In metastatic colorectal cancer (mCRC), after the exhaustion of standard chemotherapy lines (FOLFOX, FOLFIRI) and bevacizumab, the treatment strategy is primarily determined by the tumour's molecular profile (RAS, BRAF,…
In metastatic colorectal cancer (mCRC), after the exhaustion of standard chemotherapy lines (FOLFOX, FOLFIRI) and bevacizumab, the treatment strategy is primarily determined by the tumour's molecular profile (RAS, BRAF, microsatellite status/dMMR, HER2) and general performance status. In later lines, investigational and accepted options include targeted therapies, re-challenge strategies, and specific clinical trials. The presented trials and data represent investigational options, do not constitute a general standard of care, and the median survival data (PFS, OS) reported in clinical trials are group-level results that do not guarantee survival for an individual patient.
In refractory metastatic colorectal cancer, the combination of trifluridine-tipiracil (FTD-TPI) with bevacizumab was evaluated in a randomized phase III trial (SUNLIGHT), where the combination demonstrated longer group-level survival compared with FTD-TPI given as monotherapy (median OS: 10.8 months vs. 7.5 months).
In the presence of targeted molecular alterations, such as the BRAF V600E mutation, targeted combination therapies (for example, encorafenib- and cetuximab-based regimens) represent a clinically validated therapeutic approach following progression.
In refractory patients who previously responded to earlier treatments and subsequently progressed, chemotherapy re-challenge (potentially complemented with targeted agents) represents an option that can be investigated in phase II clinical trials (for example, in the study registered under NCT03485027). In addition, trials are ongoing in specific molecular phenotypes (e.g., cetuximab-based continuation in RAS/BRAF wild-type cases in the NCT05312398 and NCT07389265 trials, or immunotherapy combined with toripalimab in pMMR/MSS tumours in the NCT07106034 and NCT06525428 phase II trials).
In non-small cell lung cancer (NSCLC) harboring a KRAS G12A mutation, there are currently no approved therapies specifically targeted to the G12A variant or standard targeted agents (specific KRAS inhibitors available o…
In non-small cell lung cancer (NSCLC) harboring a KRAS G12A mutation, there are currently no approved therapies specifically targeted to the G12A variant or standard targeted agents (specific KRAS inhibitors available on the market are largely restricted to the G12C mutation). In clinical practice, patient management follows general NSCLC protocols, or is possible on an investigational basis within clinical trials. In trial registries, there are currently two active, early-phase trials that may enroll lung cancer patients harboring a KRAS G12A mutation: NCT05786924 (a Phase 1/2 study evaluating the investigational agent S241656 in advanced/metastatic NSCLC and other solid tumors, recruiting) and NCT06917079 (a Phase 1 study with the pan-KRAS inhibitor BBO-11818 in solid tumors, recruiting). Trial sites available in a given country (e.g., in Hungary) and precise eligibility details are not available in the current database results.
Angiogenesis inhibitors (antiangiogenic agents) are drugs that prevent the formation of new blood vessels (angiogenesis).
Angiogenesis inhibitors (antiangiogenic agents) are drugs that prevent the formation of new blood vessels (angiogenesis). Because growing tumours require oxygen and nutrients to proliferate and survive, angiogenesis is a crucial mechanism in tumour growth and metastasis. Angiogenesis inhibitors primarily target the vascular endothelial growth factor (VEGF) signalling pathway: either by binding to the ligand itself to inhibit its activity (such as the monoclonal antibody bevacizumab or the fusion protein aflibercept), or by inhibiting receptor tyrosine kinases with small-molecule kinase inhibitors (TKIs, such as sunitinib or sorafenib). In addition, they can induce what is known as vascular normalisation of the abnormal tumour vasculature, which can improve blood perfusion and enhance the efficacy of co-administered chemotherapy or immunotherapy. Their use can be associated with characteristic adverse effects, such as hypertension and proteinuria.\n\nIn addition to ligand and receptor blockers, bispecific antibodies (such as faricimab, which dual-targets VEGF-A and Ang-2) are also being investigated and used to inhibit neovascularisation in ophthalmologic conditions (such as neovascular age-related macular degeneration) and tumours.
Lung carcinosarcoma (pulmonary carcinosarcoma) is a rare and aggressive lung tumour combining carcinomatous and sarcomatous components.
