemotherapy.

A schwannoma is a benign nerve sheath tumor derived from Schwann cells. They are usually small and solitary tumors more frequently localized in cranial nerves and the spinal cord and rarely in the limbs. Some cases have been reported involving extremities (mainly the upper ones) but with a small size. Cases of big size schwannomas unrelated to a neurofibromatosis are very rare. We report the case of a 25 year old patient, with a giant schwannoma which invaded the ischiatic region reaching the triceps surae.

Immunoglobulin G (IgG) has been implicated in the progression of various cancers. This study explored the role of IgG in the proliferation, apoptosis, cell cycle and in vitro invasive properties of LNCaP prostate cancer cells. We used IGHG1 small interfering RNA to silence IgG1 expression in LNCaP cells. The efficacy of IgG1 gene knockdown was confirmed using qPCR and western blotting. The colony formation, proliferation, migration and invasion abilities of LNCaP cells after transfection were assessed using colony-forming, flow cytometry and transwell assays. The expressions of PCNA and caspase-3 proteins in LNCaP cells after transfection were detected with immunofluorescence staining and western blotting. IgG1 silencing significantly decreased the colony formation, survival, cell cycle progression, migration and invasion of LNCaP cells (p < 0.05). IgG1 silencing also reduced the amount of the proliferation marker PCNA and induced formation of the apoptotic marker caspase-3 (p < 0.05). Our results show that IgG1 produced by LNCaP cells confers advantages for tumor cell survival, proliferation, migration and invasion, suggesting that IgG1 is a potential target for prostate cancer treatment.

Bcl2-associated athanogene 2 (BAG2) shares a similar molecular structure and function with other BAG family members. Functioning as a co-chaperone, it interacts with the ATPase domain of the heat shock protein 70 (dHsp70) through its BAG domain. It also interacts with many other molecules and regulates various cellular functions. An increasing number of studies have indicated that BAG2 is involved in the pathogenesis of various diseases, including cancers and neurodegenerative diseases. This paper is a comprehensive review of the structure, functions, and protein interactions of BAG2. We also discuss its roles in diseases, including cancer, Alzheimer's disease, Parkinson's disease and spinocerebellar ataxia type-3. Further research on BAG2 could lead to an understanding of the pathogenesis of these disorders or even to novel therapeutic approaches.

miR-126 is a key regulator of oncogenic processes. It is functionally linked to cellular proliferation, survival and migration. Vascular endothelial growth factor A (VEGF-A), which is regarded as a tumorgenesis activator, could directly target miR-126 in several tumors. However, the mechanism in esophageal cancer remains unclear.

Human papillomaviruses (HPV) are widespread DNA viruses that can infect epithelial cells of the skin and mucosa. Most HPV infections remain clinically unapparent and clear spontaneously. In few cases, however, HPV infections persist and can cause benign and malignant neoplasms at different anatomic locations. Malignant HPV-induced neoplasms are caused by distinct types of HPV (oncogenic or high-risk (HR) HPV types) and present in the anogenital (anus, penis, uterine cervix, vagina and vulva) and head and neck (particularly oropharynx) region. In the anogenital region defined precancerous stages precede invasive cancer. In the head and neck region there is clear evidence only for the invasive stage of HPV-induced neoplasia. In early infection stages the HPV oncogenes (E6/E7) are under tight control in the basal and parabasal cell layers. In more advanced precancerous stages increased expression of the HPV oncogenes E6 and E7 occurs (transforming infection) that may result in transformation of these cells. The defined carcinogenesis in the anogenital tract enables cancer early detection, particularly at the uterine cervix where cytologic and molecular tests contribute to early diagnosis and treatment at a non-invasive stage. Up to now, the treatment of HPV-related precancerous stages (high-grade intraepithelial neoplasia) and cancer is not specifically targeting molecular characteristics of the virus. This article reviews the current state and new developments in epidemiology, prevention, diagnosis and treatment of HPV-associated neoplasia in various anatomic locations.