Lung carcinosarcoma (pulmonary carcinosarcoma) is a rare and aggressive pulmonary neoplasm that combines carcinomatous and sarcomatous components. Currently, international clinical trial registries do not contain open clinical trials specifically dedicated to lung carcinosarcoma; patients are most frequently enrolled into broader protocols targeting advanced non-small cell lung cancer (NSCLC) or solid tumours. Based on literature case reports and observational data, the main directions for experimental and personalised systemic therapies include immunotherapy (immune checkpoint inhibitors, such as nivolumab), targeted therapy based on molecular alterations (for example, osimertinib in the presence of an EGFR mutation, tyrosine kinase inhibitors such as anlotinib, or multi-kinase inhibitors such as pazopanib), as well as newer modalities investigated in other pulmonary sarcomatoid carcinomas, such as Trop-2-targeted antibody-drug conjugates (ADCs).
Due to the rarity of lung carcinosarcoma, the majority of research evidence derives from individual case reports and small cohorts. Case studies have described the efficacy of nivolumab in PD-L1-positive metastatic disease, the combination of osimertinib with neoadjuvant chemotherapy in an EGFR-mutant tumour, and the use of pazopanib or anlotinib supplemented with stereotactic body radiation therapy. In addition, high Trop-2 expression demonstrated in pulmonary sarcomatoid carcinomas raises the potential for future investigation of anti-Trop-2 antibody-drug conjugates.
For the treatment or alleviation of diarrhea occurring during chemotherapy for colorectal cancer (CRC), certain herbal-based formulas and phytotherapeutic preparations are being researched in clinical trials, but curren…
For the treatment or alleviation of diarrhea occurring during chemotherapy for colorectal cancer (CRC), certain herbal-based formulas and phytotherapeutic preparations are being researched in clinical trials, but they do not currently replace standard pharmacological care (e.g., loperamide, supportive therapy) as standard oncological therapy. Among clinical trials, the traditional multi-component herbal preparation called Xiao-Chai-Hu-Tang has been studied in combination with irinotecan-based chemotherapy, where preliminary data showed no severe-grade diarrhea. In addition, the TiaoPi AnChang decoction (TPACD) reduced the overall side effects caused by CAPOX chemotherapy in a randomized, double-blind trial, and the effect of Huangqin Houpo decoction on gut flora and its diarrhea-reducing potential have also been studied at preclinical and network pharmacology levels. However, an oral nanoformulation of curcumin did not show a significant effect in preventing chemotherapy-induced diarrhea in a randomized trial. Before using any herbal remedy or dietary supplement, consultation with an oncologist is essential to avoid potential drug interactions.
The Xiao-Chai-Hu-Tang (XCHT) multi-herbal formulation was evaluated in a pilot phase human clinical trial in advanced colorectal cancer patients receiving irinotecan-based (FOLFIRI) chemotherapy; during treatment, no grade 3–4 severe diarrhea occurred, and the pharmacokinetic profile showed no unfavorable changes in the metabolism of irinotecan.
A randomized, double-blind, placebo-controlled clinical trial with the TiaoPi AnChang decoction (TPACD) demonstrated a reduction in CAPOX-associated side effects and gastrointestinal symptoms in colorectal cancer patients diagnosed with spleen deficiency syndrome.
In contrast, according to a randomized trial in patients with metastatic colorectal cancer, orally administered nano-curcumin (3 × 40 mg daily) did not prove effective in preventing diarrhea induced by chemotherapy (XELOX/FOLFOX-6) compared to placebo.
A nodule found in the lung (pulmonary nodule) is a well-circumscribed, round or oval area on a CT scan, typically measuring less than 3 cm.
A nodule found in the lung (pulmonary nodule) is a well-circumscribed, round or oval area on a CT scan, typically measuring less than 3 cm. A shadow (opacity) may denote a more diffuse, extensive lesion. Nodules are extremely common: in a screening study, they were detectable in up to 51% of smokers (pmid:16244247). Most such lesions are benign; they may represent scar tissue (granuloma) resulting from prior inflammation or infection (e.g., tuberculosis, fungal infection), a benign tumour (e.g., hamartoma), or part of an autoimmune disease (e.g., a rheumatoid nodule). Malignant nodules most frequently arise from primary lung cancer (adenocarcinoma, squamous cell carcinoma, small cell lung cancer) or from metastases originating from other organs.
The radiologist assesses multiple features on the CT scan that help estimate the risk of malignancy. These include nodule size (nodules larger than 10 mm are more likely to be malignant, whereas multiple, tiny nodules are more suggestive of benignity – pmid:42066465), margin irregularity (spiculation, lobulation – these are independent risk factors, pmid:42577057), density (purely solid, ground-glass opacity, or mixed/part-solid), and growth rate. It is an especially concerning sign if the nodule is newly identified or growing compared to a prior examination; according to a large study, growing nodules carry a nearly 20-fold risk, and newly emergent nodules a 4-fold risk, of malignancy (pmid:41850482). The persistence of ground-glass opacity can often indicate early-stage lung adenocarcinoma, while a purely solid, rapidly growing nodule may suggest a more aggressive tumour.
Management is determined by the nodule's characteristics and the patient's individual risk factors (age, smoking history, family history). Based on the Fleischner Society guidelines (pmid:16244247) and the Lung-RADS classification (pmid:41667372), regular follow-up CT surveillance (e.g., at 3, 6, or 12 months) is sufficient for most small nodules. For larger, suspicious nodules, further imaging (PET/CT) or histological sampling (CT-guided biopsy, bronchoscopy) is required. It is important to emphasise that the overwhelming majority of nodules discovered on CT are not cancer, especially those smaller than 6 mm. Nevertheless, a pulmonologist or oncologist should always be consulted for accurate interpretation of the findings and a personalised follow-up plan. Modern artificial intelligence tools increasingly assist radiologists in detecting and characterising nodules, but a biopsy is often required for a definitive diagnosis.
A variety of benign and malignant processes may underlie nodules and shadows found in the lungs. Benign causes include residual scars following prior infections (e.g., tuberculosis, fungal infections, bacterial abscesses), termed granulomas; benign tumours such as hamartoma, fibroma, or the rare sclerosing pneumocytoma; as well as autoimmune conditions such as rheumatoid arthritis, which can cause pulmonary nodules. Chronic inflammatory changes are also common in smokers. In the case of malignant nodules, these represent primary lung cancer (adenocarcinoma, squamous cell carcinoma, small cell carcinoma) or metastases from another organ (e.g., breast, colon, kidney). The characteristics of the nodules—such as size, growth rate, and patient history—help in differentiation.
Detailed analysis of the CT scan is crucial in evaluating the nature of the nodule. Radiologists assess the following features:
- Size: nodules larger than 10 mm have a higher probability of malignancy (pmid:42066465).
- Shape and margins: irregular, spiculated, or lobulated margins suggest malignancy (pmid:42577057).
- Density: ground-glass opacity (GGO) and mixed (part-solid, part-GGO) nodules often indicate early-stage adenocarcinoma; purely solid nodules may be more aggressive.
- Growth: new or growing nodules represent an elevated risk (pmid:41850482).
- Location: nodules located in the upper lobes are more likely to be malignant.
The Fleischner Society 2005 guidelines (pmid:16244247) provide recommendations for the timing of follow-up CT scans based on size and the patient's risk category. Modern artificial intelligence systems detect and classify nodules with increasing accuracy, but they do not replace clinical decision-making.
If a nodule or shadow is identified on a CT report, the next step depends on the nodule's risk stratification. For low-risk, small nodules (e.g., under 6 mm), a follow-up CT scan at 6–12 months is generally sufficient, as recommended by the Fleischner guidelines. For intermediate- or high-risk nodules (e.g., larger than 8–10 mm, growing, or in a high-risk patient), further imaging (FDG-PET/CT) or histological sampling may become necessary. Biopsy can be performed via CT-guided percutaneous puncture, bronchoscopy, or even navigational techniques. The Lung-RADS system (pmid:41667372) helps standardise the classification of nodules detected during screening examinations. It is important that the patient always consults a specialist in pulmonology or oncology, who will determine the necessary course of action based on the overall clinical picture. The majority of nodules are benign, so panic is unnecessary; however, regular follow-up and adherence to specialist instructions are essential.
In its early stages, lung cancer is often completely asymptomatic or presents with non-specific complaints, which is why a significant proportion of patients are diagnosed only at an advanced stage.
In its early stages, lung cancer is often completely asymptomatic or presents with non-specific complaints, which is why a significant proportion of patients are diagnosed only at an advanced stage. The most common initial symptoms include a persistent cough or a change in the character of a chronic cough, dyspnea, chest pain, and haemoptysis. In addition, general systemic symptoms often appear, such as unexplained loss of appetite, weight loss, and chronic fatigue. In rarer cases, due to mediastinal extension or metastases of the tumour, difficulty swallowing (dysphagia) or paraneoplastic neurological syndromes may also be the first observed complaints. An investigation is indicated in all cases where respiratory symptoms (especially a cough persisting for more than 2–3 weeks, shortness of breath, or chest pain) do not resolve, when the character of a cough changes in smokers, or when an isolated episode of haemoptysis and unexplained weight loss occur. Furthermore, in high-risk individuals (particularly those with a significant smoking history), organised or individual screening with low-dose chest computed tomography (LDCT) is recommended even in an asymptomatic state.\n\nBased on data from clinical trials and cohorts, the early detection of lung cancer represents a serious challenge, as in more than 70% of patients the diagnosis is made only after the onset of symptoms, often in an advanced stage. In cases detected via screening (LDCT) or as incidental findings, the proportion of early stages treatable with curative intent is substantially higher, and overall survival is significantly longer.\n\nAccording to structured diagnostic protocols, upon detection of suspicious symptoms, a chest X-ray or low-dose chest CT is indicated as a first-line radiological examination. In the presence of an abnormal imaging finding or high clinical suspicion, a multidisciplinary investigation—including contrast-enhanced CT, tissue sampling, and organ-specific functional tests—must take place within targeted time windows in order to minimise therapeutic delay.