Human Papillomaviruses (HPVs) are double-stranded DNA viruses, that infect epithelial cells and are etiologically involved in the development of human cancer. Today, over 200 types of human papillomaviruses are known. They are divided into low-risk and high-risk HPVs depending on their potential to induce carcinogenesis, driven by two major viral oncoproteins, E6 and E7. By interacting with cellular partners, these proteins are involved in interdependent viral and cell cycles in stratified differentiating epithelium, and concomitantly induce epigenetic changes in infected cells and those undergoing malignant transformation. E6 and E7 oncoproteins interact with and/or modulate expression of many proteins involved in epigenetic regulation, including DNA methyltransferases, histone-modifying enzymes and subunits of chromatin remodeling complexes, thereby influencing host cell transcription program. Furthermore, HPV oncoproteins modulate expression of cellular micro RNAs. Most of these epigenetic actions in a complex dynamic interplay participate in the maintenance of persistent infection, cell transformation, and development of invasive cancer by a considerable deregulation of tumor suppressor and oncogenes. In this study, we have undertaken to discuss a number of studies concerning epigenetic regulations in HPV-dependent cells and to focus on those that have biological relevance to cancer progression.

Human papillomaviruses are small DNA viruses with a tropism for squamous epithelia. A unique aspect of human papillomavirus molecular biology involves dependence on the differentiation status of the host epithelial cell to complete the viral lifecycle. A small group of these viruses are the etiologic agents of several types of human cancers, including oral and anogenital tract carcinomas. This review focuses on the basic molecular biology of human papillomaviruses.

Human papillomaviruses (HPVs) are the causative agents of 5% of all human cancers, with cervical cancer being the most important. Two viral oncoproteins, E6 and E7, are essential for the development and maintenance of malignancy. Both proteins function by targeting critical pathways that are essential for maintaining cellular homeostasis. As a consequence of these activities, this produces an environment that is favourable for the normal viral life cycle, but when perturbed, can result in the initiation of changes to the host cell, which ultimately results in the development of a malignancy. In this review we discuss the role of these different functions of the viral oncoproteins during the viral life cycle and carcinogenesis, with an emphasis on how induction of DNA damage by the viral oncoproteins, in conjunction with the stem like nature of the target cells, can ultimately result in the development of cancer.

The human papillomavirus (HPV) infection may be associated with the development and progression of non-small cell lung cancer (NSCLC). However, the role of HPV-16 oncoproteins in the development and progression of NSCLC is not completely clear. Epithelial-mesenchymal transition (EMT), a crucial step for invasion and metastasis, plays a key role in the development and progression of NSCLC. Here we explored the effect of HPV-16 oncoproteins on EMT and the underlying mechanisms. NSCLC cell lines, A549 and NCI-H460, were transiently transfected with the EGFP-N1-HPV-16 E6 or E7 plasmid. Real-time PCR and Western blot analysis were performed to analyze the expression of EMT markers. A protein microarray was used to screen the involved signaling pathway. Our results showed that overexpression of HPV-16 E6 and E7 oncoproteins in NSCLC cells significantly promoted EMT-like morphologic changes, downregulated the mRNA and protein levels of EMT epithelial markers (E-cadherin and ZO-1), and upregulated the mRNA and protein levels of EMT mesenchymal markers (N-cadherin and vimentin) and transcription factors (ZEB-1 and Snail-1). Furthermore, the HPV-16 E6 oncoprotein promoted STAT3 activation. Moreover, WP1066, a specific signal transducer and activator of transcription 3 (STAT3) inhibitor, reversed the effect of HPV-16 E6 on the expression of ZO-1, vimentin, and ZEB-1 in transfected NSCLC cells. Taken together, our results suggest that overexpression of HPV-16 E6 and E7 oncoproteins enhances EMT, and the STAT3 signaling pathway may be involved in HPV-16 E6-induced EMT in NSCLC cells.

Peritoneal carcinomatosis represents widespread metastatic disease throughout the abdomen and/or pelvis. Cytoreductive surgery/hyperthermic intraperitoneal chemotherapy (CRS/HIPEC) improves the overall survival compared to standard therapy alone. The role palliative care (PC) plays however, remains poorly studied among these patients.

Gastric cancer is a common cancer with a poor prognosis. Chemokines play important roles in the tumor microenvironments to support tumor growth and metastasis. The effects of C-C motif chemokine ligand 22 (CCL22) in gastric cancer remain unclear.