In its early stages, ovarian cancer is often oligosymptomatic or presents with non-specific complaints, which frequently delays diagnosis.
In its early stages, ovarian cancer is often oligosymptomatic or presents with non-specific complaints, which frequently delays diagnosis. According to clinical research and guidelines (such as the Goff symptom index and NICE recommendations), the most characteristic and frequent symptoms include: abdominal or pelvic pain and discomfort, persistent bloating or an increase in abdominal circumference, difficulty eating, early satiety or loss of appetite, and changes in urinary habits (increased urinary frequency or urgency). In addition, alterations in bowel habits (such as constipation, dyspepsia), unusual or extreme fatigue, back pain, and unexplained weight loss may also occur. Suspicion is warranted if these complaints are of new onset, are persistent, or occur frequently on a monthly basis (such as on more than 12 days per month).\n\nInternational tools used for symptom assessment—such as the BEAT campaign (Bloating, Eating difficulties, Abdominal pain, Toilet changes)—highlight that the constellation and unusual persistence of these mild gastrointestinal or urological complaints warrant thorough gynaecological and imaging investigations.
A positive human papillomavirus (HPV) test indicates that the genetic material (DNA) of HPV is present in the cervical epithelium, but this does not automatically mean cervical cancer.
A positive human papillomavirus (HPV) test indicates that the genetic material (DNA) of HPV is present in the cervical epithelium, but this does not automatically mean cervical cancer. HPV infection is extremely common among the sexually active population, and in the vast majority of cases the immune system spontaneously eliminates the virus without causing neoplastic changes. The development of cervical cancer primarily requires a persistent, long-term infection with high-risk HPV types (especially HPV16 and HPV18), which over years or decades can give rise to precancerous conditions (dysplasia, e.g., CIN2/CIN3 lesions) before progressing to invasive cancer. In the case of a positive test, the condition of the epithelium and the necessary follow-up are determined by cytology or colposcopy.
In screening programs, a positive high-risk HPV (hrHPV) result is supplemented with triage tests, such as cytology (Pap test) or genotyping, to clarify whether any cytological or histological epithelial lesion has developed.
In metastatic gastric cancer, the treatment strategy is primarily based on systemic therapies that are tailored according to molecular biomarkers (HER2, PD-L1, microsatellite instability [MSI/dMMR], and CLDN18.2).
In metastatic gastric cancer, the treatment strategy is primarily based on systemic therapies that are tailored according to molecular biomarkers (HER2, PD-L1, microsatellite instability [MSI/dMMR], and CLDN18.2). In the first-line setting, the standard backbone consists of fluoropyrimidine- and platinum-based chemotherapy combinations (such as FOLFOX, CAPOX, or SOX), which are supplemented according to biomarker status. For HER2-positive tumours, chemotherapy is combined with anti-HER2 therapy (such as trastuzumab, potentially combined with pembrolizumab); following progression, antibody-drug conjugates (ADCs) such as trastuzumab deruxtecan are considered. In the case of HER2-negative tumours showing PD-L1 positivity or high MSI, the addition of immune checkpoint inhibitors (such as nivolumab or pembrolizumab) to chemotherapy has been shown to improve survival (particularly in cases with PD-L1 CPS ≥ 5). Furthermore, in CLDN18.2-positive cases, targeted therapy incorporating agents such as zolbetuximab represents a modern option. In the second- and subsequent-line settings, common choices include paclitaxel combined with ramucirumab (an anti-VEGFR2 antibody) or ramucirumab monotherapy, as well as irinotecan-based regimens, oral tyrosine kinase inhibitors, or trifluridine/tipiracil. In selected cases (for instance, in oligometastatic disease following an excellent response to treatment), conversion surgery may be considered, and for peritoneal metastases, cytoreductive surgery and hyperthermic intraperitoneal chemotherapy (HIPEC), as well as symptomatic/palliative interventions, may also be considered.
The systemic treatment of metastatic pancreatic cancer fundamentally depends on the patient's general condition (performance status) and molecular profile.
The systemic treatment of metastatic pancreatic cancer fundamentally depends on the patient's general condition (performance status) and molecular profile.
1. First-line chemotherapy options:
In patients with good general condition (ECOG 0–1), multi-component chemotherapy combinations form the basis of care: NALIRIFOX (liposomal irinotecan, oxaliplatin, 5-fluorouracil and leucovorin), classical or modified FOLFIRINOX (5-FU, leucovorin, irinotecan, oxaliplatin), and the combination of gemcitabine plus nab-paclitaxel. In patients with poorer general condition or elderly, frail patients, gemcitabine monotherapy may represent a less toxic alternative.
2. Second-line and later therapies:
After progression on first-line therapy, switching to previously unused agents is recommended. Following gemcitabine-based treatment, the combination of liposomal irinotecan with a fluoropyrimidine (e.g., nal-IRI + 5-FU/LV), fluoropyrimidine- and oxaliplatin-based regimens (e.g., FOLFOX), or modified FOLFIRINOX can be given. After FOLFIRINOX, the combination of gemcitabine and nab-paclitaxel can be used.
3. Molecularly targeted therapies and new directions:
- For patients with homologous recombination deficiency (HRD) or germline BRCA1/2 mutations, after a favourable response to platinum-based chemotherapy, PARP inhibitor maintenance therapy (e.g., olaparib) may be considered.
- RAS/KRAS targeting: In advanced, previously treated patients, daraxonrasib (a pan-RAS/RAS[ON] inhibitor) has demonstrated a significant survival benefit compared to conventional chemotherapy.
- For rare alterations (e.g., rare BRAF mutations, RET or NTRK fusions), targeted inhibitors may be considered in specific indications or within clinical trials.
4. Supportive and local treatments:
Alongside chemotherapy, supportive and palliative care (e.g., coeliac plexus block for pain relief, enzyme substitution in case of exocrine pancreatic insufficiency) is essential, and in selected oligometastatic cases stereotactic body radiotherapy (SBRT) may also be considered.
Melanoma, basal cell carcinoma (BCC), and squamous cell carcinoma (SCC) are the three most common types of skin tumours, which fundamentally differ in their cellular origin, clinical behaviour, aggressiveness, and metas…
Melanoma, basal cell carcinoma (BCC), and squamous cell carcinoma (SCC) are the three most common types of skin malignancies, fundamentally differing in their cellular origin, clinical behaviour, aggressiveness, and metastatic potential. Melanoma originates from pigment-producing melanocytes and, although less frequent, is the most aggressive and dangerous type, as it can rapidly metastasise systemically to lymph nodes and distant organs even at an early stage. In contrast, basal cell carcinoma and squamous cell carcinoma are known as non-melanoma skin cancers (keratinocyte carcinomas). Basal cell carcinoma is the most common skin cancer; it grows slowly, can be locally invasive, but metastasises extremely rarely, resulting in negligible mortality. Squamous cell carcinoma arises from the more superficial keratinocytes of the epidermis, frequently develops from precancerous lesions (such as actinic keratosis), can be locally more aggressive than BCC, and carries a moderate potential to metastasise to regional lymph nodes and distant organs. Surgical excision is fundamental in the treatment of all three types; however, in advanced or metastatic cases, melanoma requires systemic immunotherapy or targeted therapy, whereas for unresectable BCC and SCC, specific targeted agents (such as Hedgehog inhibitors in BCC) or immunotherapy may play a role.
The cell of origin and biological characteristics of these tumours show marked differences: melanoma arises from melanocytes located in the basal layer, whereas basal cell carcinoma and squamous cell carcinoma are keratinocyte carcinomas resulting from the malignant transformation of keratinocytes. When examining matrix metalloproteinases (MMPs), it has been observed that the expression of MMP-3, MMP-9, and MMP-14 is intense in melanoma, reflecting the tumour's prominent invasiveness and angiogenesis, whereas in basal cell carcinoma, expression primarily serves local stromal remodelling, lacking metastatic potential.
In terms of incidence and prognosis, basal cell carcinoma accounts for the absolute majority of skin tumours, followed by squamous cell carcinoma, whereas melanoma is the rarer entity responsible for the highest mortality. In diagnostic and surgical approaches, dermoscopy is critical for all three to achieve clear-margin excision or Mohs surgery; in advanced tumours, melanoma frequently relies on BRAF or MEK inhibitors, as well as immune checkpoint inhibitors, whereas in extensive non-melanoma skin cancers, Hedgehog pathway inhibition or anti-PD-1 therapy represents a therapeutic option.
The treatment strategy for metastatic prostate cancer depends on the disease's hormone sensitivity (metastatic hormone-sensitive [mHSPC] or castration-resistant prostate cancer [mCRPC]), the extent of metastases (low- o…
The treatment strategy for metastatic prostate cancer depends on the disease's hormone sensitivity (metastatic hormone-sensitive [mHSPC] or castration-resistant prostate cancer [mCRPC]), the extent of metastases (low- or high-volume disease), and its molecular/genetic characteristics.
1. Metastatic hormone-sensitive prostate cancer (mHSPC):
- The cornerstone of therapy is continuous androgen deprivation therapy (ADT; GnRH agonists or antagonists, or surgical castration).
- According to current clinical guidelines, intensified combination therapy is the standard of care: combining ADT with a novel androgen receptor pathway inhibitor (ARPI: e.g., abiraterone, enzalutamide, apalutamide, darolutamide) or docetaxel chemotherapy (doublet therapy).
- In the case of high tumour volume (high-volume), triplet therapy is also frequently used (ADT + docetaxel chemotherapy + an ARPI, such as darolutamide or abiraterone).
- In low-volume, de novo metastatic disease, radiotherapy to the primary prostate tumour (PDT) improves progression-free and overall survival as an adjunct to systemic therapy.
2. Metastatic castration-resistant prostate cancer (mCRPC):
- Alongside the continuation of ADT, additional targeted ARPI therapy (abiraterone, enzalutamide) or taxane-based chemotherapy (docetaxel, or cabazitaxel in case of progression) can be administered.
- Molecular profiling (genomic testing): in tumours with homologous recombination deficiency (HRR gene mutations, particularly BRCA1/BRCA2), PARP inhibitors (e.g., olaparib, talazoparib as monotherapy or combined with an ARPI) are effective.
- Radioligand therapy: in PSMA-positive tumours that have previously received chemotherapy and ARPI therapy, radiopharmaceutical-based treatment (e.g., 177Lu-PSMA-617) may be used; in exclusively bone-metastatic, symptomatic cases, radium-223 is also an option.
3. Local and supportive treatments:
- In oligometastatic disease, stereotactic body radiotherapy directed to metastases (MDT) can be considered, as well as the use of bone-protective agents (bisphosphonates, denosumab) to prevent skeletal-related events.
Melanoma is a malignant skin tumour arising from melanocytes, the early detection of which is of critical importance for successful treatment.
Melanoma is a malignant skin tumour arising from melanocytes, the early detection of which is of critical importance for successful treatment. The most widespread clinical and self-examination tool for identifying suspicious skin lesions and naevi is the so-called ABCDE rule. This acronym designates the following clinical warning signs: "A" (Asymmetry): one half of the lesion does not match the other in shape; "B" (Border): the borders are irregular, scalloped, or blurred; "C" (Color): the pigmentation is uneven, exhibiting multiple shades (shades of brown, black, reddish, bluish, or white areas); "D" (Diameter): the diameter of the lesion exceeds 6 millimetres (although early or small-diameter melanomas may be smaller than this); "E" (Evolution): rapid or gradual changes in the size, shape, or colour of the lesion, or newly emerging symptoms (such as elevation, itching, or bleeding). In clinical practice, the accuracy of the diagnosis is ensured by dermatoscopy and specialist examination, and, in cases of suspicion, by histological excision.
The ABCDE criteria system is a triage tool developed for naked-eye examination, which is applied in conjunction with the "ugly duckling" sign and dermatoscopic analysis. According to literature data, morphological change occurring over several months or weeks (Evolution) and colour variegation possess prominent predictive value in differentiating a malignant process, whereas in the case of nodular melanomas, the EFG rule (Elevation, Firm, Growing) serves as an additional criterion assisting early identification.
In most cases, early-stage prostate cancer is completely asymptomatic and is often detected only through an elevated PSA (prostate-specific antigen) level during screening or via physical examination.
In most cases, early-stage prostate cancer is completely asymptomatic and is often detected only through an elevated PSA (prostate-specific antigen) level during screening or via physical examination. When symptoms do occur—for example, due to tumor growth and urethral compression—they manifest as lower urinary tract symptoms (LUTS). These include difficulty or hesitancy in initiating urination, a weak or interrupted urinary stream, post-micturition dribbling, increased urinary frequency (especially at night, i.e., nocturia), sudden urinary urgency, or a sensation of incomplete bladder emptying. Additional symptoms may include blood in the urine (hematuria), and less frequently, blood in the semen or erectile dysfunction. Because these identical symptoms are also characteristic of benign prostatic hyperplasia (BPH) and prostatitis, the symptoms alone do not provide a definitive diagnosis, thus requiring urological evaluation (PSA test, physical examination, and imaging).\n\nThe evaluation of lower urinary tract symptoms (LUTS) coded in primary care, macroscopic or microscopic hematuria, and newly onset erectile dysfunction is significantly associated with the detection of clinically significant prostate cancer.\n\nDuring urological investigations, specific urinary complaints such as nocturia (nighttime urination), urge incontinence, and post-micturition dribbling have shown a statistically significant correlation with the presence of histologically confirmed malignant prostate tumors.
During its dissemination, breast cancer can produce regional lymph node metastases and distant metastases.
During its dissemination, breast cancer can produce regional lymph node metastases and distant metastases. In terms of distant metastases, the most frequently affected organs are the bones, lungs, liver, and central nervous system (brain); in addition, among regional lymph nodes, involvement of the axillary lymph nodes is the most common. Less frequently, it may also metastasize to other sites, such as the gastrointestinal tract, peritoneum, ovaries, or thyroid gland.\n\nAccording to summaries of the clinical literature, the most common distant targets of breast cancer are the bones, lungs, liver, and brain (pmid:41835638, pmid:41025019, pmid:40698488). Bone metastasis occurs in a significant proportion of patients, and the bone microenvironment provides favorable conditions for cellular colonization (pmid:42591313, pmid:40749014). Furthermore, the early and primary metastatic pathway of breast cancer leads toward regional, particularly axillary, lymph nodes (pmid:42370387, pmid:41752719).\n\nCertain histological subtypes, such as invasive lobular carcinoma (ILC), can also exhibit distinctive and less common organ distributions, including the gastrointestinal tract, peritoneum, as well as the ovaries and gynecological organs (pmid:42298254, pmid:42449801, pmid:39829946). Additionally, metastases have been sporadically described in the thyroid gland (pmid:42266215), urinary bladder (pmid:41835638), as well as the optic nerve and ocular tissues (pmid:41080317, pmid:41378304).
The treatment strategy for metastatic breast cancer fundamentally depends on the molecular subtype of the tumour (hormone receptor status, HER2 status, and specific genetic mutations), as systemic therapy is the corners…
The treatment strategy for metastatic breast cancer fundamentally depends on the molecular subtype of the tumour (hormone receptor status, HER2 status, and specific genetic mutations), as systemic therapy is the cornerstone of managing the disease.
In hormone receptor-positive (HR+), HER2-negative breast cancer, the first-line standard of care is endocrine therapy (such as an aromatase inhibitor or fulvestrant) combined with cyclin-dependent kinase 4/6 (CDK4/6) inhibitors (e.g. ribociclib, palbociclib, abemaciclib), which significantly improves progression-free and overall survival. When resistance develops, targeted agents can be administered based on molecular testing (tissue or liquid biopsy ctDNA): in the presence of an ESR1 mutation, next-generation oral selective estrogen receptor degraders (SERDs, e.g. elacestrant), whereas when the PI3K/AKT/PTEN pathway is altered, combinations involving PI3K or AKT inhibitors (e.g. alpelisib, capivasertib, inavolisib) are recommended.
In HER2-positive metastatic breast cancer, dual HER2 blockade (trastuzumab and pertuzumab) combined with chemotherapy was the standard for decades; however, antibody-drug conjugates (ADCs), particularly trastuzumab deruxtecan (T-DXd) or trastuzumab emtansine (T-DM1), as well as newer tyrosine kinase inhibitors (e.g. tucatinib), have revolutionised treatment both in the first-line setting and following progression. Furthermore, T-DXd has also proven effective in HER2-low (showing low HER2 expression) tumours.
In triple-negative breast cancer (TNBC) and in later treatment lines, alongside conventional cytotoxic chemotherapy, immunotherapy (immune checkpoint inhibitors, e.g. pembrolizumab in the case of PD-L1 positivity), PARP inhibitors in the presence of a germline BRCA mutation, and antibody-drug conjugates targeting TROP-2 (e.g. sacituzumab govitecan, datopotamab deruxtecan) offer targeted treatment alternatives.
The role of local therapies (such as breast surgery or radiotherapy) in metastatic breast cancer is primarily limited to symptom relief and palliative purposes; routine resection of the primary tumour has not been proven to improve overall survival compared with comprehensive systemic therapy, but in oligometastatic or oligoprogressive cases, local ablative treatments may be considered to maintain systemic control.
Yes, stage IV lung cancer is treatable. Although stage IV (metastatic) disease is generally not permanently curable according to current medical consensus, with modern oncological therapies the disease can often be cont…
Yes, stage IV lung cancer is treatable. Although stage IV (metastatic) disease is generally not permanently curable according to current medical consensus, with modern oncological therapies the disease can often be controlled over the long term, quality of life can be improved, and survival can be significantly prolonged. The treatment strategy depends on the histological subtype (non-small cell lung cancer [NSCLC] or small cell lung cancer [SCLC]) and molecular profiling (biomarkers).
In the case of non-small cell lung cancer (NSCLC), targeted therapies (such as EGFR tyrosine kinase inhibitors or ALK inhibitors) can be used based on targets identified during molecular testing, providing a significant survival benefit for patients harbouring mutations. In the absence of driver mutations, PD-1/PD-L1 inhibitor immunotherapies alone (in the setting of high PD-L1 expression) or combined with chemotherapy constitute the first-line standard of care.
In extensive-stage small cell lung cancer (ES-SCLC), the cornerstone of first-line therapy is the combination of platinum-based chemotherapy and immunotherapy, supplemented by next-generation bispecific T-cell engagers or other systemic options following progression.
Systemic treatments can be complemented by supportive and palliative care, as well as targeted radiotherapy and local interventions for oligometastatic or symptomatic lesions, facilitating symptom relief and the safe continuation of active treatments.
Small cell lung cancer (SCLC) and non-small cell lung cancer (NSCLC) are the two primary histological and biological categories of lung malignancies, which fundamentally differ in their biological behaviour, incidence r…
Small cell lung cancer (SCLC) and non-small cell lung cancer (NSCLC) are the two primary histological and biological categories of lung malignancies, which differ fundamentally in their biological behaviour, incidence rates, and therapeutic approaches. Non-small cell lung cancer accounts for approximately 85% of all lung cancer cases and is subdivided mainly into adenocarcinoma, squamous cell carcinoma, and large cell carcinoma, whereas small cell lung cancer is a less common type exhibiting neuroendocrine characteristics. NSCLC may have a slower growth rate, surgical resection represents an essential curative treatment modality in its early stages, and in its advanced forms, targeted therapies based on molecular genetic alterations (such as EGFR, ALK, KRAS, ROS1) and immunotherapies constitute the cornerstones of management. In contrast, SCLC is biologically markedly aggressive, possesses an extremely rapid doubling time, and in the vast majority of patients at the time of diagnosis, early micrometastases or widespread distant metastases are already present, which is why primary surgical management is very rarely indicated. The standard management of SCLC is systemic in nature: a combination of chemotherapy and immunotherapy, alongside radiotherapy, forms its backbone; this may initially demonstrate a good tumour response, but rapid recurrence and treatment resistance frequently develop. Furthermore, differences are also observed in the therapeutic toxicity profiles of the two histological types; for instance, in the context of antibody-drug conjugate (ADC) administration, the rate of overall pulmonary adverse events is higher in small cell lung cancer, whereas pneumonitis is more common in NSCLC.
During systemic treatments, including the administration of antibody-drug conjugates (ADCs), it has been demonstrated that the distribution of pulmonary adverse events differs between the two entities: in small cell lung cancer, any-grade pulmonary adverse events are significantly more frequent (52.1% vs. 22.5%), whereas in non-small cell lung cancer, the incidence of pneumonitis is higher (12.1% vs. 2.8%). Furthermore, during the treatment of EGFR-mutant non-small cell lung cancers with tyrosine kinase inhibitors (TKIs), transformation into small cell lung cancer (T-SCLC) may also occur as an acquired resistance mechanism, which entails an altered immune microenvironment and the necessity of therapeutic modification.
Breast cancer metastasis can manifest as locoregional lymph node spread, as well as hematogenous or lymphogenous dissemination affecting distant organs.
Breast cancer metastasis can manifest as locoregional lymph node spread, as well as hematogenous or lymphogenous dissemination affecting distant organs. The most commonly affected distant target organs are the bones, lungs, liver, and central nervous system (brain). The pattern of metastasis depends significantly on the molecular subtype and histology of the tumor: hormone receptor-positive (ER+) tumors metastasize to the bone with notable frequency, whereas HER2-positive and triple-negative breast cancers are more prone to visceral metastases (liver, lungs) as well as the formation of brain metastases. In addition to these classic targets, breast cancer—particularly the invasive lobular carcinoma (ILC) subtype—can also metastasize to rarer sites, such as the peritoneum, ovaries, uterus/cervix, gastrointestinal tract, eyelid/orbit, or thyroid.
The most common regional metastatic targets are the axillary and supraclavicular lymph node chains. During systemic dissemination, the tumor most frequently affects the skeleton (bone involvement occurs in approximately 70% of metastatic cases, most commonly in the spine, ribs, and pelvis), followed by lung, liver, and brain metastases.
Histological and molecular subtypes display distinct tropisms: while ductal carcinomas tend to spread to the bones and lungs, invasive lobular carcinomas, due to their infiltrative nature resulting from the loss of E-cadherin, can also disseminate to the peritoneum, retroperitoneum, ovaries, uterus, or the gastrointestinal tract.